[Two-dimensional echocardiographic recognition of dilated cardiomyopathy: comparison with postmortem studies]

To elucidate the pathophysiology of dilated cardiomyopathy (DCM), the relationship of two-dimensional echocardiographic wall motion abnormalities (asynergy) to histopathological findings was evaluated in autopsied patients including seven with DCM, five with old myocardial infarction (OMI) and three with the normal heart. The DCM cases were classified morphologically in two groups, namely four of type I and II and three of type III, according to Shozawa's classification. Three short-axis views of the left ventricle were divided into 19 segments; the wall motion was assessed visually and classified as normal motion, hypokinesis, akinesis and dyskinesis. The postmortem specimens were immersed in 10% formalin; transverse sections and wall divisions were prepared corresponding to the two-dimensional echocardiographic views, and the area of each segment was determined by a computer planimetry excluding the papillary muscles and trabeculae. Fibrosis (%) was measured histologically by the point counting method with light microscopy. The results were as follows: In DCM, fibrosis (%) increased with increasing severity of asynergy: 17.1% fibrosis in normal motion; 28.7% in hypokinesis; 40.7% in akinesis and dyskinesis. In OMI, fibrosis (%) also increased with increasing severity of asynergy. On comparison of DCM with OMI, no difference was established relating to fibrosis (%) in the asynergic segments; moreover, in both groups, asynergy was detected more frequently in the segments in which fibrosis (%) exceeded 21%. On comparison of type I+II DCM with type III DCM, fibrosis (%) of type III was significantly less than that of type I+II in the same degree of asynergic segments. Moreover, fibrosis (%) of type I+II tended to be greater in the outer layer than in the inner layer, while fibrosis (%) of type III was evenly distributed throughout the myocardium, or greater in the inner layer than in the outer layer. In type I+II, wall thinning was marked with increasing severity of asynergy; in contrast, these correlations were not observed in type III. In type I+II, a higher fibrotic rate was observed in the left ventricular free wall and an abnormal Q wave appeared frequently on ECG. This tendency was not found in type III. These findings indicate that fibrosis is one of the most important factors in decreasing cardiac muscular contractility in DCM, and suggest that there is a different pathogenesis between type I+II and type III fibrosis.