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. 11.13 ). These molecules include myoglobin, cardiac troponins T and I (TnT, TnI), creatine kinase (CK;
Fig. 11.12 Reperfusedmyocardialinfarction.(A)Thetransverseheartslice(stainedwithtriphenyltetrazoliumchloride)exhibitsalargeanteriorwallmyocardialinfarctionthatishemorrhagicbecauseofbleedingfromdamagedvessels.Theposteriorwallisatthetop. (B)Hemorrhageandcontractionbands,visibleasprominenthypereosinophiliccross-striationsspanningmyofibers(arrow), areseenmicroscopically.
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Relative concentration(=multiples of upper reference limit)
Hours after onset of chest pain
Fig. 11.13 Acuteincreasesinmyocardium-derivedtroponinI,myocardialcreatinekinase(CK-MB),andmyoglobinfollowlingmyocardialinfarction.ThekineticsofenzymeelevationscanbeusedtoestimatethetimingoftheMI.Myoglobincanalsobemeasured,butissubstantiallylesssensitiveandspecificformyocardialinjury.
specifically the myocardial isoform, CK-MB), and lactate dehydrogenase. Troponins (and to a lesser extent CK-MB) have high specificity and sensitivity for myocardial damage.
CK-MB has long been the biomarker of myocardial injury, but is now tested for less frequently in favor of the more sensitive cardiac-specific troponins. Total CK activity is not a reliable marker of cardiac injury since various isoforms of CK are found in non-cardiac tissues. However, the CK-MB isoform—principally derived from myocardium, but also present at low levels in skeletal muscle—is a 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. Persistence of elevated troponin levels allows the diagnosis of an acute MI to be made 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.
Consequences and Complications of Myocardial Infarction
Extraordinary progress has been made in improving patient outcomes after acute MI; the overall in-hospital death rate for MI is approximately 7% to 8%, with MI associated with ST segment elevations (approximately 10% mortality) experiencing higher mortality rates than those without (approximately 6%). Unfortunately, out-ofhospital mortality is substantially poorer: one third of individuals with STEMIs die, usually of an arrhythmia within 1 hour of symptom onset, before they receive appropriate medical attention. Such statistics make the rising rate of coronary artery disease in developing countries with scarce hospital facilities all the more worrisome.
Nearly three fourths of patients experience one or more of the following complications after an acute MI (
Fig. 11.14