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Hassebo, et al., J Gen Pract 2015, 3:3
http://dx.doi.org/10.4172/2329-9126.1000196
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ISSN: 2329-9126
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Correlation between P Wave Dispersion, QRS Duration and QT Dispersion
in Hospital Events in Cases of Acute Coronary Syndrome
Mohmoud Ferky Hassan Hassebo2*, Muhammad Nasr eldin El Sayed1, Mohamed Mostafa Abd El Salam Megahed1 and Tarek Hussein El
Badawy1
1
2
Department of Cardiology & Angiology, Alexandria University, Egypt
Department of Critical Care Medicine, Alexandria University, Egypt
Abstract
Background: The acute coronary syndromes encompass a spectrum of unstable angina to trans-mural myocardial infarction.
The definition of acute coronary syndrome depends on the specific characteristics of each element of the triad of clinical presentation,
electrocardiographic changes and biochemical cardiac markers.
Objectives: To assess Correlation between P wave dispersion, QRS duration and QT dispersion in hospital events in patients
with Acute Coronary Syndrome [ACS].
Methods: This prospective study was conducted on 60 patients with acute coronary syndrome admitted to critical care units of
Alexandria University Hospitals from first of January 2012 to end of August 2012. An informed consent was taken from relatives of
every patient included in the study. This study was approved by ethical committee of Alexandria Faculty of Medicine.
Results: During the observation up to 5 days, 1 patient [1.6%] developed AF. There was no significant correlation between P
wave Dispersion [PD] in the three studied groups and No significant relation between its and the whole complications developed
in failed thrombolysis group [p>0.05]. PD alone couldn’t predict AF in this study, as the mean was 20.0 milliseconds, which was
too small to predict AF alone.There was no significance difference between QRS duration in the three groups [unstable angina,
successful thrombolysis and failed thrombolysis respectively with mean value [75.7 ± 14.02, 75.2 ± 10.88, 73.36 ± 8.81] [p>0.05]
and the relationship between the QRS duration and the development of complications was non-significant in this study. This study
showed that there was a significant relation among the three groups and highly significant correlation between QTD duration and
prediction of complications. It was clear that ICU length of stay was longer in patients with failed thrombolysis in comparison with the
other two groups [p<0.05].
Conclusions: Importance of measurements of QT Dispersion to patients with acute coronary syndrome especially at admission.
Failed thrombolysis patients should be under close observation and Monitoring till another option is available like coronary
intervention.
Abbreviations:
ACS: Acute Coronary Syndrome; ACUITY: Acute Catheterization
and Urgent Intervention Triage Strategy; AF: Atrial Fibrillation; AHA:
American Heart Association; AMI: Acute Myocardial Infarction; BBB:
Bundle Branch Block; CAD: Coronary Artery Disease; CHF: Congestive
Heart Failure; DM: Diabetes Mellitus; ECG: Electrocardiogram;
HTN: Hypertension; LMWH: Low Molecular Weight Heparin; MI:
Myocardial Infarction; ms: Mill Second; NSTEMI: Non–ST-Segment
Elevation Myocardial Infarction; PCI: Percutaneous Coronary
Intervention; PPIs: Proton Pump Inhibitors; PWD: P Wave Dispersion;
QTD: QT Dispersion; WPW: Wolff-Parkinson-White syndrome
Introduction
Acute Coronary Syndrome [ACS] refers to a spectrum of clinical
presentations ranging from those for ST-Segment Elevation Myocardial
Infarction [STEMI] to presentations found in Non–ST-segment
Elevation Myocardial Infarction [NSTEMI] or in unstable angina. In
terms of pathology, ACS is almost always associated with rupture of
an atherosclerotic plaque and partial or complete thrombosis of the
infarct-related artery.
In some instances, however, stable Coronary Artery Disease [CAD]
may result in ACS in the absence of plaque rupture and thrombosis,
when physiologic stress [e.g, trauma, blood loss, anemia, infection,
and tachyarrhythmia] increases demands on the heart. The diagnosis
of acute myocardial infarction in this setting requires a finding of the
typical rise and fall of biochemical markers of myocardial necrosis in
addition to at least one of the following [1]:
•
Ischemic symptoms
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
•
Development of pathologic Q waves
•
Ischemic ST-segment changes on Electrocardiogram [ECG]
or in the setting of a coronary intervention
The terms transmural and non-transmural [sub-endocardial]
myocardial infarction are no longer used because ECG findings in
patients with this condition are not closely correlated with pathologic
changes in the myocardium. Therefore, a transmural infarct may occur
in the absence of Q waves on ECGs, and many Q-wave myocardial
infarctions may be sub endocardial, as noted on pathologic examination.
Because elevation of the ST segment during ACS is correlated with
coronary occlusion and because it affects the choice of therapy [urgent
reperfusion therapy], ACS-related myocardial infarction should be
designated STEMI or NSTEMI.
In 2010, the American Heart Association [AHA] published new
*Corresponding author: Mohmoud Ferky Hassan Hassebo, Department of
Critical Care Medicine, Alexandria University, Iran, E-mail: mahmoudhassebo@
yahoo.com
Received August 06, 2015; Accepted August 08, 2015; Published August 11,
2015
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015)
Correlation between P Wave Dispersion, QRS Duration and QT Dispersion in
Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi:
10.4172/2329-9126.1000196
Copyright: © 2015 Hassebo MFH, et al. This is an open-access article distributed
under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the
original author and source are credited.
Volume 3 • Issue 3 • 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 2 of 22
guideline recommendations for the diagnosis and treatment of ACS.
Acute Coronary Syndrome [ACS] is caused primarily by
atherosclerosis. Most cases of ACS occur from disruption of a previously
non severe lesion [an atherosclerotic lesion that was previously hemodynamically insignificant yet vulnerable to rupture]. The vulnerable
plaque is typified by a large lipid pool, numerous inflammatory cells
and a thin fibrous cap.
Elevated demand can produce ACS in the presence of a highgrade fixed coronary obstruction, due to increased myocardial oxygen
and nutrition requirements, such as those resulting from exertion,
emotional stress, or physiologic stress [e.g., from dehydration, blood
loss, hypotension, infection, thyrotoxicosis, or surgery].
ACS without elevation in demand requires a new impairment in
supply, typically due to thrombosis and/or plaque hemorrhage.
A syndrome consisting of chest pain, ischemic ST-segment and
T-wave changes, elevated levels of biomarkers of myocyte injury, and
transient left ventricular apical ballooning [takotsubo syndrome] has
been shown to occur in the absence of clinical CAD, after emotional or
physical stress. The etiology of this syndrome is not well understood but
is thought to relate to a surge of catechol stress hormones and/or high
sensitivity to those hormones.
The severity and duration of coronary artery obstruction, the
volume of myocardium affected, the level of demand, and the ability of
the rest of the heart to compensate are major determinants of a patient’s
clinical presentation and outcome. A patient may present to the ED
because of a change in pattern or severity of symptoms.
Typically, angina is a symptom of myocardial ischemia that appears
in circumstances of increased oxygen demand. It is usually described
as a sensation of chest pressure or heaviness that is reproduced by
activities or conditions that increase myocardial oxygen demand. A
new case of angina is more difficult to diagnose because symptoms
are often vague and similar to those caused by other conditions [eg,
indigestion, anxiety] [1].
Clinical presentation
A summary of patient complaints is as follows:
•
Palpitations, Pain, which is usually described as pressure,
squeezing, or a burning sensation across the precordium and may
radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm
•
Exceptional dyspnea that resolves with pain or rest
•
Diaphoresis from sympathetic discharge
•
Nausea from vagal stimulation
•
Decreased exercise tolerance
Stable angina involves episodic pain lasting 5-15 minutes, is
provoked by exertion, and is relieved by rest or nitroglycerin. In
unstable angina, patients have increased risk for adverse cardiac events,
such as myocardial infarction or death. New-onset exertion angina can
occur at rest and is of increasing frequency or duration or is refractory
to nitroglycerin. Variant angina [Prinzmetal angina] occurs primarily
at rest, is triggered by smoking, and is thought to be due to coronary
vasospasm.Increasing public awareness of the typical and atypical
presentations of ACS is of the utmost importance for optimal and
timely treatment. Many patients do not recognize that their symptoms
are cardiac in origin and therefore may delay seeking medical help.
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
Guidelines from the European Society of Cardiology [ESC]/American
College of Cardiology [ACC]/American Heart Association [AHA]
recommend that patients with established CAD call emergency medical
services if they have chest pain that does not resolve after they take a
sublingual nitroglycerin tablet.
Diagnosis
As previously mentioned, stable Coronary Artery Disease [CAD]
may result in ACS in the absence of plaque rupture and thrombosis,
when physiologic stress [e.g., trauma, blood loss, anemia, infection,
tachyarrhythmias] increases demands on the heart. In such cases, the
diagnosis of acute myocardial infarction can be made if workup reveals
the typical rise and fall of biochemical markers of myocardial necrosis
along with either the development of pathologic Q waves or the presence
[on ECG or in the setting of a coronary intervention] of ischemic STsegment changes. [However, the presence of ischemic symptoms can be
substituted for the Q-wave or ST-segment evidence.] [1-4].
Non–ST-Segment Elevation Myocardial Infarction [NSTEMI] is
distinguished from unstable angina by elevated levels of cardiac enzymes
and biomarkers of myocyte necrosis. Differentiation is generally based
on three sets of biomarkers measured at 6- to 8-hour intervals after the
patient’s presentation to the ED. The current definition of NSTEMI
requires a typical clinical syndrome plus elevated troponin [or creatine
kinase isoenzyme MB [CK-MB]] levels to over 99% of the normal
reference [with a coefficient of variation of <10% for the assay]. Given
this definition, nearly 25% of patients who were previously classified as
having unstable angina now fulfill the criteria for NSTEMI.
Measure cardiac enzyme levels at regular intervals, starting at
admission and continuing until the peak is reached or until 3 sets of
results are negative. Biochemical biomarkers are useful for diagnosis
and prognostication.
Of note, cardiac-specific troponins are not detectable in the blood
of healthy individuals; therefore, they provide high specificity for
detecting injury to cardiac myocytes. These molecules are also more
sensitive than CK-MB for myocardial necrosis and therefore improve
early detection of small myocardial infarctions. Although blood
troponin levels increase simultaneously with CK-MB levels [about 6 h
after the onset of infarction], they remain elevated for as long as 2 weeks.
As a result, troponin values cannot be used to diagnose reinfarction.
New methods of detecting troponins in the blood can measure levels as
low as 0.1-0.2 ng/mL.
Minor elevations in these molecules can be detected in the blood of
patients without ACS in the setting of myocarditis [pericarditis], sepsis,
renal failure, acute Congestive Heart Failure [CHF], acute pulmonary
embolism, or prolonged tachyarrhythmias.
Guidelines released by the European Society of Cardiology [ESC]
in August 2011 for the management of non-ST-segment elevation ACSs
recommend a scoring system to score the risk of an ischemic event in
the short-to-midterm. The guidelines state that bleeding risk can be
stratified using the CRUSADE [Can Rapid risk stratification of Unstable
angina patients Suppress Adverse outcomes with Early implementation
of the ACC/AHA guidelines] risk score [5].
Electrocardiography: ECGs should be reviewed promptly. Involve a
cardiologist when in doubt. Recording an ECG during an episode of the
presenting symptoms is valuable. Transient ST-segment changes [>0.05
mV] that develop during a symptomatic period and that resolve when
the symptoms do are strongly predictive of underlying CAD and have
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 3 of 22
prognostic value. Comparison with previous ECGs is often helpful.
In the emergency setting, ECG is the most important ED diagnostic
test for angina. It may show changes during symptoms and in response
to treatment, confirm a cardiac basis for symptoms. It also may
demonstrate preexisting structural or ischemic heart disease [left
ventricular hypertrophy, Q waves]. A normal ECG or one that remains
unchanged from the baseline does not exclude the possibility that chest
pain is ischemic in origin. Changes that may be seen during anginal
episodes include the following:
•
Transient ST-segment elevations
•
Dynamic T-wave changes - Inversions, normalizations, or
hyperacute changes
•
ST depressions - May be junctional, downsloping, or
horizontal
In patients with transient ST-segment elevations, consider LV
aneurysm, pericarditis, Prinzmetal angina, early repolarization, and
Wolff-Parkinson-White syndrome as possible diagnoses. Fixed changes
suggest acute myocardial infarction.
Diagnostic sensitivity may be increased by performing right-sided
leads [V4 R], posterior leads [V8, V9], and serial recordings.
Measurement of CK-MB levels: CK-MB, the iso enzyme specific to
the heart muscle, was the principal biomarker of cardiac injury until
troponin supplemented it. In the setting of myocardial infarction,
plasma CK-MB concentrations typically rise about 4-6 hours after the
onset of chest pain. They peak within 12-24 hours and return to baseline
levels within 24-48 hours. Serial measurements obtained every 6-8
hours [at least 3 times] are warranted until peak values are determined.
Measurement of troponin levels: The cardiac troponins are
sensitive, cardio specific, and provide prognostic information for
patients with ACS. They have become the cardiac markers of choice
for patients with ACS. Initial studies on the cardiac troponins revealed
a subset of patients with rest unstable angina in whom CK-MB levels
were normal but who had elevated troponin levels. These patients had
higher adverse cardiac event rates [acute myocardial infarction, death]
within the 30 days after the index admission and a natural history that
closely resembled patients with NSTEMI.As previously mentioned an
elevated troponin level also enables risk stratification of patients with
ACS and identifies patients at high risk for adverse cardiac events [i.e,
myocardial infarction, death] up to 6 months after the index event [3,4].
In a study by Antman et al. [3], the initial TnI level on admission in
patients with ACS correlated with mortality at 6 weeks. CK-MB levels,
although sensitive and specific for the diagnosis of acute myocardial
infarction, were not predictive of adverse cardiac events and had no
prognostic value.
The 2007 American College of Cardiology [ACC] guidelines for
NSTEMI recommend that serial troponins be obtained for a definitive
rule out at baseline and 6-9 hours later. To establish the diagnosis of
acute myocardial infarction, only 1 elevated level above the established
cutoff is required. The demonstration of a rising or falling level is
needed to distinguish persistently elevated troponin levels [eg, in some
patients with renal failure] from those patients with acute myocardial
infarction [6].
If myocardial injury is suspected despite negative cardiac-specific
troponin findings, additional, sensitive laboratory assays are indicated
[7].
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
Measurement of myoglobin level: Myoglobin is not cardiac specific,
but it may be detected as early as 2 hours after myocardial necrosis
starts. However, myoglobin results should be supplemented with other,
more specific cardiac biomarkers, such as CK-MB or troponin.
Myoglobin values have a high negative predictive value when blood
is sampled in the first 4-8 hours after onset.
Complete blood count determination: The CBC count helps in
ruling out anemia as a secondary cause of ACS. Leukocytosis has
prognostic value in the setting of acute myocardial infarction.
Basic metabolic panel: Obtain a basic metabolic profile, including
a check of blood glucose level, renal function, and electrolytes levels
for patients with new-onset angina. Close monitoring of potassium and
magnesium levels is important in patients with ACS because low levels
may predispose them to ventricular arrhythmias. Routine measurement
of serum potassium levels and prompt correction are recommended.
Creatinine levels must be considered before using an AngiotensinConverting Enzyme [ACE] inhibitor and particularly if cardiac
catheterization is considered. Use of N-acetylcysteine and adequate
hydration can help prevent contrast material–induced nephropathy [8].
A study by Charpentier et al. [9] suggests that a serum glucose level
of more than 140 mg/dL is associated with non-ST elevation ACS in
patients admitted to an ED for chest pain. However, when this level of
blood glucose is added to the conventional diagnostic tools, the result is
only a small increase in the ability to classify ACS.
New biomarkers: Levels of brain natriuretic peptide [BNP]
and N-terminal pro-BNP [NT-pro-BNP] are elevated in acute MI
and provide predictive information for risk stratification across the
spectrum of ACS [10,11].
Cavusoqlu et al. [12] suggests that elevated baseline levels of plasma
interleukin-10 are associated with long-term adverse outcomes in
patients with ACS.
Chest radiography: Chest radiography helps in assessing
cardiomegaly or it may reveal complications of ischemia, such as
pulmonary edema. It may also provide clues to alternative causes of
symptoms, such as thoracic aneurysm or pneumonia [which can be a
precipitating cause of ACS].
Echocardiography: Echocardiograms may play an important
role in the setting of ACS. Regional wall-motion abnormalities can
be identified with this modality, and echocardiograms are especially
helpful if the diagnosis is questionable.
An echocardiogram can also help in defining the extent of an
infarction and in assessing overall function of the left and right ventricles.
In addition, an echocardiogram can help to identify complications,
such as acute mitral regurgitation, LV rupture, and pericardial effusion.
Absence of segmental wall-motion abnormality on echocardiography
during active chest discomfort is a highly reliable indicator of a
nonischemic origin of symptoms, although echocardiography is of
limited value in patients whose symptoms have resolved or who have
pre-existing wall-motion abnormalities.
Myocardial perfusion imaging: A normal resting perfusion
imaging study has been shown to have a negative predictive value of
more than 99% in excluding myocardial infarction. Observational and
randomized trials of rest and stress imaging in the ED evaluation of
patients with chest pain have demonstrated reductions in unnecessary
hospitalizations and cost savings compared with routine care.
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 4 of 22
Perfusion imaging has also been used in risk stratification after
myocardial infarction and for measurement of infarct size to evaluate
reperfusion therapies. Novel “hot spot” imaging radiopharmaceuticals
that visualize infarction or ischemia are currently undergoing evaluation
and hold promise for future imaging of ACS.
Cardiac angiography: For high-risk patients with ACS without
persistent ST elevation, angiography with glycoprotein IIb/IIIa
inhibition has been recommended. The earlier that coronary
angiography is performed, the lower the risk of recurrent ischemia [13].
This also shortens the hospital stay for those patients.
Computed tomography coronary angiography and CT coronary
artery calcium scoring: CT coronary artery scoring is emerging as an
attractive risk stratification tool in patients who are low risk for ACS.
This imaging modality exposes the patient to very little radiation [1-2
msV]. No contrast is needed, and the study does not have a requirement
for heart rate [14].
Other techniques
Optical coherence tomography [OCT], palpography, and virtual
histology are being studied for use in identifying vulnerable plaques.
Noninvasive whole-blood test prior to coronary angioplasty may be
useful for assessing obstructive CAD in patients without diabetes [15].
Stress cardiac magnetic resonance imaging [MRI] in an observation
unit setting has shown to reduce the medical costs, compared with
inpatient care, for patients who present with emergent, non-low-risk
chest pain, without missing acute coronary syndrome [16].
Diagnostic Consideration [D.D].
In patients presenting to the ED with chest pain, a structured
diagnostic approach that includes time-focused ED decision points,
brief observation, and selective application of early outpatient
provocative testing appeared both safe and diagnostically efficient in a
study by Scheuermeyer et al. [5] However, some patients with ACS may
be discharged for outpatient stress testing on the index ED visit.
Differentials
•
Anxiety
•
Aortic Stenosis
•
Asthma
•
Esophagitis
•
Gastroenteritis
•
Hypertensive Emergencies in Emergency Medicine
•
Myocardial Infarction
•
Myocarditis
•
Pericarditis and Cardiac Tamponade.
•
Cardiomyopathy, Dilated
Treatment
Attention to the underlying mechanisms of ischemia is important
when managing ACS. A simple predictor of demand is rate-pressure
product, which can be lowered by beta blockers [eg, metoprolol or
atenolol] and pain/stress relievers [eg, morphine], while supply may
be improved by oxygen, adequate hematocrit, blood thinners [eg,
heparin, IIb/IIIa agents such as abciximab, eptifibatide, tirofiban, or
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
thrombolytics], and/or vasodilators [eg, nitrates, amlodipine].
Approach consideration
Initial therapy for acute coronary syndrome should focus on
stabilizing the patient’s condition, relieving ischemic pain, and
providing antithrombotic therapy to reduce myocardial damage and
prevent further ischemia. Morphine [or fentanyl] for pain control,
oxygen, sublingual and/or IV nitroglycerin, soluble aspirin 162-325
mg, and clopidogrel with a 300- to 600-mg loading dose are given as
initial treatment.
In complete vessel occlusion without collateralization of the infarctrelated vessel, there is little utility in “pushing nitrates.”
High-risk patients with non-ST-segment elevation myocardial
infarction [NSTEMI ACS] should receive aggressive care, including
aspirin, clopidogrel, unfractionated heparin or low–molecular weight
heparin [LMWH], intravenous platelet glycoprotein IIb/IIIa complex
blockers [eg, tirofiban, eptifibatide], and a beta blocker. The goal is early
revascularization.
Intermediate-risk patients with NSTEMI ACS should rapidly
undergo diagnostic evaluation and further assessment to determine
their appropriate risk category.
Low-risk patients with NSTEMI ACS should undergo further
follow-up with biomarkers and clinical assessment. Optimal medical
therapies include use of standard medical therapies, including
beta blockers, aspirin, and unfractionated heparin or LMWH. The
Clopidogrel in Unstable Angina to Prevent Recurrent Events [CURE]
study showed that clopidogrel would be beneficial even in low-risk
patients [17].
Patients presenting with cardiogenic shock should undergo
percutaneous coronary intervention [PCI] as soon as possible.
Cardiogenic shock is associated with a high mortality rate. Pressor
agents, such as dopamine, and inotropic agents, such as dobutamine,
may be needed.
Pharmacologic ant ischemic therapy
Nitrates: Nitrates do not improve mortality [18]. However, they
provide symptomatic relief by means of several mechanisms, including
coronary vasodilation, improved collateral blood flow, decrease in
preload [venodilation and reduced venous return], and decrease
in afterload [arterial vasodilation]. Care should be taken to avoid
hypotension, because this can potentially reduce coronary perfusion
pressure [diastolic BP - LV diastolic pressure].
. Beta-blockers: Beta-blockers are indicated in all patients unless
they have the following contraindications:
yy
Systolic blood pressure less than 90 mm Hg
yy
Cardiogenic shock
yy
Severe bradycardia
yy
Second- or third-degree heart block
yy
Asthma or emphysema that is sensitive to beta agonists
yy
Peripheral vascular disease
yy
Uncompensated CHF
Pharmacologic antithrombotic therapy
Aspirin: Aspirin permanently impairs the cyclooxygenase pathway
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 5 of 22
of thromboxane A2 production in platelets, in this way inhibiting
platelet function. Aspirin reduces morbidity and mortality and is
continued indefinitely [19].
Clopidogrel: Clopidogrel [thienopyridine] inhibits adenosine
5’-diphosphate [ADP]–dependent activation of the glycoprotein IIb/
IIIa complex, a necessary step for platelet aggregation. This process
results in intense inhibition of platelet function, particularly in
combination with aspirin. In the CURE trial, thienopyridine reduced
the rate of myocardial infarction by 20% [17].
Clopidogrel is a class I recommendation for patients when an early
noninterventional approach is planned in therapy for at least 1 month
and ideally up to 1 year. When percutaneous coronary intervention
[PCI] is planned, clopidogrel 300-600 mg should be given as early
as possible before or at the time of PCI. Clopidogrel, 75 mg daily, is
continued for at least 12 months after PCI, if the patient is not at high
risk for bleeding, according to 2011 ACCF/AHA guidelines [class I
recommendation] [20].
Clopidogrel can be considered an alternative to aspirin in patients
with aspirin intolerance or who are allergic to aspirin.
The group’s findings and recommendations are listed below:
yy Clopidogrel reduces major CV events compared with placebo or
aspirin.
yy Dual antiplatelet therapy with clopidogrel and aspirin, compared
with aspirin alone, reduces major CV events in patients with
established ischemic heart disease, and it reduces coronary stent
thrombosis but is not routinely recommended for patients with
prior ischemic stroke because of the risk of bleeding [21].
yy Clopidogrel alone, aspirin alone, and their combination are all
associated with increased risk of GI bleeding.
Clopidogrel requires metabolic activation by cytochrome P450 2C19
[CYP2C19]. PPIs that inhibit CYP2C19 are commonly co administered
with clopidogrel to reduce the risk of GI bleeding. A study by Simon
et al. showed that PPI use is not associated with an increased risk of
cardiovascular events or mortality in patients who have been treated
with clopidogrel for a recent MI, regardless of CYP2C19 genotype [22].
Prasugrel: Like clopidogrel, prasugrel is a thienopyridine ADP
receptor inhibitor that inhibits platelet aggregation. It has been
approved in the United States and has been shown to reduce new and
recurrent myocardial infarctions[23].
Ticagrelor: Ticagrelor [Brilinta] was approved by the US Food and
Drug Administration in July 2011 and is the first reversible oral P2Y
receptor antagonist. Results from the platelet inhibition and patient
outcomes [PLATO] trial showed ticagrelor provides faster, greater, and
more consistent ADP-receptor inhibition than clopidogrel [24].
Abciximab, eptifibatide, and tirofiban: Glycoprotein IIb/IIIa
receptor antagonists include abciximab [25,26], eptifibatide [27] , and
tirofiban [28] . These drugs inhibit the glycoprotein IIb/IIIa receptor,
which is involved in the final common pathway for platelet adhesion
and aggregation.
Pharmacologic anticoagulation therapy
Un-fractionated heparin: A study by Oler et al. [29] found
that unfractionated heparin was associated with a 33% reduction in
the risk of myocardial infarction or death in patients with unstable
angina who were treated with aspirin plus heparin, compared with
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
patients who were treated with aspirin alone. The FUTURA/OASIS-8
randomized trial found that low-dose unfractionated heparin, 50 U/kg
[regardless of use of glycoprotein IIb/IIIa inhibitors], compared with
standard-dose unfractionated heparin, 85 U/kg [60 U/kg with Gp IIb/
IIIa inhibitors], did not reduce major peri-PCI bleeding and vascular
access-site complications [30].
Low-molecular-weight heparin: LMWHs might be superior to
unfractionated heparin in reducing cardiovascular outcomes, with a
safety profile similar to that of heparin in patients receiving medical
care.
Aside from the possible medical benefits of using LMWH in place
of unfractionated heparin, advantages of LMWH include ease of
administration, absence of need for anticoagulation monitoring, and
potential for overall cost savings. Although 3 LMWHs are approved for
use in the United States, only enoxaparin is currently approved for use in
unstable angina. Lev et al. [31] found that the combination of eptifibatide
with enoxaparin appears to have a more potent antithrombotic effect
than that of eptifibatide and unfractionated heparin.
Factor Xa inhibitors: Use of the oral Xa inhibitor, rivaroxaban
[Xarelto], in addition to dual antiplatelet therapy in patients with ACS
was recently investigated in the ATLAS ACS2-TIMI 51 trial. Low-dose
rivaroxaban [2.5 mg twice daily] resulted in a significant reduction in
overall and cardiac mortality whereas use of the higher dose [5 mg
twice daily] did not result in a significant mortality reduction. However,
both doses were associated with an increased risk of bleeding compared
with placebo. Rivaroxaban is not currently approved by the US Food
and Drug Administration [FDA] for use in ACS. Another factor Xda
inhibitor, fondaparinux [Arixtra], has been studied for use in patients
with STEMI who do not undergo PCI [32].
In the Fifth Organization to Assess Strategies in Ischemic Syndromes
[OASIS-5] trial, fondaparinux reduced major bleeding and improved
net clinical outcome compared with enoxaparin in patients receiving
GP IIb/IIIa inhibitors or thienopyridines for ACS [33]. Fondaparinux is
not currently FDA approved for use in ACS.
Thrombolysis: Prehospital thrombolysis allows eligible patients
to receive thrombolysis 30-60 minutes sooner than if treatment were
given in the ED; however, prehospital thrombolysis is still under
investigation and has not become a trend, as a result of unproven benefit
and an increase in the availability of PCI in many medical centers as an
alternative to thrombolysis for STEMI.
Although PCI is the preferred treatment for STEMI, the distance
to primary PCI centers and the inherent time delay in delivering
primary PCI limits widespread use of this treatment. Prehospital
electrocardiographic [ECG] diagnosis and direct referral for primary
PCI enables patients with STEMI living far from a PCI center to achieve
a system delay comparable to patients who are closer to a PCI center
[34].
Coronary intervention: An early invasive strategy is also indicated
in initially stabilized unstable angina/NSTEMI patients who do not
have serious comorbidities or contraindications to such procedures and
who have an elevated risk for clinical events.
According to the 2011 American College of Cardiology Foundation/
American Heart Association [ACCF/AHA] guidelines, an early invasive
strategy [ie, within 12-24 hours of admission] is a reasonable choice for
initially stabilized high-risk patients with unstable angina/NSTEMI; for
patients not at high risk, a delayed invasive approach is also reasonable
[class IIa recommendation] [20].
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 6 of 22
Concomitant therapy: Current guidelines for patients with
moderate- or high-risk ACS recommend an early invasive approach
with concomitant antithrombotic therapy, including aspirin,
clopidogrel, and unfractionated or LMWH. The Acute Catheterization
and Urgent Intervention Triage Strategy [ACUITY] trial evaluated
the role of thrombin-specific anticoagulation with bivalirudin in
this patient population. In patients with moderate- or high-risk ACS
who were undergoing invasive treatment with glycoprotein IIb/
IIIa inhibitors, bivalirudin was associated with rates of ischemia and
bleeding that were similar to those with heparin. Bivalirudin alone was
associated with similar rates of ischemia and significantly lower rates of
bleeding [35].
ECG and arrhythmia pathogenesis
Cardiac activation: impulse formation, and conduction: The heart
can be considered as a dipole with a positive and a negative charge.
At any given time, cardiac cells are in various stages of activation [i.e.,
depolarization and repolarization].
The formation [i.e., pacemaking] and timely conduction of an
electrical impulse depend on cardiac cells that are strategically placed
and arranged in nodes, bundles, and an intraventricular network that
end in Purkinje cells. All these specialized cells lack contractile capability,
but they can act as pacemakers [i.e., spontaneously generate electrical
impulses] and alter conduction speed. The intrinsic pacemaking rate is
fastest in the sinus node, located in the right atrium, and is slowest in
the Purkinje cells.
The intraventricular conduction network includes the common
bundle of His and its right and left bundle branches, which extend along
the septum toward their respective ventricles. The left bundle branch is
a diffuse structure that fans broadly over the septum toward the two
mitral valve papillary muscles. In the left bundle branch, two divisions
can usually be distinguished; they are called anterior and posterior but
are indeed superior and inferior, respectively. Because the right bundle
branch remains compact until it reaches the distal interventricular
septal surface [where it branches into the septum and toward the lateral
right ventricular wall], many authors consider the intraventricular
conduction system to be trifascicular [36].
These intraventricular conduction pathways are composed of
Purkinje cells with both pacemaking and rapid impulse conduction
capabilities. Purkinje fibers branch into networks that extend just
beneath the endocardial surface.
The normal activation sequence begins at the midseptum, continues
in the epicardial right ventricular wall near the apex, then at the lateral
and basal LV, and ends at the basal septum.
The wavefront departs from the sinus node and travels through
the right and left atria in a centrifugal manner. On arrival at the
atrioventricular [AV] node, the impulse is delayed, allowing for a
sequential, rather than simultaneous, contraction of the ventricles after
the atria. Because the Purkinje system provides a specialized path for
rapid activation, the entire ventricular mass can be depolarized in a
short time [similar to the depolarization timing of the much smaller
atria]. The impulses then proceed slowly from endocardium to
epicardium throughout both ventricles [37].
Electrical bases for electrocardiography and vectorcardiography:
Differences in cardiac potentials of a single cardiac cell or a small group
of cells do not produce enough current to be detected on the body
surface. Electrical representation on the ECG depends on the activation
of most of the atrial and ventricular masses. The depolarization process
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produces a relatively high-frequency ECG waveform. The earliest QRS
complex is recorded in right precordial leads. While depolarization
persists, the ECG recording returns to baseline. Repolarization is then
represented by the ST segment and the T and U waves. Once the cells
are in their resting state, the ECG records a flat baseline.
Normal electrocardiographic waveforms
Overview: The waves on the ECG represent a coincident voltage
gradient generated by cellular electrical activity within the heart.The
origin of the cardiac impulse in the sinus node is electrocardiographically
mute; the initial recordable wave for each cardiac cycle is the P
wave, which represents the spread of activation through the atria.
Ventricular activation results in the QRS complex, which may appear
as one [monophasic], two [diphasic], or three [triphasic] individual
waveforms. Low-amplitude or narrow waves are denoted by lowercase
letters [e.g., q wave] and taller, wider waves are denoted by capital
letters [e.g., Q wave].
The T wave represents ventricular recovery and is sometimes
followed by a small upright deflection, the U wave. The ST segment is
the interval between the end of ventricular activation [the plateau phase
of the action potential] and the beginning of ventricular recovery. The
QT interval measures the time from ventricular activation onset to end
of ventricular recovery. At low heart rates the PR, ST, and TP segments
are at the same horizontal level [i.e., the isoelectric line], considered the
baseline for measuring various waveform amplitudes [38].
P wave: The first part of the P wave represents the activation in
the right atrium, and the middle and final sections of the P wave are
recorded during left atrial activation. The normal P wave is rounded
and upright in leads I and II and from V2 to V6. Its maximum amplitude
is 0.25 mV in lead II [or 25% of the R wave], and its duration is 0.08
second. The P-wave axis is approximately 60 degrees. The intrathoracic
position of the right and left atria determines that the activation front
be directed first anteriorly, then posteriorly. The right atrium faces lead
V1, in which the initial portion of the P wave appears positive while its
terminal part appears negative.
Ta segment: The Ta segment [or Ta wave] represents atrial
repolarization and may be seen in physiologically normal individuals,
but it is more often obscured by the QRS complex and the early part of
the ST segment. The Ta wave direction is opposite that of the P wave. It
represents the atrial repolarization .Normally not seen as it is buried in
the large QRS. Prominent Ta wave may produce PR segment depression
and mimic a pathologic Q wave.
PR interval: The time from onset of the P wave to onset of the QRS
complex [whether its first wave is a Q or an R wave] is the PR interval.
It encompasses the time between the onset of atrial depolarization in
the myocardium adjacent to the sinus node and the onset of ventricular
depolarization in the myocardium adjacent to the Purkinje network.
A major portion of it is inscribed during the slow conduction through
the AV node. The normal PR interval measures 0.12 to 0.22 second.
The PR interval increases with age. It shortens as heart rates increases;
this effect depends on higher sympathetic and lower vagal tones.
Incremental atrial pacing at rest, however, prolongs the PR interval.
The time from the end of the P wave to the onset of the QRS complex is
called PR segment and repesents the conduction delay in the AV node.
QRS complex: The QRS complex represents ventricular activation.
The contour of the QRS complex is peaked because it is composed
of high-frequency signals. The normal ventricular activation can be
summarized in four vectors : [a] initial septal activation from left to
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 7 of 22
right and anteriorly [inferiorly or superiorly], producing a positive
deflection [R wave] at right recording sites; [b] an overlapping wave of
excitation involving both ventricles, with the vector directed inferiorly
and slightly to the left, which inscribes the midportion of the QRS
complex; [c] unopposed activation of the apical and central portions
of the LV and of the right ventricle with a resultant vector oriented
posteriorly, inferiorly, and to the left; the posteriorly positioned LV is
much thicker, and its activation predominates over that of the more
anterior right ventricle, with a resulting negative deflection [i.e., S wave]
in aVR and in right precordial leads and in an R wave in leads I, II, III,
aVL, and left precordial leads; and [d] activation of the posterior basal
portion of the LV and septum with a vector directed superiorly and
posteriorly, which completes the S wave in V5 and V6.
The QRS complex measures 0.07 to 0.10 second and increases
with the subject’s height [39]. The QRS complex is measured from
the beginning of the first appearing Q or R wave to the end of the last
appearing R, S, or R’ wave. It tends to be slightly longer in male patients.
The onset of the QRS complex is not recorded simultaneously in all ECG
leads; this has implications when measuring QRS duration. The earliest
QRS onset is recorded in right precordial leads [40]. Computerized
QRS measurements have the advantage of integrating information from
the 12 leads.
Q waves: A Q wave is a negative deflection at the onset of the
QRS complex. It indicates that the net direction of early ventricular
depolarization forces is oriented away from the positive axis of the
recording lead at least by 90 degrees. Normal septal activation results in
a rapid q wave in leads I, II, III, aVL, V5, and V6. The presence of Q waves
in V1, V2, and V3 or the absence of small q waves in V5 and V6 is abnormal
. Positional factors may also result in the inscription of prominent but
narrow Q waves. If the septal vector is horizontal, Q waves may appear
in lead aVF; if the electrical axis is vertical, Q waves may appear in aVL.
Precordial lead electrodes misplaced in a high position may determine
the inscription of Q waves and a pseudoinfarction pattern. In right
precordial leads, qr and qS complexes may be normal.
R waves: The first positive wave of the QRS complex is the R
wave, regardless of whether it is preceded by a Q wave. The second
activation vector results in an R wave in leads II and III, and the
third vector produces an R wave in leads I, II, III, aVL, aVF, V5, and
V6. The precordial leads provide a panoramic view of the cardiac
electrical activity progressing from the right ventricle to the thicker LV;
consequently, the R wave increases its amplitude and duration from
V1 to V4 or V5. An rS pattern in leads V3R and V4R is normal. The R
wave amplitude in V5 and V6 varies directly with LV dimension during
exercise and with positional changes. Reversal of the normal sequence
with larger R waves in V1 and V2 can be produced by right ventricular
enlargement. When a second positive deflection occurs in any lead, it
is called R.
S waves: A negative deflection following an R wave is an S wave.
The third vector produces an S wave in leads a Vr, V1, V2, V3, and
occasionally, V4. The S wave in the precordial leads is large in V1,
larger in V2, and then progressively smaller from V3 through V6. This
sequence could be altered by ventricular enlargement. The last vector
directed superiorly and posteriorly, may result in a terminal S wave in
leads I, V5, and V6. Leads V4R and V3R show an rS morphology in 80%
of normal subjects [41].
ST segment: The ST segment represents the time period in which
the ventricular myocardium remains depolarized. The term ST segment
is used whether the QRS complex ends in an R wave or in an S wave. At
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its junction with the QRS [i.e., J point], the ST segment forms a nearly
90-degree angle and then proceeds horizontally until it curves gently
into the T wave. Slight upsloping [particularly in leads V1 to V3, and in
V4R V3R], downsloping, or horizontal depression of the ST segment may
occur as a normal variant. The ST-segment length and appearance are
influenced by factors that alter the duration of ventricular activation,
such as exercise and BBB.
T wave: The T wave represents exclusively uncanceled potential
differences of ventricular repolarization [i.e., both spatial and temporal
dispersion of repolarization] among the epicardium, M cells, and
endocardium. The T wave accounts for 8% or less of the total timevoltage product of the heart. The T wave has a rounded but asymmetric
shape, with the initial deflection longer than the terminal deflection. The
peak of the T wave marks repolarization completion of the epicardial
cells. The end of the T wave is temporally aligned with repolarization
of the M cells. The M-cell repolarization is outlasted by that of the
Purkinje cells, itself unlikely to generate an ECG wave.
The T-wave amplitude does not normally exceed 0.5 mV in limb
leads or 0.10 mV in precordial leads. The T-wave vector and polarity
are concordant with the R-wave vector. The T wave is always positive in
lead I, nearly always positive or isoelectric in lead II, and may have any
polarity in leads III and a VF. In precordial leads, the T wave is usually
upright.
U wave: When present, the U wave is a small, rounded wave
following the T wave. It is most prominent in leads V2 to V3 and it
usually shows the same direction as its preceding T wave, but in some
patients it may be discordant [42].
The U wave results from the last repolarization components.
It may be generated by repolarization of the Purkinje network or by
repolarization of the M cells [43,44].
QT interval: The QT interval measures the time from the beginning
of the QRS complex until the end of the T wave. It estimates the
duration of both ventricular depolarization and repolarization, but it is
used mainly as an estimate of ventricular recovery time. The term QT is
used whether the QRS complex begins with a Q or an R wave.
Accurate QT measurements are elusive. One reason is that on a
given ECG, the end of the T wave is not always obvious; its terminal
portion may be isoelectric or merge with a U wave. This partially
explains why the precise duration of the QT interval is notoriously
difficult to determine, even by cardiologists, and to standardize [45].
The problem has not been satisfactorily solved by automated programs,
because of technical factors regarding acquisition of digital ECG signals.
The duration of the QT interval is affected by numerous physiologic
variables. These include autonomic influences, circadian rhythms,
electrolytes, and hormones. For example, the JT interval [i.e., the
interval between the J point and the end of the T wave] is significantly
shorter in men than in women, probably because repolarization is
modulated by testosterone [46]. Repolarization and the QT interval
are also affected by drugs, an important reason to monitor QT-interval
duration.
Another main factor influencing the QT interval is heart rate
between the QT and the RR intervals is an inverse relationship that is
nonlinear: as the heart rate increases, the QT interval initially shortens
markedly and then shortens more gradually. Thus, QT-interval values
require adjustment. The normal QT-interval values for a given heart
rate are determined with mathematic formulas that estimate the
corrected QT interval [QTc]. Of the several QT correction formulas,
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 8 of 22
that of Bazett [QTc=QT/RR] is the most widely used. The normal value
of QTc is up to 0.39 second in men and 0.44 second in women. Yet with
the Bazett formula, the QTc remains undercorrected [i.e., artificially
shortened] during bradycardia, whereas it paradoxically lengthens at
faster rates [47].
Abnormal electrocardiogram [WAVES]
P-wave abnormalities: Abnormalities of the P wave reflect disorders
of atrial pressure or volume, or an anomalous origin of the cardiac
impulse.
Right atrial abnormality: Right atrial enlargement has classically
been diagnosed in the presence of the following: [a] tall, peaked P
waves in leads II, III, and aVF [0.25 mV in lead II] [P pulmonale]; [b]
a P-wave axis 75 degrees; and [c] a positive deflection of the P wave in
V1 or V2 0.15 mV [48]. These ECG signs, however, correlate poorly with
anatomic findings. The P-wave amplitude may paradoxically decrease
as right ventricular hypertrophy progresses. Also, P-wave signs have
relatively low sensitivity to detect pure right atrial enlargement. The
most sensitive ECG manifestations of right atrial abnormality in
patients with low prevalence of coronary disease, no chronic pulmonary
disease, and no left-sided heart disease seem to be QRS changes in lead
V1 [R/S ; presence of Q] [in the absence of RBBB]. In addition, STsegment depression 0.05 mV in II or aVF [probably representing a
prominent atrial repolarization [Ta] wave] is highly specific.
Left atrial abnormality: Left atrial enlargement is characterized
by the following: [a] a notched P wave with a duration 0.12 second
[mitral], best observed in leads II and V1; and [b] a wide terminal
negative deflection in lead V1 [0.1 mV amplitude per 0.4 second
duration] . The terminal force of the P wave correlates better with left
atrial volume and weight than with atrial pressure. No characteristic of
the P wave correlates with atrial size [49]. The left atrial enlargement
pattern signals an intraatrial conduction disturbance; thus, the term left
atrial abnormality is preferred.
The term pseudo-P pulmonale denotes a prominent P wave in
inferior leads that is caused by left, rather than right, atrial abnormality.
The P wave revealed is enlarged only in its terminal portion, which in
V1 is markedly negative.
Biatrial enlargement: Biatrial enlargement is characterized by tall P
waves in lead II and notched and broad P waves in leads I and II, with a
terminal negative deflection in V1.
Ta wave: Ta waves may be prominent in atrial hypertrophy or
infarction and during pericarditis that has not been promptly detected.
In the presence of atrial enlargement, the Ta wave is prolonged and may
displace the ST segment, which appears depressed.
PR interval: A short PR interval in the presence of a normal P-wave
axis suggests an abnormally rapid conduction pathway within the AV
node or its surroundings [i.e., a bundle of cardiac muscle connecting
atria directly with ventricles]. An impulse that bypasses the AV node
leads to early activation of the ventricular myocardium [ventricular
preexcitation]. This creates the potential for the electrical impulse
to reenter into the atria, producing a tachyarrhythmia [the WolffParkinson-White [WPW] syndrome]. When a short PR interval is
accompanied by an abnormal P-wave direction, the site of impulse
origin has moved from the sinus node to a position closer to the AV
node. A prolonged PR interval with a normal P-wave axis indicates a
delay in impulse transmission at some point in the pathway between
the atrial and ventricular myocardium.
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QRS complex: The absence of R-wave progression from V1 to V5 may
indicate LV necrosis. In precordial leads, the notching or slurring of the
QRS complex is more sensitive than the presence of Q waves to detect
anterior infarction, but it is less specific [50]. A cause of apparent loss
of left precordial R waves is the rightward mediastinal shift induced by
a left pneumothorax [51]. In dextrocardia, normal R-wave progression
may be observed by recording leads V1 to V5R.
Q waves: Conditions associated with abnormal Q waves include
myocardial infarction or injury, LV hypertrophy [LVH] or dilatation,
and intraventricular conduction disturbances [left BBB [LBBB],
ventricular pacing and WPW syndrome]. Less frequent causes of Q
waves include infiltrative myocardial disease, chronic obstructive
pulmonary disease [in precordial leads], acute pulmonary embolism,
pneumothorax, and misplacement of precordial electrodes [52].
ST segment: Alterations of the ST segment include elevation and
depression, which depend on either of the following two cellular
mechanisms, or both: [a] an injury current resulting from a difference
in resting membrane potentials between injured and uninjured
myocardium; and [b] a voltage gradient generated by a difference in AP
plateau amplitudes.
The most important cause of ST-segment elevation is myocardial
injury. Another cause is ventricular asynergy, which can produce a
pseudoinfarction pattern [53]. Depression of the ST segment occurs
during myocardial ischemia and when ventricular repolarization is
altered.
QT Interval
Long QT interval: The malfunction of cardiac channels may lead
to an intracellular excess of positive ions [sodium or potassium]. This
excess prolongs ventricular repolarization and, consequently, the QT
interval. A prolonged QTc is a predictor of cardiovascular mortality
even in the absence of overt heart disease [54]. Causes of long QT
interval include myocardial ischemia, cardiomyopathies, hypokalemia,
hypocalcemia, autonomic influences, drug effects, hypothermia, and
genetics [congenital long QT syndrome].
Ischemia: Acute myocardial ischemia may induce an initial, transient
QT shortening followed by extreme QT prolongation. Changes in the
QT interval often accompany T-wave or U-wave inversion [55]. The
QT interval usually normalizes within 72 hours, while inverted T waves
may persist.
Hypertrophic cardiomyopathy: The QT and QTc are prolonged in
patients with hypertrophic cardiomyopathy, as a consequence of the
increased LV mass [56].
Hypothermia: Hypothermia [core temperatures 35°C] is associated
with sinus bradycardia, which, in turn, is associated with prolongation
of the QT interval. In some patients, however, the QTc interval is also
abnormal.
Autonomic dysfunction: Patients with diabetes, alcoholism, and
other disorders that cause autonomic dysfunction may show prolonged
QT and QTc intervals [57].
Drugs: Antiarrhythmic drugs, the antibiotics erythromycin and
ketoconazole, the antihistamine agents astemizole and terfenadine,
the phenothiazines, and terodiline all have been associated with
prolongation of both the QT and QTc intervals, with torsade de pointes,
and with sudden death [58].
When new drugs are under clinical development, it is important to
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 9 of 22
test for a propensity to dangerous arrhythmias such as torsade. Because
this is unfeasible, regulatory agencies instead require testing for drugrelated changes in the QT interval [59].
Recently, the selective serotonin reuptake inhibitors and the newer
antipsychotic agents [e.g. clozapine, risperidone] have been reported
to be associated with arrhythmias and prolonged QTc interval [60]. A
list of drugs associated with QT-interval prolongation is continuously
updated on the Internet [61].
Congenital long QT syndrome: Various mutations in ion channel
genes cause congenital long QT syndrome [QTc >0.46 seconds]. 5 to
10% of gene carriers for this disorder, however, have QTc durations
within normal range [62]. Patients with the syndrome may also have
marked sinus bradycardia. The T wave is often notched or biphasic,
or it alternates its morphology or polarity [T-wave alternans] [63-65].
Prominent U waves may also be present. The extreme prolongation of
the QT interval can result in pseudo 2:1 AV block when every other P
wave falls during or before the preceding T wave. The long QT-3 variety
seems to be caused by mutations in the SCN5A gene, which may also
underlie the Brugada syndrome.
Short QT interval: In the short QT syndrome, QTc intervals
measure less than 320 milliseconds [66]. Patients [including children]
have a high incidence of ventricular tachyarrhythmias, syncope, sudden
cardiac death, or atrial fibrillation.
T wave: Abnormalities of the T wave [usually consisting of inverted
T waves] are seen in a number of conditions. The T wave is a sensitive
detector of repolarization differences over the myocardium, but the
magnitude of T-wave changes is not proportional to the extent of
myocardium with repolarization abnormalities [67]. Negative T waves
have classically been classified in primary when they result from
changes in the duration, shape, or amplitude of ventricular action
potentials [as in ischemia, myocarditis, pericarditis, drug effects], and
as secondary when changes affect not the ventricular action potential
but the activation sequence [as in BBB, ventricular pacing, ventricular
hypertrophy, cardiomyopathies, and WPW syndrome] [68]. This
mechanistic dichotomy, however, may be challenged in light of the
phenomenon of T-wave memory and perhaps also by that of T-wave
alternans, changes that could result from a combination of mechanisms
or from ventricular electrical remodelling [69].
The term T-wave abnormality has been called into question by the
finding that negative T waves that develop in infarct-related ECG leads
shortly after thrombolysis are associated with improved survival.[70]
It appears, however, that such T waves must be dynamic [i.e., revert
to positive over time, with exercise, or with dobutamine] to predict
myocardial viability and favorable outcome[71,72]. Abnormalities
of the T wave on a resting ECG of male patients have been shown,
conversely, to predict cardiovascular mortality [73].
Ischemic heart disease
Myocardial ischemia and injury: Occlusion of a coronary artery
or one of their branches leads to interruption of the blood supply and
causes myocardial ischemia and injury. During myocardial ischemia,
myocytes partially depolarize, and their membrane resting potential
is reduced [i.e., becomes less negative]. The action potential duration
and amplitude then decrease. Local injury currents develop between
ischemic and nonischemic cells that manifest in the ECG as ST-segment
deviation toward the specifically involved area.
The first ECG change is the development of peaked, tall T waves,
followed by elevation of the ST segment [74]. The ischemic zone is
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ISSN: 2329-9126 JGPR, an open access journal
electrically more negative than its surrounding myocardial area during
the recovery phase. Thus, while ST-segment elevation is still present
or after it has subsided, the T waves become inverted in relation to the
QRS complexes. The T-wave inversion may regress within minutes
or may persist for several months [75]. These T-wave changes are not
specific or sensitive for the diagnosis of myocardial ischemia. Factors
other than ischemia [e.g., reperfusion, sympathetic denervation] may
conceivably have a role in the genesis of negative T waves.
For the diagnosis of myocardial injury, one of the following criteria
is required:
[a] Elevation of the origin of the ST segment at the J point of 0.10
mV in two or more limb or precordial leads V4 to V6 or 0.20 mV in two
or more precordial leads V1 to V3 or
[b] Depression of the origin of the ST segment at the J point of
0.10 mV in two or more leads V1 to V3 or ST-segment elevation greater
than 0.10 mV in two or more leads V7 to V9. Severe degrees of ischemia
are associated with distortion of the later part of the QRS complex,
which reverses after the acute phase [76].
A highly specific marker of myocardial injury is alternans of the
ST segment. Electrical alternans consists of alternans of the degree
of ST-segment elevation, and it is secondary to variations in action
potential duration or amplitude. Alternating ST-segment elevation and
depression have not been reported. The classic notion that transmural
injury is characterized by ST-segment elevation while nontransmural
[subendocardial] injury is characterized by ST-segment depression has
not been confirmed with imaging studies [77].
When insufficient coronary blood flow persists after the myocardial
metabolic reserves have been depleted, the process of necrosis or
myocardial infarction begins [78]. Permanent new Q waves develop at
some point after ST-segment elevation or depression has occurred. In
ECG leads in which rapid q waves are normally present, these waves
may become pathologically wide.
Subendocardial injury: Ischemia secondary to an increased metabolic
demand [e.g., exercise] initially affects the subendocardium. Myocytes
are less susceptible to ischemia during electrical depolarization than
during electrical recovery; this is why the ECG changes involve mainly
the ST-T waveforms [and much less the QRS complex].
Initial changes include a depression of the J point of at least 0.10
mV and a horizontal or downward sloping of the ST segment toward
the T wave. The T wave may or may not be altered in the same
direction as the ST segment. T-wave inversion may be secondary to
ST-segment depression or it may change as a direct manifestation of
delayed repolarization in the ischemic myocardium. The ST-segment
depression of subendocardial injury resolves rapidly after removal of
the cardiovascular stress. When the ST-segment depression persists in
the absence of increased LV workload, the diagnosis of subendocardial
infarction should be considered. Ischemia-related ST-segment
depression may also occur as a mirror phenomenon of injury that has
induced ST-segment elevation in the myocardial area opposite the
surface electrode.
Acute ST-Segment Elevation Myocardial Infarction
The evolutionary changes during acute infarction include [a] STsegment elevation often preceded by tall T waves, [b] abnormal Q
waves, and [c] return of ST-segment elevation to baseline with T wave
inversion. The most typical change involves ST-segment elevation,
which decreases significantly after the first 12 hours of chest pain [79].
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 10 of 22
In some patients, multiple episodes of ST-segment elevation and
resolution occur after thrombolytic therapy. Moderate ST-segment
elevation usually persists for several days; its persistence beyond 2
weeks suggests ventricular aneurysm. If coronary reperfusion is rapidly
achieved, Q waves may not develop.
Clinical Value of the Electrocardiogram during Acute
Myocardial Infarction.
In general, the 12-lead ECG is specific but only moderately sensitive
to detect acute myocardial injury [80,81]. Systematically recording
leads V4R, V8, and V9 [i.e., a 15-lead ECG] increases the probability of
detecting ST-segment elevation, with no decrease in specificity [82].
The infarction descriptors anterior, inferior, and lateral have classically
been attributed to occlusions of the LAD, right coronary artery [RCA],
and left circumflex artery [LCX], respectively. Other terms such as
apical, septal, high lateral,and posterior are also in use. However, the
12-lead ECG is only moderately accurate to determine the anatomic
location of acute infarction, and the correspondence of some ECG
terms with the pertinent site of infarction is rather poor. The ECG is
most sensitive to detect acute occlusion of the LAD and is least sensitive
for involvement of the circumflex artery. Automated diagnoses [i.e.,
provided by the electrocardiographer] are specific but not sensitive;
their most promising application is in the prehospital setting [83-85].
Among patients presenting to the emergency department with chest
pain and ST-segment elevation in the 12-lead ECG, the cause of STsegment elevation is often uncomplicated LVH [86].
Established myocardial infarction: Most infarctions consist of
areas of both transmural and nontransmural necrosis that change
quantitatively over time and whose correlation with the development
of Q waves or their absence, respectively, is poor. The classification of
Q-wave versus non Q-wave infarcts discriminates between larger and
smaller infarcts [87].
During acute myocardial injury and while the ST segment is still
elevated, abnormal Q waves begin to develop as a consequence of both
the loss of electrical forces in the necrotic area and the effect of the
resultant force directed away from the area. Pathologic Q waves can be
recorded from all myocardial regions that depolarize early during the
cardiac cycle. The posterobasal area depolarizes late, thereby producing
positive QRS waveforms in the precordial leads opposing this zone [i.e.,
V1 and V2].
The Q waves of infarction correlate with percent scar tissue [88].
Although in most patients Q waves persist indefinitely, in 15% to 30%
of cases they disappear or regress. Small, rapid r waves may also result
from post reperfusion recovery of electrical activity. Other patients
presenting with chest pain accompanied by biologic markers of cardiac
necrosis develop repolarization changes followed by non-pathologic,
small q waves or r waves of diminished amplitude. Some of these non
Q-wave infarctions result from injury of the left inferoposterior wall.
In these cases, in leads V1 to V4 of the initial ECG, there is usually
horizontal ST-segment depression, as opposed to the downsloping STsegment depression of anterior infarcts.
For many patients with non Q-wave infarction, the underlying
angiographic finding is a recanalized vessel [89]. The prognosis of non
Q-wave infarction is markedly predicted by the admission ECG [90].
Electrocardiogram During and After Reperfusion Therapy
Approximately half of patients arriving to a medical center within
1 hour of chest pain present with abnormal Q waves. These Q waves
predict a larger infarct size but do not offset the benefits of reperfusion
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
therapy [91]. Thrombolytic therapy and primary percutaneous coronary
intervention, when successful, accelerate the ECG evolutionary changes
of acute infarction. The early appearance of T-wave inversion and rapid,
complete resolution of ST-segment elevation [even in one single ECG
lead] have been associated with patency of the infarct-related artery and
with improved survival [92-94].
Conversely, incomplete resolution of either the ST-segment
elevation or a concomitant ST-segment depression predicts increased
mortality [95].
Clinical Value of the Electrocardiogram in Established
Myocardial Infarction
Autopsy, echocardiographic, and angiographic studies have shown
that the 12-lead ECG has a limited capability to diagnose established
myocardial infarction [96,97]. The accuracy of the ECG depends
on both the infarct location and size, and it may be hampered by
the presence of intraventricular conduction defects, LAFB, Q-wave
regression, multiple infarctions [e.g., an anterior infarct may reduce tall
R waves in V1 to V2 from a previous posterior infarct], and LVH.
Infarct size: Several methods have been developed to estimate the
area of damaged myocardium after an acute coronary event. It appears
that, in terms of prognosis, the most accurate scoring system is the
Cardiac Infarction Injury Score [CIIS] [98].
The future: The clinical use of the ECG has withstood the passage
of time. The ECG is often the initial test demonstrating cardiovascular
abnormalities, a role now expanded with the use of ECG in prehospital
diagnosis and telemedicine [99].
Current emphasis in ECG research is on the study of dynamic
patterns inherent in certain parameters [especially ventricular
repolarization] with the aid of ambulatory recordings and newer,
potent digital storage and analysis techniques. Attempts at improving
the resolution of standard electrocardiography have relied on an
increase in the number of recording electrodes [body surface mapping]
and on an improvement in the signal-to-noise ratio of the higherfrequency signals by averaging and filtering [signal-averaged ECG].
These techniques are promising, but their roles in clinical practice are
still unclear.
Pathogenesis of Arrhythmia after acute coronary syndrome
The initiation and maintenance of life-threatening ventricular
arrhythmias [ventricular tachycardia and ventricular fibrillation] in the
setting of myocardial ischemia and infarction result from the complex
interaction of multiple factors. These include damaged myocardium,
arrhythmia triggers, reperfusion, and various modulating factors.
The pathogenesis may be different, with scar formation being of
primary importance, with ventricular arrhythmias occurring one
week or more after myocardial infarction [MI]. This card will review
these mechanisms in detail, with particular attention to arrhythmias
occurring in the first 48 hours
Mechanisms of arrhythmia formation
Life-threatening periinfarction ventricular arrhythmias result from
interplay among three basic components:
1- The damaged myocardium, which produces a substrate
capable of developing reentrant circuits. It has been observed that
complex ventricular arrhythmias are associated with a larger infarction
and with early left ventricular dilatation and remodeling, perhaps due
to ventricular stretching and electromechanical feedback [100,101].
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 11 of 22
2- Arrhythmia triggers, including spontaneous ventricular
arrhythmias, variations in cycle length, and heart rate.
3- Modulating factors, such as electrolyte imbalance,
dysfunction of the autonomic nervous system, elevated levels of
circulating catecholamine’s, continued ischemia, and impaired left
ventricular function. These factors may act on both substrate and
triggers to induce arrhythmias.
The proper milieu for the development and maintenance of
ventricular arrhythmias is ultimately based upon the rapid and profound
effects acute myocardial ischemia has on the electrophysiological
characteristics of the myocyte. Changes in the resting membrane
potential and in the inward and outward ionic fluxes during the
action potential lead to alterations in conduction, refractoriness, and
automaticity of cardiac muscle cells, all of which contribute to the
occurrence of ventricular arrhythmias [102].
An increase in QT dispersion on the electrocardiogram, which
reflects differences in ventricular repolarization times between normal
myocardium and myocardium within the periinfarction ischemic zone,
may predict an increase in risk for ventricular fibrillation early in the
course of a myocardial infarction [103]. Early coronary reperfusion
after an acute myocardial infarction reduces QT dispersion which may
reduce electrical instability [104].
Cardiac denervation: Sympathetic efferent fibers en route to the
left ventricle cross at the atrioventricular groove, travel within the
superficial subepicardium in a base-to-apex direction and penetrate the
myocardium to innervate the endocardium. A transmural myocardial
infarction can damage the sympathetic fibers and result in functional
denervation of the myocardium apical to the area of the infarction.
Animal and human studies have shown that, after an infarction, regions
of the ventricular myocardium below the infarcted zone have no uptake
of iodine-123-metaiodobenzylguanidine [MIBG], a radiolabeled
guanethidine analog that is actively taken up by sympathetic nerve
terminals, even though this tissue remains viable, as indicated by
persistent thallium uptake [105-107].
Moreover, this denervated tissue fails to exhibit afferent reflexes in
response to bradykinin or nicotine and its refractoriness is not altered
by stimulation of the vagus nerve or the stellate ganglion [108].
However, this zone does manifest denervation hypersensitivity
and is supersensitive to infused norepinephrine or isoproterenol;
it has a greater shortening in refractoriness compared to normal
myocardial tissue. The resulting heterogeneity in refractoriness,
induced by circulating catecholamines, is a potential mechanism for
arrhythmogenicity after infarction. Reinnervation of the periinfarction
area, but not the infarcted tissue, and the loss of supersensitivity occur
within 12 months after the infarction [109].
Role of thrombus and ischemic preconditioning
The incidence of life-threatening ventricular arrhythmias in the
presence of intracoronary thrombus is greater than that associated with
coronary artery ligation or balloon occlusion, despite a similar amount
of ischemia [110,111].
In one animal study, for example, an increased incidence of
ventricular fibrillation due to more conduction slowing during the
first few minutes was noted with ischemia induced by intracoronary
thrombus compared to coronary artery ligation [111].
The electrophysiologic effect of the thrombus lasted only a
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
few minutes, suggesting an association between thrombin and
the rapid release of ischemic metabolites, such as LPGs and
lysophosphatidylcholines, and their accumulation in ventricular
myocytes [112-114].
The occurrence of reperfusion arrhythmias follows a bell-shaped
curve:
As the duration of ischemia increases in experimental animals,
so do reperfusion arrhythmias. The peak incidence occurs at 5 to 10
minutes after the onset of ischemia, presumably due to depletion of
ATP stores become depleted [115,116].
These experimental observations may be applicable to humans. A
recent pooled analysis of intracoronary thrombolytic trials suggested
that life-threatening arrhythmias during reperfusion were more
likely to occur when the interval between the onset of infarction and
thrombolytic therapy was short [analogous to animal models] [117].
The rate of lysis may also be important. Serious arrhythmias are
more common when thrombolytic agents are given directly into
the coronary artery and lysis is rapid; they are less frequent when
intravenous thrombolytic agents are used [117].
Thrombolytic therapy is usually given clinically more than two
to four hours after the onset of coronary occlusion, when significant
myocardial infarction is already present. It therefore seems likely, from
the preceding observations, that ischemia rather than reperfusion is
responsible for the majority of serious arrhythmias seen in patients
with acute MI. This hypothesis is supported by trials of intravenous
thrombolytic therapy that did not demonstrate any increase in lifethreatening arrhythmias that could be attributed to reperfusion,
although frequent ventricular premature beats and accelerated
idioventricular rhythm do occur and may be a marker of reperfusion
[118,119].
Reperfusion arrhythmias should be managed in an identical
fashion to other types of arrhythmias, although data suggest that
antiarrhythmic drugs are less effective in this setting. At present, there
are no prophylactic therapeutic maneuvers that have been proven to
reduce the incidence of these events, but there is interest in the possible
efficacy of calcium channel blocking agents and free radical scavengers,
such as superoxide dismutase and adenosine. As an example,
dipyridamole, an inhibitor of cellular uptake of adenosine that may
reduce intracellular calcium, was evaluated in one study of 61 patients
undergoing primary angioplasty for an acute anterior wall myocardial
infarction [120].
Pretreatment with dipyridamole prevented all episodes of
accelerated idioventricular rhythm and ventricular tachycardia, which
occurred in 18 and 8 percent, respectively, of patients not receiving
pretreatment. In addition, dipyridamole terminated arrhythmia in all
nine patients who developed a sustained ventricular tachyarrhythmia
after reperfusion.
Correlation between ECG waves and events
Atrial fibrillation [AF] is a frequent complication of acute
myocardial infarction [AMI], with reported incidence of 7% to 18%.
The incidence of congestive heart failure, in-hospital mortality, and
long-term mortality is higher in AMI patients with AF than in AMI
patients without AF. P wave duration on signal-averaged ECG [PWD]
and P wave dispersion on standard ECG [Pd] are noninvasive markers
of intra-atrial conduction disturbances, which are believed to be the
main electrophysiological cause of AF.
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 12 of 22
PWD and Pd both measured in a very early period of AMI are
useful in predicting AF [121].
QRS prolongation with or without bundle branch block [BBB] has
been associated with adverse outcome in myocardial infarction; we
examined the relationship between QRS duration and outcome in a
broad spectrum of patients with acute coronary syndrome [ACS].
In patients presenting with a broad spectrum of suspected ACS, QRS
prolongation—particularly in the setting of LBBB—is an independent
predictor of in-hospital and 1-year mortality [122].
For patients with chest pain and non-diagnostic initial ECG, ACS
risk is high if QTD and QTcD values are greater than 40 Ms. Therefore,
QTD and QTcD can help identify patients with acute coronary
syndrome who present with chest pain and a nondiagnostic initial
ECG. However, poor operator characteristics of QT dispersion could
limit its value as a diagnostic test in the clinical setting [123].
Aim of the Work
The aim of this work was to assess the correlation between P wave
dispersion, QRS duration and QT dispersion in hospital events in
patients with acute coronary syndrome [ACS].
•
•
ECG.
Typical anginal pain.
ST segment elevation in two or more contagious leads in
•
High Cardiac enzymes.
•
Signs of success after thrombolytic therapy [two from three]:
1- Resolution of chest pain.
2- Regression of ST elevation by at least 50 % in ECG.
3- Occurrence of reperfusion arrhythmias [e.g. idioventricular
rhythm].
II) Group 2: [ST segment elevation myocardial infarction with
failed thrombolysis]:
•
•
ECG.
Typical anginal pain.
ST segment elevation in two or more contagious leads in
•
High Cardiac enzymes.
•
Signs of failure after thrombolytic therapy :
Patients and Methods
1- Resistant chest pain.
Patients
2- No regression of ST elevation by at least 50% in ECG.
3- No Occurrence of reperfusion arrhythmias.
This prospective study was conducted on 60 patients with acute
coronary syndrome admitted to critical care units of Alexandria
University Hospitals from first of January 2012 to end of August
2012.An informed consent was taken from relatives of every patient
included in the study. This study was approved by ethical committee of
Alexandria faculty of medicine.
Inclusion criteria
The study included patients with Acute Coronary Syndrome [ACS]
who had two from three of the following criteria:
•
Clinical manifestation [Typical anginal pain usually with
nausea and sweating].
•
Electrocardiographic changes [ECG].
•
Myocardial markers [CK, CKmb, Troponin I].
Exclusion Criteria:
Excluded from the study patients with any of the following:
ECG in which Q-T interval could not be assessed:
1.
Unclear QT interval in at least seven ECG leads.
2.
Bigeminal ventricular systole, atrial fibrillation, a pacemaker.
3. Current drug use affecting QT interval e.g quinidine,
Amiodarone, psychogenic agents [tricyclic antidepressant, tetracyclic
agents].
4.
Patients on hemodialysis.
5.
Post Coronary Artery Bypass Graft [CABG].
The patients included in the study will be classified into three
groups:
I) Group 1: [ST segment elevation myocardial infarction with
successful thrombolysis]:
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
III) Group 3 : [Unstable angina] :
•
Typical anginal pain.
•
ECG changes [without ST segment elevation].
•
Negative cardiac enzymes.
Methods:
1)
Full history taking including :
•
Age.
•
Sex.
•
Character of pain.
•
Medical history including: Diabetes Mellitus, Hypertension,
Previous heart disease and Drug intake.
2)
Clinical Examination including :
•
Pulse rate [beat/min.].
•
Blood Pressure [mmHg].
•
Temperature [c º].
•
Chest and heart examination.
3) Electrocardiography: A 12-lead ECG record was done on
admission, before and after thrombolytic [if given] and once daily till
discharge.
A paper speed of 25 mm/s and amplification of 10 mm/mV was
used for recording 12- lead ECG and the following parameters were
calculated:
a- P wave Dispersion [PWD] is the difference between the
longest [P max] and the shortest P wave duration [P min] recorded
from multiple different surface ECG leads was calculated as [PWD=P
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 13 of 22
max – P min] by milliseconds [ms].
b-
Correlation was done between quantitative and qualitative variables
using Spearman correlation test and scatter dot graph.
QRS duration was measured [ms].
c- QT interval was calculated from the onset of the QRS
complex to the point of return of the T wave to the isoelectric line.
Three sequential complexes were measured and the mean value was
used for QT interval calculation [ms].
The difference between the maximum and minimum QT intervals,
occurring in any of the 12 leads, was measured as QTD. QTc max and
QTc min will be determined with the Bazett formula [QTc=QT /√RR],
and the difference between QTc max and QTc min was calculated as
QTcD[9] , together with assessment of other ischemic ECG change [T
wave changes, S-T segment changes].
4) Cardiac markers [CPK [u/l], CK MB [u/l], Troponin I [ng/
ml]] on admission and after six hours.
5)
Plain chest X – ray
6)
Management:
All patients were managed according to the following Protocol
which includes:
I] Patients with ST segment elevation myocardial infarction
[STEMI] will receive:
1- Oxygen [3-5 l / min].
2- Morphine [4 mg I.V. As a pain killer].
3- Nitroglycerine
according to response].
[sublingual
then
intravenous
titrated
4- Antiplatelets [Acetyl salycilic acid 81 mg 4 tablets on
admission then once daily and clopidogrel 75 mg 4 tablets on admission
then once daily].
5- Thrombolytic therapy [streptokinase in a dose of 1.5 million
units over one hour].
6- Anticoagulants
enoxaparine 1 mg/kg].
[low
molecular
weight
heparin
e.g.
II] Patients with unstable angina will receive:
The same treatment except thrombolytic therapy
7)
Outcome as regards:
Every patient was followed up for five days [patients who died
before fifth day will be excluded due to insufficient data needed for
follow up]:
1-
Duration of stay in ICU:
2- Morbidity: dysrhythmias, heart failure, cardiogenic shock,
mechanical ventilation.
3-
Mortality:
8)
Statistical method:
Records of the studied cases and the results obtained after proposed
procedure were statistically analyzed using SPSS 16.0 under Microsoft
Windows XP. Continuous data were expressed in the form of mean ±
SD. Categorical variables were expressed in the form of number and
percent. One way ANOVA were utilized to compare numerical data.
Chi-square test was used to compare categorical data as appropriate.
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
Results
There was no significant difference between the gender of patients
in the three groups of patients [p >0.05], total number of males was 48,
however in females was 12.
There was also no significant difference between the three age
groups of patients [p >0.05], mean of age was similar [57.3, 57.2 and
56.3 years] respectively.
This Table 1 shows that there was significant difference in risk
factors between the studied groups as following: smoking is higher in
the groups [Successful thrombolysis and failed thrombolysis] than the
unstable angina group.
There was also significant ECG changes and Cardiac enzymes were
elevated in the [Successful thrombolysis and failed thrombolysis] than
the unstable angina group.
This Table 2 shows that there was no difference in duration of QRS
between the three groups [P >0.05], QRS mean was ranged from 73.5
MS in patients with unstable angina, and 76 MS in patients with failed
thrombolysis
This Table 3 shows that there is significant difference in QTD
between the three groups, it was longer in patients with failed
thrombolysis therapy [101 msec], than in other groups of patients, [72.3
msec] in patients with successful thrombolytic therapy, [83.5 sec] in
patients with unstable angina.
This Table 4 shows that there is a significant difference between
the three groups ICU length of stay, patients with failed thrombolysis
stayed more than 3 days in ICU, in comparison to the other groups.
This table shows that the presence of listed complications was only in
the failed thrombolysis group in comparison to the other two groups.
It was found that percent of survivors in unstable angina and
patients with successful thrombolysis was 100% in comparison with
80% of failed thrombolysis group, that was highly significant [p <
0.001*].
This table shows that there is no significant difference between
the PWD, QRS duration and the presence of complications in failed
thrombolysis group; however there is a significant difference between
the QTD and the complications in the same group.
There was a highly significant difference between QTD in relation
to occurrence of each complications, the largest one was in heart
failure [190 msec] and the smallest one was [28 msec] in Junctional
arrhythmia .
This table shows that non survived patients were 4 from 7
complicated patients [57.1%], their causes of death were [heart failure,
cadiogenic shock, AF and pulseless VT], in comparison to the survived
patients 3 from 7 complicated patients [42.9%], with a statistical
difference <0.05.
This Table 5 shows significant difference between complicated and
non complicated patients regarding ICU stay, all complicated patients
[100%] stayed more than 3 days in ICU while only 6 from 13 patients
[46%] from complicated patients stayed more than 3 days.
Discussion
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 14 of 22
Acute coronary syndrome [ACS] refers to any group of symptoms
attributed to obstruction of the coronary arteries. The most common
symptom prompting diagnosis of ACS is chest pain, often radiating to
the left arm or angle of the jaw, pressure-like in character, and associated
with nausea and sweating. Acute coronary syndrome usually occurs as
a result of one of three problems: ST elevation myocardial infarction
[30%], non ST elevation myocardial infarction [25%], or unstable
angina [38%] [124].
These types are named according to the appearance of the
electrocardiogram [ECG/EKG] as non-ST segment elevation
myocardial infarction [NSTEMI] and ST segment elevation myocardial
infarction [STEMI]. There can be some variations as to which forms
of myocardial infarction [MI] are classified under acute coronary
syndrome [125].
ACS should be distinguished from stable angina, which develops
during exertion and resolves at rest. In contrast with stable angina,
unstable angina occurs suddenly, often at rest or with minimal exertion,
or at lesser degrees of exertion than the individual’s previous angina
“crescendo angina”. New onset angina is also considered unstable
angina, since it suggests a new problem in a coronary artery.
Though ACS is usually associated with coronary thrombosis, it can
also be associated with cocaine use [126].
Patients presenting with chest pain and nondiagnostic
electrocardiograms [ECG] in the emergency department [ED] often
pose a challenge to physicians, Atrial fibrillation [AF] is a frequent
complication of acute myocardial infarction [AMI], with reported
incidence of 7% to 18%. The incidence of congestive heart failure, inhospital mortality, and long-term mortality is higher in AMI patients
with AF than in AMI patients without AF. P wave duration on signalaveraged ECG [PWD] and P wave dispersion on standard ECG [Pd] are
noninvasive markers of intra-atrial conduction disturbances, which are
believed to be the main electrophysiological cause of AF [121].
P wave dispersion, detected from the surface ECG, has been thought
to reflect left atrial enlargement and altered conduction [127]. P wave
dispersion and P wave maximal duration reflects the activation of atrial
muscle and may depend primarily upon the mass of tissue excited,
have been used in the assessment of the risk for atrial fibrillation
which is characterized by nonhomogeneous and discontinuous atrial
conduction[128,129]. P wave dispersion was defined as the difference
between the longest and the shortest P wave duration recorded from
multiple surfaces ECG leads [128]. The clinical significance of P wave
duration has been demonstrated in many clinical conditions, especially
in paroxysmal atrial fibrillation [128,130]. P wave dispersion has been
showed to be influenced by the autonomic nervous system activation,
which induces changes in left atrial size and the velocity of impulse
propagation [131].
At present, no definitive cut-off value has been determined as to
the diagnosis of high-risk patients [132].
This study was undertaken to find out the correlation between the
P wave dispersion in hospital events in patients with acute coronary
syndrome [ACS].
In Table 6 [3] there was no significant relationship between P wave
duration in the studied groups [p>0.05].
A meta- analysis study, found that Pd, Pmax, and Pmin span a wide
range of values in healthy individuals. Seemingly, abnormal values
were often reported in healthy adults. The high variability of P-wave
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
parameters in healthy individuals, and overlapping of the results with
those reported for patients with increased risk for atrial fibrillation,
might suggest that this technique has limited sensitivity and specificity.
The variability between studies may stem from methodological
issues and, therefore, there is a definite need for methodological
standardization of Pd measurements [132]. This study agreed with our
study as PWD alone couldn’t predict AF .
But, this study disagreed with [Dilaveris et al., 1999] [133] who
said that Prolonged P wave duration and PD have been reported to
represent increased risk of atrial fibrillation in patients with acute
coronary syndromes.
This study found that [case report]:
Only One patient developed AF on the 3rd day in failed
thrombolysis group, this patient was male, 66 years, diabetic, smoker,
with typical chest pain, had significant ECG changes, P wave was
measured on observing him 5 days in the intensive care unit [ICU], as
following: PWD1=20, PWD2=40, PWD3=0 .0 [AF], PWD4=0.0[AF]
and PWD5=0.0[AF] milliseconds, he died on the 5th day.
Prolonged QRS duration, and the presence of intraventricular
conduction abnormalities, usually indicates the presence of changes
in the myocardium due to underlying heart disease. Prolonged QRS
duration is often associated with depressed ejection fraction or enlarged
left ventricular volumes, but several studies have demonstrated that
this simple ECG measure provides independent prognostic value, after
adjusting for relevant clinical covariates [134].
Post-infarction patients with prolonged QRS duration have a
significantly increased risk of mortality, although data associating
QRS prolongation specifically with sudden death is less supportive. In
non-ischemic cardiomyopathy, there is no evidence that QRS duration
has prognostic significance in predicting mortality or sudden death.
Prolonged QRS duration, and especially presence of left bundle branch
block, seems to predict a benefit from cardiac resynchronization
therapy in both ischemic and non-ischemic cardiomyopathy patients.
Therefore, QRS duration and morphology should not only be considered
a predictor of death or sudden death in patients after myocardial
infarction, and in those suspected of coronary artery disease, but also
as a predictor of benefit from cardiac resynchronization therapy in
patients with heart failure, whether of an ischemic or non-ischemic
origin [135].
This present study agreed with Bryneo et al. [135] , as evaluation of
the presenting electrocardiogram in Alexandria University Hospital’s
intensive care patients [n=60] showed that there was no significance
difference between QRS duration in the three groups [unstable angina,
successful thrombolysis and failed thrombolysis respectively with mean
value [73.7 ± 14.02, 76.2 ± 10.88, 72.36± 8.81] [p>0.05] (Table 7) and
the correlation between the QRS duration and the development of
complications was non-significant in this study, tp=0.104 (Table 8).
However Petrina et al. found the contrast which discovered that
QRS prolongation-particularly in the setting of LBBB-is an independent
predictor of in-hospital and 1-year mortality [134-137].
The QT interval represents the total duration of ventricular
depolarization and repolarization. QT interval is calculated from the
onset of the QRS complex to the point of return of the T wave to the
isoelectric line. The normal value of QTc is up to 0.39 second in men
and 0.44 seconds in women. The difference in the QT intervals between
the derivations from ECG leads as “QT dispersion” [QTD] and noted
that it represents the degree of the repolarization heterogeneity. “QTD”
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 15 of 22
Unstable angina 20
case
Successful thrombolysis
20 case
Failed thrombolysis 20
case
No
%
No
%
No
Male
14
70.0
19
95.0
15
75.0
Female
6
30.0
1
5.0
5
25.0
p
%
Sex
MC
p=0.124
Age (years)
Min.-Max.
39.0-75.0
30.0-73.0
47.0-70.0
Mean ± SD
57.35 ± 9.87
57.20 ± 11.37
56.30 ± 8.24
Median
56.50
60.0
52.0
p=0.937
F
p: p value for comparing between the studied group.MC: Monte Carlo test.F: F test (ANOVA).*Statistically significant at p ≤ 0.05.
Table 1: Comparison between the different studied groups according to demographic data.
Unstable
angina
Successful thrombolysis
No
%
No
+ve
11
55.0
4
-ve
9
45.0
16
Failed thrombolysis
%
No
%
20.0
7
35.0
80.0
13
65.0
p
DM
0.022
χ2p1
χ2p
p=0.070
χ2p
p=0.139
0.204
*
p2
0.015*
FE
Hypertension
+ve
11
55.0
7
35.0
5
25.0
-ve
9
45.0
13
65.0
15
75.0
+ve
15
75.0
18
90.0
13
65.0
-ve
5
25.0
2
10.0
7
35.0
+ve
4
20.0
15
75.0
9
45.0
-ve
16
80.0
5
25.0
11
55.0
Heart disease
MC
p=0.201
Smoking
χ2p
p1
χ2p
p2
<0.001*
χ2p
p=0.002*
0.091
0.053
Cardiac enzymes
+ve
0
0.0
20
100.0
20
100.0
-ve
20
100.0
0
0.0
0
0.0
χ2p
p1
<0.001*
χ2p
p <0.001*
<0.001*
p2
ECG changes
Non significant change
8
40.0
0
0.0
0
0.0
Positive change
12
60.0
20
100.0
20
100.0
p1
FE
p2
0.003*
MC
p <0.001*
0.003*
-
P: p value for comparing between the studied group.p1: p value for comparing between unstable angina with each other groups. p2: p value for comparing between
successful thrombolysis and failed thrombolysis.MC: Monte Carlo test.FE: Fisher Exact test.χ2: Chi square test.*Statistically significant at p ≤ 0.05.
Table 2: Comparison between the different studied groups according to medical history.
is defined as the difference between the maximum and minimum QT
intervals, occurring in any of the 12 leads. Prolonged QTD is associated
with an increased risk of serious ventricular arrhythmias in patients
with long QT syndrome, hypertrophic cardiomyopathy, chronic heart
failure or myocardial infarction [Suzuki et al.] [105].
Experimental work has shown that increased dispersion of electrical
recovery after activation is a key factor in the development of serious
and fatal arrhythmias associated with ischemia [Janse and Wit., 1989].
This agreed with our study, 53 patients had QTD [mean=79.95]
millisecond with no complications, however 7 patients who developed
complications, had QTD between 28 and 190 Millisecond respectively,
Table 8.
Table 9, showed that there was a highly significant correlation
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
between QTD duration and prediction of complications, tp=0.022*
which is agreed with Pekdemir et al. [123] who described the same
results in his study which showed that QTD can help identify patients
with acute coronary syndrome who present with chest pain and a nondiagnostic initial ECG. However, poor operator characteristics of QT
dispersion could limit its value as a diagnostic test in the clinical setting.
Regarding the complications, it had been found that all of them had
occurred in patients with failed thrombolysis therapy, in comparison to
the other two groups, 7 patients [35%], [p<0.05] (Table 9).
In the present study ICU length of stay was longer [>3 days] in
patients with failed thrmbolysis [13 patients] in comparison with the
other two groups, 11 patients with successful thrmbolysis, and one
patient with unstable angina stayed more than 3 days in ICU [p<0.05]
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 16 of 22
Unstable angina
Successful thrombolysis
Failed thrombolysis
(n=20)
(n=20)
(n=18)
PWD
Min.-Max.
20.0-60.0
20.0-60.0
20.0-60.0
Mean ± SD
48.0 ± 13.61
47.0 ± 13.42
43.33 ± 15.72
Median
50.0
40.0
40.0
p1
0.787
MW
p2
p
p=0.624
KW
0.357
0.485
MW
p: p value for Kruskal Wallis test for comparing between the studied group.p1: p value for Mann Whitney test for comparing between unstable angina with each other groups.
p2: p value for Mann Whitney test for comparing between successful thrombolysis and failed thrombolysis.*Statistically significant at p ≤ 0.05.
Table 3: Comparison between the different studied groups according to P wave dispersion (PWD)
Unstable angina
Successful thrombolysis
Failed thrombolysis
p
QRS
Min.-Max.
50.0-100.0
40.0-120.0
50.0-90.0
Mean ± SD
73.50 ± 14.24
72.0 ± 17.95
76.0 ± 10.46
Median
80.0
70.0
80.0
Sch
p1
Sch
p2
0.948
p=0.681
F
0.863
0.687
P: p value for F test (ANOVA) for comparing between the studied group.p1: p value for Post Hoc Test (Scheffe) for comparing between unstable angina with each other
groups.p2: p value for Post Hoc Test (Scheffe) for comparing between successful thrombolysis and failed thrombolysis.*Statistically significant at p ≤ 0.05.This table shows
that there was no difference in duration of QRS between the three groups (P >0.05), QRS mean was ranged from 73.5 MS in patients with unstable angina, and 76 MS in
patients with failed thrombolysis.
Table 4: Comparison between the different studied groups according to QRS Duration:
Unstable angina
Successful thrombolysis
Failed thrombolysis
p
QTD
Min.-Max.
39.0-129.0
9.0-125.0
28.0-187.0
Mean ± SD
83.50 ± 31.11
72.30 ± 31.47
101.0 ± 36.35
Sch
p1
Sch
p2
0.566
p=0.025
F
0.239
0.025
P: p value for F test (ANOVA) for comparing between the studied group.p1: p value for Post Hoc Test (Scheffe) for comparing between unstable angina with each other
groups.p2: p value for Post Hoc Test (Scheffe) for comparing between successful thrombolysis and failed thrombolysis.*Statistically significant at p ≤ 0.05.
Table 5: Comparison between the different studied groups according to QT Dispersion (QTD)
(Table 10). This is an agreement with Craig et al. who found that lower
mortality is associated with shorter lengths of stay. Only part of these
associations could be attributed to following best practice guidelines
and lower rates of preventable complications.
Soon after resuscitation and intensive care was done to acute
coronary syndrome patients, it was claimed that survivors mostly
would return to their homes. In the present study it was found that
percent of patients with favourable outcomes in unstable angina and in
patients successfully thromboylsed 100% respectively compared with
failed thrombolysis patients [80% survived and 20% died] Tables 11 and
12.This is also an agreement with Craig et al. [138]
Summary and Conclusion
The acute coronary syndromes encompass a spectrum of unstable
angina to transmural myocardial infarction. The definition of acute
coronary syndrome depends on the specific characteristics of each
element of the triad of clinical presentation, electrocardiographic
changes and biochemical cardiac markers.
This prospective study was conducted on 60 patients with acute
coronary syndrome admitted to critical care units of Alexandria
University Hospitals from first of January 2012 to end of August
2012. An informed consent was taken from relatives of every patient
included in the study. This study was approved by ethical committee of
Alexandria Faculty of Medicine.
During the observation up to 5 days, 1 patient [1.6%] developed AF.
There was no significant correlation between P wave dispersion[PD] in
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
the three studied groups and No significant relation between it and the
whole complications developed in failed thrombolysis group [p>0.05].
PD alone couldn’t predict AF in this study, as the mean was 20.0
milliseconds, which was too small to predict AF alone.
There was no significance difference between QRS duration in
the three groups [unstable angina, successful thrombolysis and failed
thrombolysis respectively with mean value [75.7 ± 14.02, 75.2 ± 10.88,
73.36± 8.81] [p>0.05] and the relationship between the QRS duration
and the development of complications was non-significant in this study.
This study showed that there was a significant relation among the
three groups and highly significant correlation between QTD duration
and prediction of complications.
It was clear that ICU length of stay was longer in patients with
failed thrombolysis in comparison with the other two groups [p<0.05].
Recommendations
1- Importance of measurements of QT Dispersion to patients
with acute coronary syndrome especially at admission.
2- Failed thrombolysis patients should be under close
observation and monitoring till another option is available like
coronary intervention.
Acknowledgement
First and above of all, I would like to confess favor and thanks to ALLAH who
granted me the power, patience and reconciliation at all time, without his great
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 17 of 22
Unstable angina
Successful thrombolysis
Failed thrombolysis
No
%
No
%
No
<3 days
19
95.0
9
45.0
7
35.0
>3 days
1
5.0
11
55.0
13
65.0
p
%
ICU length
χ2p
p1
χ2p
p2
0.001*
<0.001*
0.519
Min.-Max.
1.0-4.0
2.0-4.0
2.0-5.0
Mean ± SD
2.45 ± 0.76
3.50 ± 0.61
3.60 ± 0.88
Median
2.50
4.0
4.0
<0.001*
<0.001*
Sch
p1
Sch
p2
p <0.001*

p <0.001*
F
0.917
P: p value for comparing between the studied groups.p1: p value for comparing between unstable angina with each other groups.p2: p value for comparing between
successful thrombolysis and failed thrombolysis.F: F test (ANOVA).Sch: Post Hoc Test (Scheffe).χ2: Chi square test.*Statistically significant at p ≤ 0.05.
Table 6: Comparison between the different studied groups according to ICU length
Unstable angina
No
Successful thrombolysis
%
Failed thrombolysis
No
%
No
%
MC
p
Complications
Absent
20
100.0
20
100.0
13
65.0
Present
0
0.0
0
0.0
7
35.0
p1
-
FE
FE
0.001*
0.008*
p2
0.008
*
Heart failure
0
0.0
0
0.0
2
10.0
Cardiogenc Shock
0
0.0
0
0.0
2
10.0
Accelerated junctiontial rythm
0
0.0
0
0.0
1
5.0
AF
0
0.0
0
0.0
1
5.0
Pulsless VT
0
0.0
0
0.0
1
5.0
-
P: p value for Monte Carlo test for comparing between the studied groups.p1: p value for Fisher Exact test for comparing between unstable angina with each other groups.
p2: p value for Fisher Exact test for comparing between successful thrombolysis and failed thrombolysis.*Statistically significant at p ≤ 0.05.
Table 7: Comparison between the different studied groups according to complications
Unstable angina
Successful thrombolysis
Failed thrombolysis
No
%
No
%
No
%
Survived
20
100.0
20
100.0
16
80.0
Non survived
0
0.0
0
0.0
4
20.0
MC
p
Survival
p1
-
FE
p2
0.029*
0.106
0.106
FE
P: p value for Monte Carlo test for comparing between the studied groups.p1: p value for Fisher Exact test for comparing between unstable angina with each other groups.
p2: p value for Fisher Exact test for comparing between successful thrombolysis and failed thrombolysis.*Statistically significant at p ≤ 0.05.
Table 8: Comparison between the different studied groups according to survival
Complications
Absent
p
Present
PWD
(n=13)
(n=7)
Min.-Max.
20.0-60.0
20.0-40.0
Mean ± SD
46.15 ± 17.10
36.0 ± 8.94
Median
60.0
40.0
QRS
(n=13)
(n=7)
Min.-Max.
50.0-90.0
80.0-80.0
Mean ± SD
73.85 ± 12.61
80.0 ± 0.0
Median
80.0
80.0
QTD
(n=13)
(n=7)
Min.-Max.
36.0-102.0
28.0-187.0
Mean ± SD
83.15 ± 17.47
121.86 ± 51.68
Median
82.0
119.0
p=0.208
MW
p=0.104
t
p=0.022*
t
P: p value for comparing between the studied groups.t: Student t-test.MW: Mann Whitney test.*Statistically significant at p ≤ 0.05.
Table 9: Relation between P Wave Dispersion (PWD), QRS Duration, QT Dispersion (QTD) and Complications in failed thrombolysis group.
J Gen Pract
ISSN: 2329-9126 JGPR, an open access journal
Volume 3 • Issue 3• 1000196
Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
Page 18 of 22
Complications
QTD (Mean ± SD)
No Complications
79.9 ± 28.39
Heart Failure
190.0 ± 00.0
Cardiogenic Shock
154 ± 00.0
AF
92.0 ± 00.0
JA
28.0 ± 0.00
187.0 ± 0.0
Pulpless VT
Anova
P value
6.95
<0.001*
*highly significant=p<0.001*.
Table 10: Relation between QTD and complications.
Complications
Absent
(n=13)
Present
(n=7)
No
p
No
%
%
Survived
13
100.0
3
42.9
Non survived
0
0.0
4
57.1
Survival
0.007*
P: p value for Fisher Exact test for comparing between the two studied groups.*Statistically significant at p ≤ 0.05.
Table 11: Relation between survival and complications in failed thrombolysis group.
Complications
Absent (n=13)
No
Present (n=7)
%
No
p
%
ICU length
<3 days
7
53.8
0
0.0
>3 days
6
46.2
7
100.0
Min.-Max.
2.0-4.0
4.0-5.0
Mean ± SD
3.23 ± 0.83
4.29 ± 0.49
Median
3.0
4.0
p=0.044*
FE
p=0.007*
t
p: p value for comparing between the studied group.t: Student t-test.FE: Fisher Exact test.*Statistically significant at p ≤ 0.05.
Table 12: Relation between ICU length and complications in failed thrombolysis group.
blessing, I would never accomplish my work. No word could express my feeling of
gratitude and respect to Prof. Dr. Tarek Hussein El Badawy, Professor of Cardiology
and Angiology, Faculty of Medicine, University of Alexandria for his supervition,
useful advices, marvelous effort and support during this study.
I would like to express my sincere gratitude and appreciation to Prof. Dr.
Muhammad Nasr eldin El Sayed, Professor of Critical Care Medicine, Alexandria
University Hospitals, for his kind advice, valuable supervision and constructive
encouragement in conducting the study.
My deep appreciation to Dr. Mohamed Mostafa Abd El Salam Megahed,
Assistant Professor of Critical Care Medicine, Faculty of Medicine, University of
Alexandria, for his continuous supervision and expert guidance.
Finally, warmest thanks should go to my family for their endless help, support
and encouragement.
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Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
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Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
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Citation: Hassebo MFH, Sayed MNEE, Megahed MMAES, Badawy THE (2015) Correlation between P Wave Dispersion, QRS Duration and QT
Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
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Dispersion in Hospital Events in Cases of Acute Coronary Syndrome. J en Pract 3: 196. doi: 10.4172/2329-9126.1000196
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