Faculty Bibliography

Two-dimensional echocardiography at rest was used to analyze segmental wall motion abnormalities for detecting coronary artery disease in patients with and without a history of myocardial infarction. One hundred twenty-five echocardiograms were analyzed in a randomized, blinded fashion. They were obtained from 55 consecutive patients found to have significant coronary artery disease at angiography, 59 consecutive normal subjects and 11 patients with dilated cardiomyopathy. The overall sensitivity of two-dimensional echocardiography was relatively low at 67%. However, specificity was 99%. The sensitivity was higher in patients with past myocardial infarction than in those without myocardial infarction (81 versus 42%), as expected. Echocardiography can detect segmental wall motion abnormalities in some patients with coronary artery disease and no overt prior myocardial infarction. This was highlighted by nine such patients with coronary artery disease and no prior myocardial infarction or electrocardiographic Q waves who were found to have segmental wall motion abnormalities. A semiquantitative, two-dimensional echocardiographic segmental wall motion score was derived for 47 patients and was correlated with angiographic left ventricular ejection fraction (r = 0.71). This score differentiated patients with a normal ejection fraction (greater than 50%) from those with a depressed ejection fraction (less than 50%): 1.1 +/- 1.6 versus 6.9 +/- 3.1 (p less than 0.001). Almost all patients (92%) with an echocardiographic score of five or more had an abnormal ejection fraction of less than 50%. In patients with chronic congestive heart failure, the echocardiogram separated those with dilated cardiomyopathy from those with coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

A case of discrete subvalvular aortic stenosis with anomalous insertion of a papillary muscle to the base of the anterior mitral valve leaflet and continuous with the discrete subaortic stenosis is described. Two-dimensional echocardiographic and pathologic data showing the contribution of the anomalous papillary muscle to left ventricular outflow tract obstruction are presented.

This study was designed to investigate whether isolated genetic factors, controlled by genes in the HLA chromosomal region, could be indicted as independent contributing influences in the genesis of premature coronary artery disease (CAD). Nineteen patients with fixed obstructive CAD documented by coronary angiography had no coronary risk factors with respect to age; levels of serum cholesterol, fasting triglycerides, and blood glucose; blood pressure; obesity; history of diabetes mellitus or hypertension; and cigarette-smoking history. Sixteen patients had a family history of CAD. HLA typing was restricted to antigens of the A and B loci. Control subjects (n = 1,157) were normal. At the A locus, no antigens demonstrated an observed frequency significantly higher than that expected from the control population. At the B locus, BW 38 had a statistically significant greater frequency (p less than 0.01) in the study group with CAD (21 percent) than in the control population (4 percent). The association between BW 38 and premature CAD lost its statistical significance when conservatively corrected for the number of HLA antigens tested by the Bonferroni adjustment. The relative risk for CAD if a patient had antigen BW 38 was 6.2. Our data suggest a statistically significant trend between the presence of HLA BW 38 and premature CAD. Whether the HLA tissue antigens are involved directly in the pathogenesis of CAD, act as markers for immune response genes, or serve as markers of other yet undefined genetic factors needs further study.