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

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.

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.

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.

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.

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.