Increased age, male, hypertension, hypercholesterolemia, diabetes, smoking, and family history of coronary artery disease are the risk factors for myocardial infarction.

Patients under the age of 40 with no cardiovascular risk factors and older healthy patients (e.g., 60-year-old swimmer) with no cardiovascular risk factors are highly unlikely to be having an MI. Pain that is reproducible by palpation is more suggestive of musculoskeletal pain. Localized pain that is described as being sharp is also less likely to be related to heart disease, as is chest pain related to certain foods or eating.

Chest pain, diaphoresis, anxiety, tachycardia, tachypnea, and nausea/vomiting are classic findings. If there is a large area of ischemic damage to the heart, the patient may have heart failure presenting with bilateral rales (pulmonary edema), jugular venous distention, new S3 or S4 heart sounds, new murmurs, and hemodynamic instability (i.e., cardiogenic shock).

Postmenopausal women are at higher risk for MI. In fact, heart disease is the leading cause of death in women over the age of 40. The decline in estrogen levels is believed to contribute to a higher cardiovascular disease risk profile. Estrogen promotes growth and maintenance of the intimal layer of the arterial wall, maintaining its ability to expand and accommodate blood flow.

Acute coronary syndrome entails varying degrees of acute myocardial ischemia, the end result of coronary artery disease. There are three types of acute coronary syndrome: unstable angina (UA), non-ST segment elevation myocardial infarction (NSTEMI), and ST segment elevation myocardial infarction (STEMI).

What is the Difference Between UA, NSTEMI, and STEMI?

Thrombus formation following plaque rupture is the primary mechanism involved in coronary vessel obstruction leading to ischemia and, eventually, myocyte necrosis and tissue death.

The left anterior descending (LAD) artery is the most commonly affected coronary vessel.

Yes. MIs are classified based on whether or not there is a primary coronary event, such as a plaque rupture with subsequent thrombosis. Causes of MI not associated with a primary cardiac event include decreased oxygen supply (e.g., hypoxia, hypotension, anemia) and increased myocardial oxygen demand (e.g., sepsis, tachyarrhythmias). Postoperative MIs often result from a combination of factors other than primary coronary events. Primary coronary events require urgent intervention, while MIs resulting from non-primary coronary events will often resolve as the underlying cause is addressed.

Prinzmetal angina is characterized by episodic chest pain unrelated to exertion. Coronary artery vasospasms are responsible for transient decreased perfusion to the heart which causes reversible injury to myocytes. ECG shows ST segment elevation secondary to transmural ischemia, similar to what is seen in unstable angina. However, Prinzmetal angina is not due to coronary artery disease.

In addition to a relevant history (i.e., prior MI, chest pain) and physical exam, the patient should have a 12-lead ECG and a blood test for cardiac enzymes. A chest radiograph will help rule out other diagnoses like pneumothorax and aortic dissection.

Cardiac enzymes, including troponin-I and creatine phosphokinase myocardial fraction (CKMB), are measured every 8 hours in the first 24 hours of a suspected MI. CKMB is the first to rise but it has a low specificity. Troponin-I has the highest sensitivity for MI and increases in 3 hours, peaks in 6 hours, and gradually decreases over 7 days.

CKMB is the best marker to look for secondary MI following a recent MI. Its levels peak within 12–40 hours following MI and decreases after 2–3 days. Therefore, in a subsequent MI, there will be a new increase in CKMB.

ECG will help determine whether there is actually ischemia or infarction and, if so, the location of the ischemia or infarction (Table 5.1). ECG may potentially identify nonischemic causes of the patient’s symptoms, such as pericarditis, pulmonary embolism, and arrhythmia.