A simple method to interpret cardiac and aortic anatomy from chest radiographs.
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Biomedical subjects
Publications and source records attributed to W C Roberts.
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Porcine bioprostheses implanted in both the mitral and aortic valve positions simultaneously in 5 patients aged 20 to 61 years (mean 45) were reexamined 18 to 107 months (mean 51) later. In 4 patients, the degenerative changes were distinctly more severe in the bioprostheses in the mitral than in the aortic valve position.
Anatomic and functional features of the normal and abnormal mitral valve are reviewed. Of 1,010 personally studied necropsy patients with severe (functional class III or IV, New York Heart Association) cardiac dysfunction from primary valvular heart disease, 434 (43%) had mitral stenosis (MS) with or without mitral regurgitation (MR): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 189 (44%) patients, and associated with aortic stenosis in 152 (35%), with pure (no element of stenosis) aortic regurgitation in 65 (15%) patients, and with tricuspid valve stenosis with or without aortic valve stenosis in 28 (6%) patients. The origin of MS was rheumatic in all 434 patients. Of the 1,010 necropsy patients, 165 (16%) had pure MR (papillary muscle dysfunction excluded): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 97 (59%) patients, and associated with pure aortic regurgitation in 45 (27%) and with aortic valve stenosis in 23 (14%) patients. When associated with dysfunction of the aortic valve, pure MR was usually rheumatic in origin, but when unassociated with aortic valve dysfunction it was usually nonrheumatic in origin. Review of operatively excised mitral valves in patients with pure MR unassociated with aortic valve dysfunction disclosed mitral valve prolapse (most likely an inherent congenital defect) as the most common cause of MR. Excluding the patients with MR from coronary heart disease (papillary muscle dysfunction), mitral prolapse was the cause of MR in 60 (88%) of the other 68 patients, and a rheumatic origin was responsible in only 3 of the 68 patients, all 68 of whom were greater than 30 years of age. Mitral anular calcification in persons aged greater than 65 years is usually associated with calcific deposits in the aortic valve cusps and in the coronary arteries. Because calcium in each of these 3 sites is common in older individuals residing in the Western World, it is most reasonable to view mitral anular calcification in older individuals as a manifestation of atherosclerosis. Mitral anular calcium appears to be extremely uncommon in persons with total serum cholesterol levels less than 150 mg/dl. Mitral anular calcium may produce mild MR and, if the deposits are heavy enough, MS.
Although percutaneous transluminal coronary angioplasty (PTCA) appears to be a relative safe and effective procedure, reported complications include coronary occlusion and dissection with or without acute myocardial infarction. Herein, a hitherto unreported complication of PTCA is described.
Certain clinical and necropsy cardiac findings are described in 3 men who had percutaneous transluminal coronary angioplasty (PTCA) of the left anterior descending (LAD) coronary artery 80, 90, and 150 days before sudden death. Each patient had a decrease in the mean transstenotic coronary gradient (17, 38, and 43 mm Hg) and an angiographic increase in the LAD luminal diameter (55, 60, and 65%). At necropsy, the LAD coronary artery in the area of the PTCA in each patient was narrowed 76 to 95% in cross-sectional area by atherosclerotic plaques. No cracks in plaques or other lesions which may have resulted from the PTCA procedure were identified histologically in the LAD coronary artery of any patient.
The presence of extravasated erythrocytes (EE), iron (I), and fibrin (F) within coronary atherosclerotic plaques and their relation to intraluminal coronary thrombus was determined in 2958 five-mm segments of 224 major epicardial coronary arteries in 57 patients with fatal coronary heart disease and in 1290 five-mm segments of 103 coronary arteries in 27 control (c) subjects. Intraplaque EE were present in 10% of the segments (controls [c] = 1%), in 35% of the arteries (c = 5%), and in 84% of the patients (c = 19%); I was present in 4% of the segments (c = less than 1%), in 14% of the arteries (c = 4%), and in 57% of the patients (c = 22%); intraplaque F was present in 2% of the segments (c = less than 1%), in 17% of the arteries (c = 3%), and in 63% of the patients (c = 7%). Intraluminal thrombus, present only in the patients with acute myocardial infarction and in none of the controls, occurred in 3% of the segments, in 8% of the arteries and in 26% of the patients. Intraplaque hemorrhage or EE occurred usually in the absence of intraluminal thrombus and conversely intraluminal thrombus occurred more frequently without than with underlying plaque hemorrhage. The frequency of intraplaque EE, I, and F was proportional to the amount of coronary atherosclerotic plaque present. Intraplaque I and F infrequently were observed in the absence of EE. The significance of extravasated erythrocytes, iron, and fibrin in atherosclerotic plaques remains unclear.
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