- 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. |Favorite Table|Download (.pdf)
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 ...