Chest pain.

Patients undergoing STEMI typically experience severe substernal pressure that they characterize as unbearable crushing or constricting pain. The pain often radiates down the arms and up to the jaw. STEMI can be differentiated from angina pectoris in that pain caused by STEMI lasts longer (20 to 30 minutes) and is not relieved by nitroglycerin. Some patients confuse the pain of STEMI with indigestion.

ECG changes.

Acute STEMI produces changes in the ECG. Why? Because conduction of electrical impulses through the heart becomes altered in the region of injury. Elevation of the ST segment, which defines STEMI, occurs almost immediately in response to acute ischemia (Fig. 53–1). Following a period of ST-segment elevation, a prominent Q wave (more than 40 milliseconds in duration) develops in the majority of patients. (Q waves are small or absent in the normal ECG.) Over time, the ST segment returns to baseline, after which a symmetric inverted T wave appears. This T-wave inversion may resolve within weeks to months. Q waves may resolve over a period of years.

Biochemical markers for MI.

When myocardial cells undergo necrosis, they release intracellular proteins (eg, cardiac troponins, creatine kinase). Hence, elevations in these proteins in blood can be diagnostic of STEMI.

Today, cardiac-derived troponins—cardiac troponin I and cardiac troponin T—are considered the best serum markers for STEMI. These proteins are components of the sarcomere, and are distinct from their counterparts in skeletal muscle. Under normal conditions, troponin I and troponin T are undetectable in blood. However, when STEMI occurs, their levels rise dramatically, often to 100-fold or more above the lower limits of detection. Cardiac troponins become detectable 2 to 4 hours after symptom onset, peak in 10 to 24 hours, and return to undetectable in 5 to 14 days. Measurements of troponin I and troponin T are more sensitive than measurements of other biochemical markers for STEMI, and produce fewer false-positive or false-negative results.

Before cardiac troponins became the preferred biomarkers for STEMI, clinicians relied on measurement of the MB isozyme of creatine kinase (CK-MB). Since CK-MB is found primarily in cardiac muscle rather than skeletal muscle, an increase in serum CK-MB is highly suggestive of cardiac injury. Following MI, serum levels of CK-MB begin to rise in 4 to 8 hours, peak in 24 hours, and return to baseline in 36 to 72 hours. In some patients, the increase in CK-MB may be too small to allow a definitive diagnosis, even though significant myocardial injury has occurred.