- Chest discomfort, usually described as “pressure,” “dull,” “squeezing,” or “aching.”
- Characteristic electrocardiographic changes.
- Elevated biomarkers, such as troponin.
- Imaging may show new regional wall motion abnormality with
preserved wall thickness.
- The elderly, women, and diabetics may have atypical presentation.
Acute myocardial infarction (MI) is a clinical syndrome that
results from occlusion of a coronary artery, with resultant death of
cardiac myocytes in the region supplied by that artery. Depending
on the distribution of the affected coronary artery, acute MI can
produce a wide range of clinical sequelae, varying from a small,
clinically silent region of necrosis to a large overwhelming area
of infarcted tissue resulting in cardiogenic shock and death. About
1.2 million people experience MI in the United States each year; every
minute, one American will die of coronary artery disease.
The risk of having an acute MI increases with age, male gender, smoking, dyslipidemia, diabetes, hypertension, abdominal obesity,
a lack of physical activity, low daily fruit and vegetable consumption, alcohol overconsumption, and psychosocial index. As much as 90% of the risk of acute MI has been attributed to the modifiable risk factors. The diagnostic criteria for acute MI are listed in Table 5–1.
Table 5–1. ESC/ACC Definition of Myocardial Infarction.
| Save Table
Table 5–1. ESC/ACC Definition of Myocardial Infarction.
|Criteria for acute MI|
Criteria for established MI
Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following:
Development of pathologic Q waves on the ECG
ECG changes indicative of ischemia (ST segment elevation or depression)
Coronary artery intervention (eg, coronary angioplasty)
Pathologic findings of an AMI
Any one of the following criteria satisfies the diagnosis for established MI:
Development of new pathologic Q waves on serial ECGs. The patient may or may not remember previous symptoms. Biochemical markers of myocardial necrosis may have normalized, depending on the length of time that has passed since the infarct
Pathologic findings of a healed or healing MI
A prolonged imbalance between myocardial oxygen supply and demand
leads to the death of myocardial tissue. Coronary atherosclerosis
is an essential part of the process in most patients. Ischemic heart disease
seems to progress through stages of fatty-streak deposition in coronary
arteries to development of fibro-fatty plaque, which then increases
in size until it causes luminal obstruction, leading to exertional
angina (see Chapter 3). However, at any stage
in this process, the atherosclerotic lesion may erode, ulcerate,
fissure, or rupture, thereby exposing subendothelial vessel wall
substances to the circulating blood. Procoagulant factors (such
as tissue factor) reside within the plaque itself and, in the absence
of counterbalancing antithrombotic factors (eg, heparin, tissue-factor-inhibitor) and fibrinolytic activities (tissue plasminogen activator [t-PA] and single-chain urokinase-type plasminogen activator) within the endothelial
cells of the coronary artery, can cause thrombosis. This potent
procoagulant stimulus results in thrombus development in this region. In
general, acute MI occurs when this thrombosis propagates and occludes flow
within the artery, resulting in ischemia of cardiomyocytes distal
to the obstruction. Recent work suggests that inflammation may play
a pivotal role in the genesis of plaque rupture. Total thrombotic
occlusion occurs most commonly in proximal coronary arteries; its presence
has been documented during the first 4 hours after infarction in
more than 85% of patients with ST-segment elevation (Figure 5–1).
Incidence of total occlusion in patients with acute myocardial infarction.
(Reproduced, with permission, from DeWood MA et al. N Engl J Med. 1980;303:897.)
A similar type of myocardial insult occurs occasionally despite angiographically normal coronary arteries and may be caused by emboli
(eg, in patients with prosthetic valves or those with endocarditis),
dissection of the coronary artery (most commonly in pregnant women),
or coronary vasospasm (on rare occasions). It can also be caused
by thrombosis in situ, the probable mechanism by which patients
who have variant angina or who abuse cocaine can suffer acute infarction. In these cases, vasoconstriction secondary to endothelial dysfunction
and a propensity to thrombosis is of sufficient magnitude and duration
to cause thrombus formation. Oxygen consumption and possibly direct myocyte toxicity also increase with cocaine use. In
addition, thrombosis in situ can apparently cause infarction among
women who take estrogens (especially if they smoke). An increasingly
recognized differential diagnosis of acute MI is stress cardiomyopathy
(also known as apical ballooning syndrome or tako-tsubo cardiomyopathy).
This entity can present with a variety of symptoms and electrocardiographic
(ECG) changes, including ST elevation, and there is akinesis of
the anterior and inferior walls and apex of the left ventricle in
the absence of coronary artery disease. It is often accompanied
by severe emotional stress. The diagnosis is one of exclusion, after
angiography demonstrates patent coronary arteries. The prognosis
is good, and recovery of ventricular function is the norm.
In addition to blockage of coronary arteries (reduced “supply”), acute MI may be seen when myocardial oxygen requirements are elevated
(increased “demand”). This often occurs when other
medical illnesses coexist with ischemic heart disease. Pulmonary
embolism, pneumonia, arrhythmia, septic shock, severe anemia, or
great emotional distress can increase myocardial oxygen demand,
reduce coronary perfusion pressure, or evoke paradoxical coronary
artery responses and lead to MI. However, these tend to be smaller
infarctions with no ECG ST elevation that are diagnosed by elevated
Libby P et al. Inflammation and atherosclerosis. Circulation. 2002 Mar 5;105(9):1135–43.
Rosamond W et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2007 update: a report from the American Heart Association Statistics
Committee and Stroke Statistics ...