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Although cardiac rupture is the second most common cause of death after ventricular failure in acute myocardial infarction, no diagnosis has ever been made before an episode of clinical compromise, and no significant predictive factors have been described. This study was designed to determine whether high serum C-reactive protein (CRP) levels could predict the incidence of subacute cardiac rupture after acute myocardial infarction. Nine consecutive patients with cardiac rupture were compared retrospectively with 28 consecutive control patients without rupture after acute myocardial infarction. In the rupture group, peak serum CRP levels increased rapidly and markedly after infarction, reaching more than 20 mg/dl on day 2, and persisted at high levels compared with those in the control group. However, the time course and levels of serum creatine phosphokinase were not significantly different between the two groups. High serum CRP levels ( > 20 mg/dl) had a high diagnostic sensitivity (89%) and specificity (96%) for cardiac rupture. Patients with persistently high serum CRP levels, particularly above 20 mg/dl, might have high probability of occurrence of sub-acute cardiac rupture after acute myocardial infarction.

In 18 consecutive patients with a new murmur following acute myocardial infarction (AMI), examination by two-dimensional echocardiography (2DE) correctly excluded ventricular septal defects (VSD) in eight patients and enabled direct visualization of the VSD in 10 patients. In three patients, 2DE was the first technique to establish the diagnosis. In all patients with VSD, 2DE diagnosis was confirmed by catheterization, surgery, and/or postmortem examination. In six patients with VSD, 2DE contrast studies were performed and were positive. 2DE enabled localization of the VSD in all patients (five inferior, five anterior). To evaluate left ventricular (LV) function, a 2DE wall motion index (WMI) was calculated using an 11 segment model of the LV. While there was no difference (p greater than 0.2) in AMI-VSD survivors versus nonsurvivors in age, kinase, and AVO2 difference, there was no overlap in WMI (p = 0.004) of survivors (0.80 +/- 0.36) versus nonsurvivors (1.66 +/- 0.19). Thus 2DE allows accurate detection and localization of postmyocardial infarction VSD and enables determination of prognosis of these patients.

Echocardiographic studies were performed on 134 consecutive patients with idiopathic mitral valve prolapse syndrome. Fifteen patients (11.2%) were noted to have ruptured chordae tendineae on M-mode examination and in 12 of them the diagnosis was confirmed by bidimensional studies. Only four patients were referred for surgery as a result of severe mitral regurgitation. At operation one patient was found to have rupture of the anterior mitral chorda and the other three had posterior mitral chordal rupture. Eleven patients with chordal rupture had either mild symptoms or were completely asymptomatic. It is concluded that chordal rupture in patients with the mitral valve prolapse syndrome does not always result in severe hemodynamic deterioration and may go undetected unless a high index of suspicion is maintained. Serial echocardiographic studies may reveal the natural history of this condition in asymptomatic patients.

To determine the relative frequency of the causes of death in the acute (less than 24 hours), early (24 hours to 3 weeks), and chronic (greater than 3 weeks) phases of myocardial infarction, data from all autopsies performed at a university hospital during a 56-month period were reviewed. Autopsies were performed in 56% of in-hospital deaths and 27% of patients dead on arrival in the emergency room (out-of-hospital deaths). In 271 cases of suspected cardiac death, a myocardial infarction of any age was identified. Death had occurred in the acute phase of a first infarction in 19 patients and was most frequently due to pump failure (37%) followed by cardiac rupture (26%) and arrhythmias (21%). Death had occurred 24 hours to 3 weeks after a first infarction in 80 patients and was most frequently due to pump failure (44%), rupture (27%), and arrhythmias (16%). Recurrent acute infarction was found in 32% of patients whose deaths were due to arrhythmias or pump failure and in 19% of those whose deaths were due to rupture. Death had occurred greater than 3 weeks after a first infarction in 172 patients. In 132 (77%) of these patients death was due to a complication of a new acute or recent infarction. Myocardial rupture was a less frequent cause of death in patients with recurrent infarction (8%) than in those dying in the acute or early phase after their first infarction (27%, p = 0.0009). A primary arrhythmia in the absence of recurrent infarction or ischemia accounted for only 14% of out-of-hospital deaths late after an infarction.(ABSTRACT TRUNCATED AT 250 WORDS)