Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations.

OBJECTIVE: To test the hypothesis that certain clinical events may precede free wall myocardial rupture and allow its prediction, we conducted a retrospective and prospective study of 70 patients with rupture. BACKGROUND: Rupture of the left ventricular free wall develops in approximately 10% of patients with fatal acute transmural myocardial infarction. Clinically, its occurrence has been considered precipitous and unexpected. Pathologically, however, rupture appears to be a stuttering, progressive process characterized in many instances by an infiltrating intramural hemorrhage and a thrombus within the tear of > or = 1 day's duration. METHODS: The clinical course and evolutionary electrocardiographic (ECG) changes in 70 consecutive patients with rupture and 100 comparison patients with acute myocardial infarction but without rupture were reviewed to ascertain whether certain clinical symptoms, signs and ECG alterations occur in patients prone to develop rupture, allowing its anticipation. In addition, a correlation was established between the site of infarction indicated by the ECG and the site of rupture determined at autopsy or surgery. RESULTS: Patients with rupture had a significantly greater incidence of pericarditis, repetitive emesis and restlessness and agitation than did patients without rupture. More than 80% of patients with rupture had two or more symptoms compared with 3% of patients without rupture (p < 0.002). A deviation from the expected evolutionary T wave pattern occurred in 94% of patients with rupture and 34% of control patients (p < or = 0.02). An abrupt transient episode of hypotension and bradycardia, probably due to the initial tearing of the epicardium with a resultant small hemopericardium, was observed in 21% of patients with rupture. Rupture of the midlateral wall was most common (32%) and usually occurred in the setting of an inferoposterolateral infarction related to an acute left circumflex artery occlusion. On the basis of these clinical and ECG changes, rupture was confirmed by echocardiography and pericardiocentesis in the two most recent patients, and the defect was successfully repaired. CONCLUSIONS: Rupture is often preceded by particular symptoms, signs--namely, one or more episodes of abrupt, transient hypotension and bradycardia and unexpected alterations of the T waves, especially directional changes of the latter. Patients displaying these symptoms, signs and ECG changes require a bedside echocardiogram and echocardiographically guided pericardiocentesis if fluid is visualized. If the pericardiocentesis identifies the fluid as blood, immediate surgery is indicated.

T wave changes consistent with epicardial involvement in acute myocardial infarction. Observations in patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis.

OBJECTIVES: This study was designed to evaluate the presence or absence of atypical T wave evolution in patients with a postinfarction pericardial effusion but without clinically recognized postinfarction pericarditis. A second purpose was to evaluate the frequency of atypical T wave evolution in a previous study of postinfarction pericarditis. BACKGROUND: Electrocardiographic (ECG) criteria involving the evolution of the T wave after an acute myocardial infarction were recently described in patients with regional postinfarction pericarditis. Atypical T wave evolution was found to have a sensitivity of 100% and a specificity of 77% for clinically recognized regional postinfarction pericarditis with or without a pericardial effusion. METHODS: The hospital records and serial ECGs of 20 patients with clinically recognized postinfarction pericarditis (Group I) were reviewed. The records and serial ECGs of 20 additional patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis (Group II) were also examined. The type of postinfarction T wave pattern, typical or atypical, was recorded in both groups. RESULTS: All 20 patients in Group I had atypical T wave evolution. Among the 20 patients in Group II, every patient also had atypical T wave evolution. Fifteen percent of all 40 patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred postinfarction pericarditis. CONCLUSIONS: The high sensitivity of atypical T wave evolution in diagnosing regional postinfarction pericarditis was confirmed. However, similar T wave alterations were also observed when a postinfarction pericardial effusion existed in the absence of clinically recognized pericarditis. Fifteen percent of patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred pericardial involvement. Thus, the presence of atypical T wave evolution may be a more sensitive indicator of a transmural infarction than the development of a Q wave.

The role of alcohol in new-onset atrial fibrillation.

Forty cases of new-onset atrial fibrillation (AF) were reviewed to establish the frequency of various causes. Alcohol intoxication caused or contributed to 14 cases (35%). Coronary artery disease (22.5%) and pulmonary disease (22.5%) were also common causes of acute AF. Among patients less than 65 years old, alcohol caused or contributed to approximately two thirds (63%) of the cases of AF. Thyrotoxicosis was uncommon (one case in 40); no patient had a diagnosis of mitral stenosis, pulmonary embolism, or pericarditis. There were no complications of AF in alcoholic patients; the majority (88.9%) converted spontaneously to a normal sinus rhythm within 24 hours. Alcohol intoxication should be considered early in the differential diagnosis of new-onset AF in young patients. Many patients may not require admission to an intensive care unit or a costly battery of diagnostic tests.

Quality of survival after out-of-hospital cardiac arrest: predictive value of early neurologic evaluation.

One hundred and seventeen patients were admitted following out-of-hospital cardiac arrest. After initial neurologic evaluation, they were followed prospectively until discharge or death. Seventeen patients were alert when admitted. Of these, four died and 10 of 13 survivors were neurologically normal. One hundred of the patients were unresponsive; of these, 60 died. Of 40 survivors, 15 were neurologically normal, at discharge; 15 could perform some self-care but were confused, and 10 required total care. Absence of pupillary light reaction, oculocephalic reflexes, purposeful response to pain, and spontaneous respirations were associated with high mortality and more severe neurologic deficits. However, some patients with usually unfavorable signs recovered good neurologic function.

Acute myocardial infarction with normal and near normal coronary arteries. Documentation with coronary arteriography within 12 1/2 hours of the onset of symptoms in two cases (three episodes).

Three instances (in two patients) of acute myocardial infarction associated with arteriographically normal or near normal coronary arteries are reported. One patient with a lateral infarction had a normal coronary arteriogram and hypokinesia of the lateral wall. Another patient had two infarctions: (1) a transmural inferior-lateral infarction associated with occlusion of the most distal segment of the posterior descending branch of the right coronary artery, and (2) a transmural anterior-lateral-superior infarction associated with occlusion of the most distal segment of the left anterior descending coronary artery. Neither occlusion was consistent with the extent of infarction. Although coronary arteriography was performed as early as 12 1/2, 3 3/4 and 11 2/3 hours, respectively, after the onset of symptoms of infarction in these three instances, the pathophysiologic features of the infarctions are obscure. Temporary occlusion of an epicardial coronary artery by spasm or platelet aggregates, or both, is suggested as a possible mechanism of the acute event.

Hemodynamic pattern resembling pericardial constriction after acute inferior myocardial infarction with right ventricular infarction.

Two patients with acute inferior myocardial infarction complicated by cardiogenic shock are presented. Cardiac catheterization 2 and 7 days after infarction, respectively, revealed a hemodynamic pattern resembling constrictive pericarditis. Right coronary occlusion proximal to the right ventricular marginal branches was present in both patients. Resolution of the constrictive hemodynamic pattern was demonstrated in the one survivor at repeat catheterization 7 weeks after infarction. The mechanism for constrictive hemodynamics in these patients is unclear.

Left ventricular outflow obstruction produced by a pedunculated fibroma in a newborn: clinical, angiographic, echocardiographic and surgical observations.

An unusual case of a one-day-old infant with significant left ventricular outflow obstruction produced by a pedunculated fibroma is described. The clinical findings were indistinguishable from severe valvular or subvalvular aortic stenosis. The tumor was difficult to detect by echocardiography. It produced an echo-free widening of the left ventricular outflow tract. Left ventricular cineangiography clearly demonstrated a mobile mass beneath the aortic valve.

The clinical distinction between regional postinfarction pericarditis and other causes of postinfarction chest pain: ancillary observations regarding the effect of lytic therapy upon the frequency of postinfarction pericarditis, postinfarction angina, and reinfarction.

Recently two types of atypical T-wave evolution were recognized as electrocardiographic (ECG) markers of regional postinfarction pericarditis. The sensitivity and specificity of these changes for this condition were 100 and 77%, respectively. The major purpose of this investigation is to show how these ECG changes can be used to differentiate among postinfarction pericarditis, postinfarction angina, and reinfarction. Even appropriately constructed serial monitor lead ECGs can be used to make this distinction. The ease of correctly distinguishing among the three causes of postinfarction chest pain utilizing a carefully elicited history and ECG criteria is discussed. In addition, a secondary objective was to assess the effect of lytic therapy on the incidence of postinfarction pericarditis. Among the 200 patients in this study, lytic therapy halved the incidence of postinfarction pericarditis, which is in accord with the larger Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) study.