SUMMARY The 10-20% incidence of cardiac rupture in acute fatal myocardial infarction has not changed in the past century, and little is known about its pathophysiology. To determine whether expansion acute dilatation and thinning of the area of infarction not explained by resorption of necrotic tissue -may be a variable predictive for rupture, we studied 110 consecutive autopsied patients who died of acute myocardial infarction. The presence and severity of expansion was determined qualitatively on a scale of 0-4+ from review of the postmortem radiographs, and quantitatively by a ratio of wall thickness adjacent to the rupture site to thickness of noninfarcted wall. By radiographs, 54 (49%) had expansion, of whom 23 (43%) had rupture in the zone of expansion; of the 56 cases without expansion only one (2%) had ruptured (p < 0.005). The severity of expansion related to rupture: 50% with 3-4+ expansion ruptured, compared with only 23% with 1-2 + expansion. Wall thickness ratios for patients without expansion were 0.93 ± 0.10; for those with expansion but no rupture, 0.62 ± 0.16; and 0.49 ± 0.13 for those with expansion and rupture (p < 0.01). Wall thinning in these three groups was noted at average postinfarction intervals of 8, 7 and 5.5 days, respectively too early to be caused by resorption.Thus, expansion of acute myocardial infarction is a previously unappreciated variable that appears to be predictive of rupture, suggesting that regional dilatation and thinning of newly infarcted myocardium may be of pathogenetic importance in the development of rupture. Since expansion can be identified with twodimensional echocardiography, and occurs over days, these findings suggest that patients at high risk for rupture might be recognized early and interventions to prevent further expansion and rupture evaluated.CARDIAC RUPTURE in acute fatal myocardial infarction has a 10-20% incidence that has not changed in the past century." 2 The effective use of antiarrhythmic drugs has reduced the mortality of myocardial infarction. Attempts are underway to limit myocardial infarct size, and to support patients with cardiogenic shock with the hope of improving mortality. Yet the percentage of patients with acute myocardial infarction who die from cardiac rupture still remains high. Cardiac rupture is estimated to account for 25,000 fatalities a year in the United States,2 and, after cardiogenic shock and arrhythmias, is the most common cause of death in patients with myocardial infarction. This mortality is especially troublesome in that most reports2-10 agree that patients who die from cardiac rupture tend to have only one relatively small transmural infarction. One would expect that if these patients had not ruptured, their prognosis would have been favorable.Little is known of the pathophysiology of rupture, a factor that limits any attempts to alter its occurrence. Postulated mechanisms for cardiac rupture include a decrease in tensile strength, a high intracavitary pressure, ruptured intramural venous channels and a paradoxi...

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SUMMARY We compared myocardial infarct size produced by permanent occlusion of the middle left anterior descending (LAD) or circumflex (LCx) coronary artery in the anesthetized dog. The dogs were killed 3-10 days later, and the occluded coronary bed was visualized by postmortem arteriography. The outlines of the infarct and occluded bed were marked on tracings of weighed left ventricular (LV) rings and the size of the infarct and occluded bed was calculated by planimetry. For both arteries, infarct size and occluded bed size were linearly related to each other, but LAD infarcts were larger relative to occluded bed size (52.0% vs 32.3%, p < 0.05). A smaller occluded bed was necessary for the appearance of an infarct after LAD occlusion than after LCx occlusion (8.3% vs 18.5% of the left ventricle, p < 0.005). Reconstructed LV ring maps indicated a significantly wider margin of noninfarcted myocardium at the lateral edge of the occluded bed for LCx infarcts than for LAD infarcts. For dogs with similar occluded bed sizes in the range of 20-35% of the left ventricle, infarct size was considerably larger for LAD occlusion (15.9% vs 6.1% of the left ventricle, p < 0.001). In this subgroup, blood pressure and heart rate 10-20 minutes after occlusion were not significantly different for the two arteries, but collateral flow, measured with 9-,u radioactive microspheres, was approximately 50% lower after LAD occlusion. The relationship between the amount of myocardium with reduced blood flow and developed infarct size was similar for the two arteries. We conclude that occlusions of the middle LAD and LCx are not equivalent. For a given occluded bed size, LAD occlusions produce larger areas of infarction, apparently related to lower levels of collateral flow delivered to the occluded region.ONE of the most popular animal models for the study of regional ischemia and infarction is the dog in which one of the major coronary arteries has been temporarily or permanently occluded. The anterior descending (LAD) and circumflex (LCx) branches of the left coronary artery are both used for this purpose and are considered more or less interchangeable. Which branch is used in a given laboratory appears to depend more on custom than on any scientific considerations.Although more proximal occlusion of a coronary artery tends to result in a larger ischemic region and a larger completed infarct, a wide variation is found in infarct size, even with occlusion at a constant anatomic site.".2 This fact stems from the variability in coronary artery anatomy and pertains to both branches of the left coronary artery. The observed variability in infarct size, at least for LCx occlusions, can be accounted for in large measure by the size of the occluded coronary bed and the severity of ischemia within the occluded region. 2 No systematic comparison of LAD and LCx distribution infarcts has been undertaken. We therefore determined the intensity of ischemia and the size of developed infarct for dogs with permanent occlusion of one of these two coronar...

SUMMARY Although clinical studies indicate that patients with idiopathic dilated congestive cardiomyopathy who develop electrocardiographic or angiographic signs of left ventricular (LV) hypertrophy may survive longer, there is little morphologic evidence for such anatomic favorable or unfavorable prognostic groups. We studied 30 autopsied patients who died of dilated cardiomyopathy; of these, 15 died within 1 year of the first symptom of their disease (short-term survivors) and 15 patients died 1-14 years after initial symptoms (long-term survivors). There were no significant differences in sex, race, clinical presentation or cause of death between the groups, but there were significant morphologic differences. In the short-term survivors, average heart weight was S40 g and LV wall thickness was 1.0 cm, whereas in the long-term survivors, the average heart weight was 759 g and LV wall thickness was 1.3 cm (p < 0.001). LV cavity dilatation as measured by maximal transverse diameter from the postmortem angiograms did not differ between the two groups. These patients were compared with 10 autopsied patients with normal hearts and no clinical cardiac disease and 10 autopsied patients with volume overload secondary to valvular regurgitation. An LV hypertrophy/dilatation index (thickness/diameter) was 0.17 i 0.07 for the short-term survivors, 0.21 i 0.07 for the long-term survivors, 0.38 ± 0.07 for volume overload patients, and 0.48 :L 0.19 for normal subjects (F = 20.24, p < 0.001). Thus, in patients with hypertrophy due to volume overload, wall thickening increased with dilatation, returning the ratio of wall thickness to cavity size toward normal. In contrast, among the idiopathic congestive cardiomyopathies, dilatation was disproportionate to hypertrophy and the difference was most marked for short-term survivors. Materials and MethodsPatients from the autopsy files of The Johns Hopkins Hospital were included in this study if (1) they had a clinical history of congestive heart failure; (2) there was evidence of biventricular dilatation; (3) the heart valves and coronary arteries were normal; and (4) both the gross specimen and postmortem angiograms were available for study. Patients were excluded if (1) they had a history of systemic hypertension; (2) there was pathologic evidence of a restrictive, infiltrative or hypertrophic cardiomyopathy; (3) they had congenital anomalies; and (4) there was histologic evidence of active myocarditis. The autopsy files for the past 15 years were reviewed and 30 cases fulfilled the criteria for inclusion. As controls, we studied 10 normal hearts from adults who had neither clinical nor pathologic evidence of cardiovascular disease and 10 adult hearts with long-standing volume overload due to pure aortic regurgitation (five hearts) or pure mitral regurgitation (five hearts). These 20 comparison hearts met the stated criteria. They were prepared postmortem, as the study hearts were, with coronary arteriography and formalin fixation in distention. Of these 10 patients, one was in ...

Three patients are described who either died suddenly or had severe, lifethreatening arrhythmias during or immediately after doxorubicin administration. Since doxorubicin and daunorubicin administration is known to be associated with acute EKG abnormalities, the acute decompensation in these patients appeared to be caused by the administration of these agents. The importance of careful observation of patients receiving doxorubicin, because of the possibility of acute cardiac arrhythmias, is stressed.