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Ischemic Heart Disease,

Myocardial Infarction and


Hypertensive Heart Disease

Clinical Features
The classic MI is heralded by severe, crushing
substernal chest pain (or pressure) that can radiate to
the neck, jaw, epigastrium, or left arm.
Silent infarcts are particularly common in patients
with underlying diabetes mellitus due to neuropathy
Dyspnea is common, attributable to impaired
myocardial contractility.

Electrocardiographic abnormalities are important for the diagnosis of MI; these


include Q waves, ST segment changes, and T wave inversions (the latter two
representing abnormalities in myocardial repolarization). Arrhythmias caused by
electrical abnormalities in ischemic myocardium and conduction system are
common; indeed, sudden cardiac death from a lethal arrhythmia accounts for the
vast majority of MI-related deaths occurring before hospitalization. The laboratory
evaluation of MI is based on measuring blood levels of macromolecules that leak
out of injured myocardial cells through damaged cell membranes (Fig. 1013);
these molecules include myoglobin, cardiac troponins T and I (TnT, TnI), creatine
kinase (CK) (specifically the myocardial isoform, CK-MB), and lactate
dehydrogenase. Troponins and CK-MB have high specificity and sensitivity for
myocardial damage. CK-MB remains a valuable marker of myocardial injury,
second only to the cardiac-specific troponins (see next entry). Total CK activity is
not a reliable marker of cardiac injury since various isoforms of CK are also found in
brain, myocardium, and skeletal muscle. However, the CK-MB isoformprincipally
derived

from myocardium, but also present at low levels in skeletal muscle


is the more specific indicator of heart damage. CK-MB activity begins
to rise within 2 to 4 hours of MI, peaks at 24 to 48 hours, and returns
to normal within approximately 72 hours.
TnI and TnT normally are not found in the circulation; however,
after acute MI, both are detectable within 2 to 4 hours, with levels
peaking at 48 hours and remaining elevated for 7 to 10 days.
Although cardiac troponin and CK-MB are equally sensitive markers
of the early stages of an MI, persistence of elevated troponin levels
for approximately 10 days allows the diagnosis of an acute MI long
after CK-MB levels have returned to normal. With reperfusion, both
troponin and CK-MB levels may peak earlier owing to more rapid
washout of the enzyme from the necrotic tissue.