Download Ischemic Heart Disease

King Saud University
Pharmacy College
Pharmacology Department
513 PHL
Ischemic
Heart Disease
Prepared by…. Asma Al-Oneazi
1. Introduction:
Ischemic heart disease refers to a condition with disturbance of cardiac function due to a
relative lack of oxygen in the myocardium. Most often this is caused by atherosclerosis in the
coronary arteries. Reduction in myocardial perfusion can be limited from other causes such as
thrombi, vascular spasms and other more rare conditions.(1)
Ischemic heart disease represent a clinical spectrum that extends all the way from unstable
angina presenting with worsening episodes of chest pain, to non-ST segment elevation
myocardial infarction (NSTEMI) with more prolonged chest pain and biochemical evidence
of myocardial injury, to ST-segment elevation myocardial infarction (STEMI) with more
extensive myocardial damage and usually the formation of Q-waves on the surface
electrocardiogram, and finally to sudden cardiac death.(5)
Ischemic heart disease mainly due to an imbalance in the myocardial oxygen supplydemand relationship. This imbalance may be caused by an increase in myocardial oxygen
demand (which is determined by heart rate, ventricular contractility, and ventricular wall
tension) or by a decrease in myocardial oxygen supply (primarily determined by coronary
blood flow but occasionally modified by the oxygen-carrying capacity of the blood) or
sometimes by both.(2) Some of the risk factor for ischemic heart disease is socioeconomic
status in both adulthood and childhood, gender, lifestyle factors, including body mass index,
and smoking, blood pressure, and high blood cholesterol level.(1)
2. Physiology of coronary blood vessels:
2.1. The normal coronary system consists of:
 Large epicardial or surface vessels that normally offer little intrinsic resistance to
myocardial flow.
 Intramyocardial arteries and arterioles, which branch into a dense capillary network to
supply basal blood flow of myocardium.
Both are in series, and total resistance is the
geometric sum; however, under normal
circumstances, the resistance in intramyocardial
arteries is much greater. The arterioles
dynamically alter their intrinsic tone in response
to demands for oxygen and other factors, and as
a result, myocardial oxygen delivery and
myocardial oxygen demand are tightly coupled
in a rapidly responsive system.
Figure-1: Anatomy of
coronary blood vessels
[2]
There are relationships among coronary blood vessels and blood flow. As resistance
increases in surface vessels owing to occlusion, Intra-myocardial vessels can vasodilate
to maintain coronary blood flow.(4)
2.2. Metabolic regulation:
Over a wide range of activity, coronary blood flow is closely matched to myocardial
metabolic requirements to maintain a consistently high level of oxygen extraction by the
heart. Even during resting conditions 70% to 80% of the oxygen perfusing the coronary
capillaries is extracted by the myocardium, so there is little ability to increase oxygen
uptake by means of increasing oxygen extraction. For this reason, increases of oxygen
demands during exercise or other stress must be met by proportionate increases in
coronary flow.(15)
So, any changes in oxygen balance lead to very rapid changes in coronary blood flow.
Although a number of mediators may contribute to these changes, such as nitric oxide,
prostaglandins, CO2, and H+, and adenosine; which is formed from (ATP) and adenosine
(AMP) under conditions of ischemia and stress, is a potent vasodilator that links
decreased perfusion to metabolically induced vasodilation. The synthesis and release of
adenosine into coronary sinus venous effluent occur within seconds of coronary artery
occlusion.(4)
2.3. Endothelial control of coronary vascular tone:
The vascular endothelium, a single-cell tissue with an enormous surface area separating
the blood from vascular smooth muscle of the artery wall, is capable of a broad range of
metabolic functions. The endothelium functions as; a protective surface for the artery
wall, as long as it remains intact and functional, it promotes vascular smooth muscle
relaxation and inhibits thrombogenesis and atherosclerotic plaque formation. Damaged
endothelium reacts to numerous stimuli with vasoconstriction, thrombosis, and plaque
formation.(4)
2.4. Endothelial cells, once thought to be passive conduits for blood flow, are now known to
perform two extremely important functions in maintaining homeostatic processes. One
function is structural, in which the cells act as a permeability barrier and regulate passage
of molecules and cells across the blood vessel wall. The second function is metabolic, in
which the cells secrete opposing mediators that maintain a balance between bleeding and
clotting of blood (including activation and inhibition of platelet functions and
fibrinolysis), constriction and dilation of blood vessels, and promotion and inhibition of
vascular cell growth and inflammation. Some of the mediators that have role in the
regulation of vasomotor tone:
Vasodilators
 Endothelial-derived hyperpolarizing factor (EDHF)
 Nitric oxide (endothelial-derived relaxing factor, or EDRF)
 Prostacyclin (prostaglandin I2)
Vasoconstrictors
 Angiotensin II
 Endothelin
 Endothelium-derived constricting factor
[3]


Platelet-derived growth factor
Thromboxane A2.(4)
2.5.Endothelium derived relaxation factor: EDRF is synthesized from L-arginine via
nitric oxide synthase and released by shear force on the endothelium. EDRF or nitric
oxide then causes relaxation of the underlying smooth muscle and may be thought of
as a paracrine homeopathic defense mechanism against noxious stimuli. Denudation
or loss of the vascular endothelium results in loss of EDRF and this protective
mechanism. Loss of the endothelial cell layer and function may occur secondary to
physical disruption (e.g., percutaneous transluminal angioplasty [PTCA]), factors
impinging from the vascular side (cyanide from smoke), or disruption of the intimalmedial layers (oxidized low density lipoprotein). Impaired endothelial function may
be related to the development of premature atherosclerosis based on recent family
studies. Endothelial function may be improved with angiotensin converting enzyme
(ACE) inhibitors, statins, and exercise.(4)
3. Pathophysiology of ischemic heart disease:
3.1. With normal cardiac function, coronary blood flow can increase to meet needs for an
increased oxygen supply with exercise or other conditions that increase cardiac workload.
When coronary arteries are partly blocked by atherosclerotic plaque, vasospasm, or
thrombi, blood flow may not be able to increase sufficiently.(11)
3.2. Impaired endothelium function (eg, by rupture of atherosclerotic plaque or the sheer force
of hypertension) leads to vasoconstriction, vasospasm, clot formation, formation of
atherosclerotic plaque, and growth of smooth muscle cells in blood vessel walls.(11)
3.3. When the endothelium is damaged, these vasodilating and antithrombotic effects are lost.
At the same time, production of strong vasoconstrictors (eg, angiotensin II, endothelin-1,
thromboxane A2) is increased. In addition, inflammatory cells enter the injured area and
growth factors stimulate growth of smooth muscle cells. All of these factors participate in
blocking coronary arteries.(11)
3.4. Atherosclerotic lesions encroaching on the luminal cross sectional area of the larger
epicardial vessels transform the relationships among coronary blood vessels and blood
flow. The response become inadequate with greater degrees of obstruction. As blood
flows across a stenotic lesion, the pressure drops owing to abrasion between blood and
the lesion and owing to the abrupt unstable expansion as blood emerges from the
stenosis. This pressure drop is dynamic and directly related to flow, giving rise to a
resistance that is not fixed but rather fluctuates as flow is changed. This relationship can
[4]
affect collateral blood flow and its response to exercise dramatically, resulting in what
has been called coronary steal. A similar situation also may occur when the epicardial or
subepicardial vessels “steal” blood flow from the endocardium in the presence of a
stenotic lesion.(4)
Figure-2: Development of atherosclerotic lesions.
3.5. Sympathetic nervous system stimulation normally produces dilation of coronary arteries,
tachycardia, and increased myocardial contractility to handle an increased need for
oxygenated blood. Atherosclerosis of coronary arteries, especially if severe, may cause
vasoconstriction as well as decrease blood flow by obstruction.(11)
3.6. When coronary atherosclerosis develops slowly, collateral circulation develops to
increase blood supply to the heart. Collateral circulation develops from anastomotic
channels that connect the coronary arteries and allow perfusion of an area by more than
one artery.(11) Collateral blood flow exists to a certain extent from birth as native
collaterals, but persisting ischemia may promote collateral growth as developed
collaterals. These two types of collaterals differ in anatomy and in their ability to regulate
coronary blood flow. Collateral development depends on the severity of obstruction, and
the presence of various growth factors (basic fibroblast growth factor [b-FGF] and
vascular endothelial growth factor [VEGF]), and endogenous vasodilators (e.g., nitrous
oxide and prostacyclin)(4) Endothelium-derived relaxing factors such as nitric oxide (NO)
can dilate collateral vessels and facilitate regional myocardial blood flow. Although
collateral circulation may prevent myocardial ischemia in the client at rest, it has limited
ability to increase myocardial perfusion with increased cardiac workload.(11)
[5]
4. Types of ischemic heart disease:
4.1. Silent Myocardial ischemia: with electrocardiographic, or radionuclide evidence of
ischemia appearing in the absence of symptoms. While some patients have only silent
ischemia, most patients who have silent ischemia have symptomatic episodes as well.
The precipitants of silent ischemia appear to be the same as those of symptomatic
ischemia.(2)
4.2. Typical angina pectoris: symptoms of angina appear when myocardial oxygen demand
increases, as with exertion. In typical stable angina, the pathological substrate is usually
fixed atherosclerotic narrowing of an epicardial coronary artery, on which exertion or
emotional stress superimposes an increase in myocardial oxygen consumption. Typical
angina is experienced as a heavy, pressing substernal discomfort (pain), often radiating to
the left shoulder, flexor aspect of the left arm, jaw, or epigastrium. However, a significant
minority of patients notes discomfort in a different location or of a different character.
Women, the elderly, and diabetics are more likely to have ischemia with atypical
symptoms. In most patients with typical angina, whose symptoms are provoked by
exertion, the symptoms are relieved by rest or by administration of sublingual
nitroglycerin. Over many years it may become unstable, increasing in frequency or
severity and even occurring at rest.(2)
4.3. Unstable angina or vasospasm (variant or Prinzmetal angina): angina symptoms may
occur without any increase in myocardial oxygen demand but rather as a consequence of
abrupt reduction in blood flow, as might result from coronary thrombosis. In variant
angina, focal or diffuse coronary vasospasm episodically reduces coronary flow. Patients
also may display a mixed pattern of angina with the addition of altered vessel tone on a
background of atherosclerotic narrowing. In most patients with unstable angina, rupture
of an atherosclerotic plaque, with consequent platelet adhesion and aggregation,
decreases coronary blood flow. Plaques with thinner fibrous caps are more "vulnerable"
to rupture.(2)
4.4. Myocardial infarction: Myocardial infarction occurs when a narrowed atherosclerotic
coronary artery gets acutely occluded leading to necrosis of the heart muscle supplied by
that artery. Affected patients generally complain of a crushing sub-sternal pain with
radiation to the neck, jaw, or left arm. The pain may be accompanied by shortness of
breath, anxiety, nausea and sweating. The highest risk of death following acute
myocardial infarction occurs during first 12 hours when the risk of ventricular fibrillation
is greatest. Within 6 months following an episode of myocardial infarction, patients are at
increased risk of an additional infarction.(3)
[6]
Myocardial infarction can be classified according to electrocardiographic changes
into ST-segment-elevation MI [STEMI] or non-ST-segment-elevation MI [NSTEMI].
Table-1: The different between NSTEMI and STEMI.
NSTEMI
STEMI
 NSTEMI does not cause changes on (ECG).
However, chemical markers in the blood
indicate that damage has occurred to the
heart muscle, and the blockage may be
partial or temporary, and so the extent of the
damage relatively minimal.(12)
 NSTEMI ischemia is severe enough to
produce myocardial necrosis, resulting in
the release of a detectable amount of
biochemical markers, mainly troponins T or
I and creatine kinase from the necrotic
myocytes, in the bloodstream(4).
 Abnormal cardiac enzymes
NSTEMI from UA.(12)
distinguish
 NSTEMI
is
usually
caused
by
atherosclerotic disease, which diminish the
blood flow to the myocardium causing
myocardial ischemia.
 Also, can be caused by a non-occlusive
thrombus such as spasm in the coronary
artery which is associated with an increased
risk for cardiac death and myocardial
infarction. (12)
[7]
 STEMI is caused by a prolonged period of
blocked blood supply. It affects a large
area of the heart muscle, and so causes
changes on the ECG as well as in blood
levels of key chemical markers.(12)
 The cause of STEMI is usually acute
atherosclerotic plaque rupture with
occlusive thrombus formation.(12)
 ST-segment changes that may be
indicative of myocardial ischemia or
injury. The elevated ST segment indicates
that a relatively large amount of heart
muscle damage is occurring because the
coronary artery is totally occluded. (12)
 Emergency treatment with thrombolytics
or percutaneous coronary intervention.(13)
Figure-3: Electrocardiogram show STEMI and NSTEMI.
5. Diagnosis of ischemic heart disease:
5.1. Cardiac markers: they are biochemical markers such as creatine kinase (CK), CK-MB
isoenzyme, lactate dehydrogenase isoenzymes, myoglobin, cardiac troponins T (cTnT)
and I (cTnI) and others are routinely used to assist cardiologists and other physicians for
the diagnosis and management of patients with ischemic heart disease. (6) These markers
detect myocardial necrosis and prognosis. Death of myocytes releases enzymes that can
be detected in the blood. Cardiac markers will be positive if there has been myocardial
necrosis and is helpful in the diagnosis, especially because the ECG does not always
detect myocardial necrosis.(12)
5.1.1. Myoglobin: Myoglobin is a protein found in both skeletal and myocardial muscle. It
is released rapidly after tissue injury and may be elevated as early as one hour after
myocardial injury, although it may also be elevated due to skeletal muscle trauma.(7)
Myoglobin released early after the onset of MI such and can be used for ruling out
MI within the first 6–9 h after the onset of chest pain, important in the triaging of
patients presenting to an emergency department.(6)
5.1.2. Creatine kinase (CK): It is composed of M and/or B subunits that form CK-MM,
CKMB, and CK-BB isoenzymes. Total CK (the activity of the MM, MB, and BB
isoenzymes) is not myocardial-specific. However, the CK-MB isoenzyme (also
called CK-2) comprises about 40% of the CK activity in cardiac muscle and 2% or
less of the activity in most muscle groups and other tissues. CK- MB is both a
sensitive and specific marker for myocardial infarction and usually becomes
[8]
abnormal three to four hours after an MI, peaks in 10–24 hours, and returns to
normal within 72 hours. It would be the marker of choice if the sole decision to be made is
MI or MI rule out. (7)
5.1.3. Troponin T and troponin I: Troponin is a complex of three proteins on the thin
filaments of skeletal and cardiac muscle fibers. During muscle contraction the
troponin complex regulates the interaction between the thick and thin filaments. This
complex consists of troponin T (TnT), troponin I (TnI) and troponin C (TnC).
Troponin C is identical in skeletal and cardiac muscle, but the amino acid sequences
of troponin T and troponin I found in cardiac muscle is different from that of the
troponins in skeletal muscle. These isoforms of cardiac troponins, cTnT and cTnI,
are very specific to cardiac muscle and their presence in blood indicates cardiac
tissue necrosis. Because of this specificity, cardiac troponin T or I is now the
preferred cardiac marker. There is some evidence that cTnI is more cardiac specific
than cTnT, but both troponins are considered to be acceptable. Cardiac troponins T
and I begin to rise 4-8 hours after an MI, peak at approximately 12 - 24 hours, and
remain elevated for up to 10 days.(8)
5.1.4. C-reactive protein (CRP): CRP is a protein found in serum or plasma at elevated
levels during a inflammatory processes. It is a sensitive marker of acute and chronic
inflammation and infection, and in such cases is increased several hundred-fold.
Several recent studies have demonstrated that CRP levels are useful in predicting the
risk for a thrombotic event (such as a blood clot causing MI). Heart patients who
have persistent CRP levels between 4 and 10 mg/L, with clinical evidence of lowgrade inflammation, should be considered to be at increased risk for thrombosis.(7)
5.1.5. Myeloperoxidase (MPO): is a well-known enzyme, mainly released by activated
neutrophils, characterized by powerful pro-oxidative and pro-inflammatory
properties. There is strong evidence that HDL is a selective in vivo target for MPOcatalyzed oxidation, that may represent a specific molecular mechanism for
converting the cardio-protective lipoprotein into a dysfunctional form, raising the
possibility that the enzyme represents a potential therapeutic target for preventing
vascular disease in humans. Recently, myeloperoxidase has been proposed as a
useful risk marker and diagnostic tool in acute coronary syndromes and in patients
admitted to emergency room for chest pain.(9)
5.2. Diagnostic tests:
5.2.1. Electrocardiogram (ECG):
The ECG is simple to perform and is the most frequently used, least invasive, It remains
the procedure of first choice for evaluation of chest pain. In its simplest interpretation,
the ECG characterizes rhythms and conduction abnormalities. However, the ECG also
provides information about the pathophysiologic changes, and hemodynamics of the
CVD system. ECG abnormalities are often the earliest sign of ischemia, and electolyte
abnormalities, and used to assess physical strength, document the prevalence of
ischemic heart disease (IHD), and identify subclinical heart disease. The ECG
frequently is used in conjunction with other diagnostic tests to provide additional data,
[9]
to monitor the patient, and to identify if abnormalities detected during tests correlate
with ECG changes.(4).
Figure-4: Normal Electrocardiogram.
Myocardial ischemia, ranging from injury to necrosis, results in T-wave
changes, ST-segment abnormalities, and changes in the QRS complex. While
myocardial infarction results in a typical pattern of ECG changes that begins with
tall peaked T waves persisting up to several hours, followed by ST-segment
elevation with a coved configuration, and inverted T waves. Development of a new
Q wave has a high specificity but low sensitivity for acute myocardial ischemia.(4).
5.2.2. Exercise tolerance test (ET):
ET is a noninvasive test used to evaluate clinical and cardiovascular responses to
exercise. ET is used frequently as an initial test, in conjunction with physical
examination and patient symptoms. The ET provides diagnostic information in patients
with known or suspected IHD and prognostic information in patients after myocardial
infarction or revascularization.(4).
The principle behind ET is to increase myocardial oxygen demand above
myocardial oxygen supply and coronary reserve, thereby provoking ischemia
(inadequate myocardial perfusion), using exercise as a stressor. Ischemia is detected by
patient symptoms, ECG changes, and/or hemodynamic changes. The type of ECG
changes, leads affected, and patient performance are used as an index of severity and
location of disease. ET is a very practical test in that it can assess patients’ functional
capacity.(4).
5.2.3. Echocardiography (ECHO):
ECHO is the use of ultrasound to visualize anatomic structures such as the valves
within the heart and to describe wall motion. Clinically, ECHO is the most frequently
used noninvasive cardiovascular test. It competes well with invasive techniques such as
cardiac catheterization with angiography for the evaluation of ischemia and valvular
abnormalities. ECHO is used often as an initial evaluative tool following auscultation
detection of an abnormality, thus providing a baseline visual characterization.(4)
[10]
ECHO remains the procedure of choice in the diagnosis and evaluation of a number
of conditions such as wall motion abnormalities associated with ischemia. Images
obtained from ECHO are used to estimate chamber wall thickness and left ventricle
ejection fraction, assess ventricular function, and detect abnormalities of the
pericardium such as effusions or thickening.(4).
5.2.4. Cardiac catheterization and coronary arteriography:
Development of the cardiac catheterization technique was a major signpost in the
diagnosis and management of CVD because it provided a physiologic and anatomic
approach to assess patency of coronary vessels and hemodynamic parameters of cardiac
function. Cardiac catheterization is the technique used to gain vascular access to the
coronary arteries by intravascular catheters and heart chambers. Once cardiac
catheterization is complete, other diagnostic and therapeutic procedures, such as
angiography, percutaneous transluminal angioplasty (PTCA), and drug administration
(e.g., thrombolytics) may be undertaken.
Catheterization is also now used commonly with PTCA and/or drug therapy in the
management of acute coronary syndromes to:
 Evaluate efficacy of the intervention.
 Help define a new management strategy.
 allows assessment of valvular function and estimation of various cardiac
performance parameters such as cardiac output, stroke volume, systemic vascular
resistance, and blood flow.
 It also allows for placement of cardiac pacemakers.
Figure-5: Cardiac catheterization
The cardiac catheterization procedure requires vascular access, usually obtained
percutaneously at brachial or femoral arteries or veins. Left-sided catheterization
provides access to the aorta, left ventricle, and left atrium. Right-sided catheterization
enables the right side of the heart, coronary sinus, pulmonary arteries, and pulmonary
[11]
wedge position to be reached. Left-sided catheterization is used for coronary
angiography and ventriculography, whereas right sided catheterization is used for
determination of cardiac performance parameters.(4)
6. Prognosis of ischemic heart disease:
Usually the outcome of IHD is development of dysrrhythmia, reinfarction, and CHF.
Death are major outcomes following ACS Approximately 30% of patients develop heart
failure at some time during their hospitalization for IHD. In-hospital death rates for patients
who present with or develop heart failure are more than threefold higher than for those who
do not. Therefore, therapeutic strategies such as use of coronary angiography,
revascularization, and pharmacotherapy should be used to reduce morbidity and mortality due
to ischemic heart disease.(4)
7. Desired outcome of treatment:
The short-term goals of therapy for IHD are to reduce or prevent the symptoms that limit
exercise capability and impair quality of life. While the long-term goals of therapy are to
prevent CHD events such as MI, arrhythmias, and heart failure and to extend the patient’s
life.(4)
8. Treatment:
8.1. Pharmacological treatment:
Patient case
Appropriate treatment
Comment
Patients with hypertension
and IHD
1) Diuretics.
2) long-acting
dihydropyridine CCBs
3) ACEIs
4) antiplatelet agents
5) β blockers
6) hypolipidemic agents.(10)
Treatment to Prevent Acute
coronary syndrome and heart
attack development.(10)
Patient with silent ischemia
CCBs and β-blockers can be
used as protective.
Modify the major risk factors
for IHD, hypertension,
hypercholesterolemia, and
smoking.(4) Is
Ischemia17
chemia17
Patient with stable
exertional angina pectoris
1) Aspirin
2) β- blockers with prior MI
3) Lipid-lowering therapy such
as statin.
4) Sublingual nitroglycerin for
immediate relief of angina.(4)
[12]
 If aspirin contraindicated
give Clopidrogrel.
 Can be add CCBs or
long-acting nitrates for
reduction of symptoms
when β-blockers are
contraindicated. Or not
successful. Or if initial
treatment with β-blockers
leads to unacceptable side
effects.(4)
 Role of β-blockers;
potential cardioprotective
effects, antiarrhythmic
 effects, lack of tolerance,
and antihypertensive
effects(4).
Patient with coronary artery
spasm and variant angina
Nifedipine, verapamil, and
diltiazem as single agents for
the initial management of
variant angina and
coronary artery spasm.
For the acute attacks;
sublingual nitroglycerin or
isosorbide dinitrate. (4)
Patients with CAD and
diabetes.
ACEIs.(4)
Patient with STEMI
1) Nitroglycerin(sublingual
every 5 minutes as needed, or
Intravenous NTG for CHF,
hypertension, or persistent
ischemia that responds to
nitrate therapy).
2) Aspirin
3) Beta-Blocker
4)ACEIs
5)Angiotensin Receptor
Blocker
6) IV morphine sulfate as
needed to control pain.
6) Anxiolytics.(13)
Patient with NSTEMI
1) Aspirin (unless
contraindicated) /
clopidogrel.
2) Beta-blockers instituted
within the first 24 hours in
absence of
contraindications.(14)
CCBs or long-acting nitrates
for reduction of symptoms
when β-blockers are
contraindicated.(4)
[13]
 Beta-blocker should be
assess for contraindications,
i.e., bradycardia and
hypotension.
 Start ACEIs
 if there is no hypotension or
known contraindications to
this class of medications.
 Start ARB orally (in
patients who are intolerant
of ACEIs) (13).
Smoking-cessation counseling
Lipid panel measurement
Also, can be prescribe ACEIs(4)
8.2.Surgical treatment: The decision to choose percutaneous coronary intervention (PCI) or
CABG for revascularization is based on the extent of CAD (number of vessels and
location/amount of stenosis) and ventricular function.(4)
8.2.1.Percutaneous coronary intervention (PCI):
PCI has been used successfully in the management of UA. PCI is often the first
treatment of choice for (STEMI), which occurs when one of the coronary arteries is
completely blocked. The goal of both thrombolysis and PCI is to prevent the death of
heart muscle cells by restoring coronary blood flow to the heart. PTC involves the
insertion of a guide wire and inflatable balloon into the affected coronary artery and
enlarging the lumen of the artery by stretching the vessel wall. This frequently causes
atheroma plaque fracture by stretching inelastic components and denuding the
endothelium, resulting in loss of nitric oxide and other vasodilators and exposure of
plaque contents to the vascular compartment. Consequently, immediate vascular recoil,
platelet adhesion and aggregation, mural thrombus formation, and smooth muscle
proliferation and synthesis of extracellular matrix may give rise to acute occlusion and
early or late restenosis.(4)
Figure-6: Percutaneous coronary intervention.
The initiation of combination therapy with aspirin, unfractionated heparin or low-molecular
weight heparin, and glycoprotein (GP) IIb/IIIa receptor antagonists and coronary artery stents
has reduced the occurrence of early reocclusion and late restenosis dramatically. Patients best
appropriate for PTCA are those with recent onset of worsening of angina without a long history
of symptoms. Also, patients with one or more lesions to be dilated in vessels and patients with
multi-vessel disease and diabetes, or abnormal LV function.(4)
[14]
8.2.2.Coronary artery bypass grafting (CABG):
Coronary artery bypass grafting commonly used approach for the management of IHD. The
objectives in performing CABG are:
(1) to reduce the number of symptomatic anginal attacks not controlled with medical
management or PCI and improve the lifestyle of the patient.
(2) to reduce the mortality associated with CAD.
CABG is recommended in:
 asymptomatic or mild angina patient.
 in stable angina include proximal but with a moderate area of possible myocardium and
ischemia on noninvasive testing.
 In STEMI, for ongoing ischemia/infarction not responsive to maximal medical therapy.
 May be used for patients who have failed PTCA if there is ongoing ischemia or
threatened occlusion with significant myocardium at risk.
 (class I).
 CABG may be repeated in patients with a previous CABG if disabling angina exists
despite maximal noninvasive therapy and if a large area of myocardium is threatened and
is subtended by passable distal vessels.
The need for nitrates and β-blockers clearly is reduced by surgery, with only 30% of
CABG patients requiring chronic medication, in contrast to 70% of their medical counterparts
who receive anginal drugs.(4)
Graft patency influences the success for symptom control and survival, and the mechanism
for early graft occlusion is probably different from that associated with late closure. Early
occlusion is related to platelet adhesion and aggregation, whereas late occlusion may be related
to endothelial proliferation and progression of atherosclerosis. Antiplatelet therapy has been
demonstrated to improve early and late patency rates and probably should be used in all
patients who do not have any contraindications. Aspirin with or without other antiplatelet
agents (dipyridamole) reduces the late development of vein graft occlusions. Late graft closure
is related to elevated lipid levels and the progression of atherosclerosis in the grafted vessels as
well as the native circulation.
Aggressive lipid lowering can stabilize the progression of CAD and may induce
deterioration in selected coronary artery segments within a patient following CABG. as well as
in the management of other coronary risk factors (e.g., hypertension), and institution of a
supervised daily exercise program is recommended. Internal mammary artery grafts should be
used for better graft survival and clinical outcomes.(4)
[15]
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disease, a systematic review of the epidemiologic evidence: Scand J Work Environ
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2) Thomas Michel. (2006). TREATMENT OF MYOCARDIAL
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7) www.Encyclopedia of Surgery.Cardiac marker tests.
8) Larry Broussard, PhD, Patsy C. Jarreau, MHS, MT, Karen A. Brown, MS, MT, Laura
D. Massey, MA, MBA, MT. Educational Commentary for the 3rd Test Event of
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9) Valentina Loria, Ilaria Dato, Francesca Graziani, and LuigiM. Biasucci, (2008).
Myeloperoxidase: A New Biomarker of Inflammation in Ischemic Heart Disease and
Acute Coronary Syndromes: Mediators of Inflammation, Hindawi Publishing
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