Download Acute myocardial infarction

MODULE 16:
Figure 1
Cardiology
PART 9
Acute myocardial
infarction
Figure 2
by Lisa Browne
2. Right coronary artery
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Acute Myocardial Infarction (AMI) or heart attack is caused
by a sudden and prolonged reduction in coronary artery blood
flow. Infarcts are defined as either ST-Elevation (STEMI) or Non-STElevation (NSTEMI) with the pathophysiological difference being
related to the degree of coronary artery occlusion.
The majority of infarcts are caused by narrowing of an epicardial blood vessel due to atheromatous plaque. This plaque
ruptures exposing the underlying membrane and resulting in
platelet aggregation, fibrin accumulation and thrombus formation. The thrombus either partially occludes the vessel causing a
NSTEMI, or completely occludes the vessel causing ST-segment
elevation on the surface ECG (STEMI) (see Figure 1).
Myocardial cells that are starved of oxygen-enriched blood go
through stages of ischaemia, injury and necrosis. This process can
take up to six hours during which time the patient may experience pain or discomfort in their chest, arms, neck or jaw; they may
be diaphoretic and short of breath. In contrast for some patients
the first manifestation of acute myocardial ischaemia is sudden
cardiac death.
Myocardial cells that are abruptly deprived of their blood supply are prone to electrical instability; this can lead to ventricular
fibrillation and cardiovascular collapse. Nearly 50% of those who
succumb to acute myocardial infarction will die within the first
30-days,1 the majority of which are caused by ventricular fibrillation or pulseless ventricular tachycardia.
Non-atherosclerotic causes of myocardial infarction occur
much less frequently and are typically related to conditions such
as primary coronary vasospasm, vasospasm secondary to cocaine
use, or indeed other factors that cause prolonged reduction in
myocardial oxygen supply, eg. severe aortic stenosis.
Heart attacks vary in size and severity, but all are significant.
Some are catastrophic with either fatal or chronically disabling
outcomes; conversely some people make a complete recovery.
The severity and subsequent prognosis are primarily influenced
by the level of obstruction/occlusion, the size of the artery
1. Aorta
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2
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3. Left anterior descending
coronary artery
4. Circumflex coronary artery
5. Left main coronary artery
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involved, and in the case of STEMI the time between onset of
occlusion and revascularisation.2
Coronary circulation
Knowledge of coronary circulation is important in managing patients with acute myocardial ischaemia, as it is possible to
estimate the site of infarction from the ECG and therefore estimate the culprit artery. This information is clinically significant as
it not only provides a reasonable prognostic indication, it is also
invaluable in predicting the type of patients who are high risk for
complications.
The exact anatomy of the myocardial blood supply varies considerably from person to person. In general there are two main
coronary arteries, the left and right (see Figure 2). The left main
(LM) coronary divides into the left anterior descending (LAD) and
circumflex branches (LCX). It originates at the base of the aorta
from the coronary ostia located behind the aortic valve leaflet.
The LAD supplies the majority of the left ventricle, the anterolateral wall, the apex, and the interventricular septum.3 An acute
occlusion of the left main is often catastrophic as a huge proportion of the myocardium is starved of its blood supply. Conversely
an occlusion in a small distal branch of the LAD (which supplies a
smaller portion of the myocardium) is likely to carry a much better prognosis particularly when treated expeditiously.
The right coronary artery (RCA) originates above the right
cusp of the aortic valve. It travels down the right atrioventricu-
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lar groove, towards the crux of the heart. In addition to supplying
the right ventricle (RV), the RCA supplies 25-35% of the left ventricle (LV). In approximately 90% of patients the RCA gives off a
posterior descending branch (PDA), this pattern of flow is known
as right dominance. For the remaining patients the PDA is a terminal branch of the left circumflex. The PDA supplies the inferior
wall, ventricular septum, and the posteromedial papillary muscle.
The RCA also supplies the sino-atrial (SA) node in 60% of patients.
The other 40% of the time, the SA nodal artery is supplied by the
left circumflex artery.3 Proximal occlusion of the RCA is therefore
likely to cause significant damage to the inferior wall, the right
ventricle and increases the risk of brady arrhythmias in people
whose sino-atrial node is supplied by the RCA.
Degree of obstruction/occlusion
As mentioned previously, the degree of coronary occlusion differentiates ST-Elevation from Non-ST-Elevation. Time to treatment
is critically important when the artery is completely occluded
(STEMI). The sooner the artery is opened and coronary perfusion
is restored the better the prognosis.4 Even in the case of NSTEMI,
there is a strong correlation between expeditious treatment and
positive patient outcomes.4
Time as a factor
Reperfusion therapy (thrombolysis or primary percutaneous
intervention (PCI)) is only indicated for STEMIs and aims to reestablish coronary artery patency. It is therefore important that
this sub-set of patients are identified and treated soon after their
arrival to hospital. The diagnosis of STEMI is made after a taking
a targeted clinical history, physical examination, and 12 lead ECG.
The clinical history should ascertain the timing of symptoms, and
the physical examination aids in differential diagnosis and in
determining the presence of any complications. The 12-Lead ECG
is central to the decision-making process because ST-Elevation
identifies patients who benefit from urgent reperfusion. For this
reason the ECG should be obtained and analysed within five minutes of the patient’s arrival to hospital
Symptoms
The history is critical in making the diagnosis of MI and sometimes may provide the only clue that leads to the diagnosis in
the initial phase of presentation. Chest pain, usually across the
anterior precordium is typically described as tightness, pressure,
or squeezing. The discomfort may radiate to the jaw, neck, arms,
and epigastrium. The left arm is more frequently affected; however the patient may experience pain or heaviness in both arms.
Dyspnoea may accompany chest pain or occur as an isolated
complaint, suggesting poor ventricular compliance in the setting
of acute ischemia.
It should be noted that the severity of symptoms do not
generally correlate well with the severity of the condition. The
public often have a pre-existing expectation of what a heart
attack should feel like. They often expect severe and dramatic
crushing chest pain. This is however a contrast to the clinical
reality. Chest discomfort is a subjective experience and patient’s
symptoms may vary from mild to more severe discomfort. Furthermore a significant minority of patients will present with
symptoms other than chest pain, this is particularly evident in
women, the elderly and diabetic patients. For some individuals
the MI can be a totally silent event, and may only be identified
retrospectively on coronary angiogram or when patients present
with evidence of left ventricular dysfunction weeks or months
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later. Despite these variations in the severity and type of symptoms, chest discomfort remains the most common clinical feature,
as such should always be taken seriously.
The physical examination can often be unremarkable, however
a targeted cardiac assessment is important before a diagnosis
is made. This will help the clinician rule out alternative causes
for symptoms; provide valuable information pertaining to the
current level of cardiac function and highlight any potential contraindications to treatment.
The ECG is critical to the diagnostic process. ECG criteria for the
diagnosis of STEMI is new ST Elevation in two or more contiguous
precordial leads (V1-V6) (Figure 1) , or more than 1mm in the limb
leads (1,11,111, AVF, AVL) or the occurrence of new LBBB. While
changes do occur in the majority of patients with ischaemic chest
pain, it should be noted that the ECG is an imperfect tool and can
be normal in the early stages of STEMI. Furthermore conditions
like pericarditis can mimic STEMI. For this reason the ECG should
always be used in light of other clinical information.
Treatment
Standard pharmacological treatment for patients with acute
myocardial infarction (both STEMI and NSTEMI) includes aspirin,
clopidogrel, oxygen, b-blockers, nitrates and statins. For those
with complete coronary occlusion (STEMI) there are two forms
of reperfusion therapy available, pharmacological (fibrinolysis) or
primary percutaneous coronary intervention (primary PCI). Fibrinolytic agents work by catalysing the conversion of plasminogen
to plasmin; thus dissolving fibrin, the thread like substance that
binds clot together. This therapy is maximised when it is administered within the first few hours of symptom onset, lesser benefits
can be seen when administered up to 12 hours.
Primary PCI has consistently been proven to be a superior
treatment to fibrinolysis.5 This treatment involves direct revascularisation of the occluded vessel by angioplasty balloon inflation
and or clot extraction. Primary PCI restores coronary artery patency in over 90% of patients whereas fibrinolytic therapy is
effective in about 50-60% of cases.4 Furthermore, it is superior in
terms of preserving myocardial function, long- and short-term
mortality and reducing major complications such as stroke.5 In
addition, this treatment is of considerable benefit to patients
who are ineligible for fibrinolytic therapy or as a rescue strategy
when fibrinolytic therapy has failed. Primary PCI is however only
provided in specialist centres that have onsite catheterisation
facilities and a skilled team of operators.
While the treatment of acute myocardial infarction has improved
significantly over the past decade, it remains a very significant
cause of death and disability within our society. The presence of
chest pain in at risk individuals should always be taken seriously
and promptly evaluated. In the business of managing acute myocardial ischaemia, time really does mean muscle, and the quicker
we act the better the patient’s chances of survival are.
Lisa Browne is an advanced nurse practitioner in cardiology at the Mater Hospital,
Dublin
References
1. Ratcliffe A, Pepper C. Thrombolysis or primary angioplasty? Reperfusion therapy for
myocardial infarction in the UK. Postgraduate Med J 2008; 84: 73-77
2. Banning A. (Ed). Managing Acute Myocardial Infarction. Medicine 2006; 34(5): 181-19
3. Morton P et al. Critical Care Nursing: A Holistic Approach. 8th ed. Lippincott Williams &
Wilkins, 2005
4. Keeley E, Hills L. Primary PCI for Myocardial Infarction with ST-Segment Elevation. NEJM
2007; 365(1): 47-54
5. Guagliumi G. Emerging data and decisions for optimizing STEMI management: the
European perspective. Eur Heart J Suppl 2009; 11(C): 19-24
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