SUMMARY To define the role of portable two-dimensional echocardiography (2-D echo) in the immediate diagnosis of acute chest pain syndrome, 80 consecutive patients were studied. Adequate 2-D echo studies were obtained in 65 (81%). Thirty-three patients had clinical evidence of transmural or nontransmural acute myocardial infarction (AMI), 18 infarction, which correlate well with pathologic data and with the site of infarction on the ECG. The purpose of this study was to investigate the role of twodimensional echocardiography in the immediate diagnosis of acute myocardial infarction in patients who present with acute chest pain to the emergency room. Materials and MethodsThe study population consisted of 80 consecutive patients with a symptom complex of prolonged chest discomfort occurring within 12 hours of admission to an intensive care unit. Patients with valvular heart disease, previous myocardial infarction, cardiomyopathy or significant periocardial effusion were excluded by clinical history, physical examination or echocardiography. M-mode and two-dimensional echocardiograms were obtained within 8 hours of admission. Fifty-four males and 26 females, ages 32-85 years, were studied. Myocardial infarction was diagnosed by a typical history of chest pain along with either characteristic electrocardiographic changes or a rise in serum CK-MB. ECGs were performed at least once daily and CK-MB was measured every 8 hours for the first 24 hours and then daily for at least 2 days. CK-MB was performed by the cellulose acetate electrophoretic method. A transmural myocardial infarction was diagnosed by the development of new Q waves > 0.04 second in more than one lead or an R: S ratio > 1 in lead V1 or V2 with at least abnormal repolarization in the inferior leads. A nontransmural myocardial infarction was diagnosed by an elevation of CK-MB enzyme without necessitating important ECG changes or classic evolution of deep symmetric T-wave inversions. The infarction was considered inferior if the Q waves or symmetrically inverted T waves occurred in leads 2, 3, or aVF; anterior if in leads V1-V,; and lateral if in leads 1, aVL or V,-V,.The clinical course was monitored in the intensive care unit and thereafter. A cardiac complication was

LVH produces multiple electrophysiological abnormalities and increased vulnerability to inducible polymorphic ventricular arrhythmia in this model of LVH. Cats that show regression of hyperthrophy have normal ventricular electrophysiology and have the same low vulnerability to inducible ventricular arrhythmia as Sham animals.

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