CLINICAL PRESENTATION



The usual patient with myocardial infarction has severe chest pain that lasts until treated. Some patients are discovered to have suffered a my­ocardial infarction by electrocardiography or non­invasive evaluation of left ventricular function without any clinical history of infarction. In many of these patients, when a very careful history is obtained, an episode can be identified that prob­ably represents the myocardial infarction. How­ever, some people, especially diabetics, have true “silent” myocardial infarctions.

The diagnosis of sub­endocardial infarction may be suspected from electrocardiographic ST and T wave changes but must be confirmed by enzyme determinations. There are no chest x-ray findings characteristic of myocardial infarction. The white blood cell count rises the first day after a myocardial infarction and returns to normal within a week; it usually peaks between 12,000 and 15,000 cells/cu mm. Acute phase reactants, such as the erythrocyte sedimentation rate, may be elevated. Several cardiac en­zymes released into the blood (Fig. 7-2) are used to diagnose myocardial infarction. Creatine kin­ase MB (the fraction characteristic of cardiac mus­cle) is the most sensitive and specific marker of myocardial necrosis, and an MB fraction exceed­ing 7 to 8 per cent is indicative of myocardial in­farction even if the total CPK is not greater than normal. Injury to skeletal muscle causes the skel­etal muscle fraction (MM) of CPK to rise. Other forms of injury to cardiac muscle, such as myo­carditis, trauma, and cardiac surgery, may release significant amounts of creatine kinase MB frac­tion. Cardioversion and CPR usually do not ele­vate the MB function. Serum lactate dehydrog­enase (LDH) may be fractionated into five isozymes. LDHj is principally from the heart, and if LDHa exceeds LDH2, myocardial infarction is likely. LDH is sometimes useful in diagnosing my­ocardial infarction in a patient who presents sev­eral days after the event, when the creatine kinase has normalized. Hemolysis can raise LDHi activ­ity, but LDH2 also elevates and exceeds LDH}. Liver and skeletal muscle contain mainly LDH4 and LDH5.

The use of infarct-avid scintigraphy has been discussed in Chapter 2. Echocardiography may demonstrate a segmental wall motion abnormality but cannot distinguish whether it is old or new.