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Biomedical subjects

B F Waller

Publications and source records attributed to B F Waller.

At least 163 records · Page 9Linked to original sources
PubMed1984

Frequency and significance of M-mode echocardiographic evidence of mitral valve prolapse in clinically isolated pure mitral regurgitation: analysis of 65 patients having mitral valve replacement.

To assess the reliability of M-mode echocardiographic patterns of mitral valve prolapse (MVP) (echo MVP) in detection of morphologic evidence of MVP (morphologic MVP), operatively excised mitral valves and corresponding M-mode echocardiograms from 65 patients with chronic, severe, isolated, pure mitral regurgitation (MR) were studied. Of the 65 patients, 45 (69%) had echo MVP (either holosystolic or mid-to-late systolic prolapse patterns on preoperative M-mode echograms) and 42 (93%) of them had morphologic MVP; of the 3 without morphologic MVP, 2 had ruptured chordae tendineae from infective endocarditis and 1 had papillary muscle dysfunction from atherosclerotic coronary heart disease. Of the 20 patients without echo MVP, 14 (70%) had no morphologic MVP (9 had papillary muscle dysfunction from coronary heart disease, 4 had infective endocarditis on previous normal valves and 1 had rheumatic heart disease). Of the 48 patients with morphologic MVP, 42 (88%) had echo MVP and most had considerably dilated mitral anulae; the other 6 had ruptured chordae tendineae with less degrees of anular dilatation. Of the 17 patients without morphologic MVP, 3 had echo MVP (coronary artery disease in 1 and infective endocarditis on a previous normal valve in 2); of the 14 with neither echo nor morphologic MVP, 9 had papillary muscle dysfunction from coronary artery disease, 4 had infective endocarditis on previously normal valves and 1 had rheumatic heart disease. The patients with very dilated mitral anuli and leaflet areas generally had holosystolic (hammocking) patterns on echo; the patients with small anuli and leaflet areas usually had mid-to-late systolic (buckling) prolapse patterns.

Adult↗
PubMed1984

Severe aortic-valve stenosis unmasked by amateur running.

Three men aged 35, 55, and 60 years had asymptomatic underlying aortic-valve stenosis unmasked by amateur running or jogging. All three men underwent aortic-valve replacement and two of the three have resumed mild exercise programs. Congenitally abnormal aortic valves were found in two of the three patients. Amateur exercise may uncover an underlying cardiovascular abnormality perhaps sooner than might be apparent without exercise.

Adult↗
PubMed1984

Transverse aortic wall tears in infants after balloon angioplasty for aortic valve stenosis: relation of aortic wall damage to diameter of inflated angioplasty balloon and aortic lumen in seven necropsy cases.

Aortic wall tears resulting from rupture of dilating balloons in infants undergoing transluminal balloon angioplasty have not been previously recognized. A 2 day old infant had percutaneous transluminal balloon angioplasty to dilate a stenotic aortic valve, and after multiple balloon inflations the balloon burst. The infant died 2 days after undergoing transluminal balloon angioplasty and at necropsy a circumferential, transverse aortic wall tear was found. To test the hypothesis that rupture of appropriately sized balloons results in similar aortic wall tears, six unfixed, intact infant aortas were subjected to transluminal balloon angioplasty at necropsy: two infants had balloon rupture with inflated balloon diameter similar to that of the aorta, two had balloon rupture with an undersized balloon and two had dilation with an oversized balloon. Transverse wall tears occurred in aortas with similar aortic and balloon diameters; no aortic wall damage occurred with rupture of undersized balloons, and aortic rupture resulted from the use of oversized balloons. Thus, intimal-medial tears in the infant aorta may result from balloon bursting during angioplasty when aortic and inflated balloon diameters are similar.

Angioplasty, Balloon↗
PubMed1984

Morphologic observations after percutaneous transluminal balloon angioplasty of early and late aortocoronary saphenous vein bypass grafts.

Clinical and morphologic observations from two patients undergoing percutaneous transluminal angioplasty of stenotic aortocoronary saphenous vein bypass grafts early (3 months) and late (56 months) after graft insertion are described. Each patient had one or more clinically successful graft dilations resulting in an angiographic increase in luminal diameter and a decrease in mean trans-stenotic gradient, and each had restenosis of the graft at the site of previous angioplasty within 2 months of dilation. Both operatively excised grafts had diffuse but variable amounts of intimal fibrous thickening and severe narrowing at the previous angioplasty site. The early graft had no evidence of dilation injury, and the intimal thickening consisted solely of fibrocollagenous tissue free of calcific deposits. In contrast, the late graft had a healing intimal dissection at the angioplasty site, and the intimal thickening consisted of atherosclerotic plaque with calcific deposits. Angiographic and morphologic correlations suggest that the mechanism of saphenous vein angioplasty early (less than or equal to 1 year) after insertion is by graft "stretching," while late (greater than 1 year) after insertion it is by atherosclerotic plaque "fracture" similar to that observed in atherosclerotic coronary arteries subjected to angioplasty procedures.

Adult↗
PubMed1983

Status of the major epicardial coronary arteries 80 to 150 days after percutaneous transluminal coronary angioplasty. Analysis of 3 necropsy patients.

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.

Adult↗
PubMed1983

Tunneled ("bridged") left anterior descending coronary artery in a newborn without clinical or morphologic evidence of myocardial ischemia.

Tunneled epicardial coronary arteries have been presumed congenital in origin, but morphologic or angiographic documentation of myocardial bridging at birth is lacking. This report describes a 42-day-old infant with a lengthy tunneled left anterior descending coronary artery observed at necropsy that produced no apparent clinical cardiac dysfunction during life despite sinus tachycardia. These observations support the concept that myocardial bridges may be congenital in origin, and suggest length of tunneling and tachycardia may not be adverse factors for myocardial bridges in infancy.

Autopsy↗
PubMed1983

Early and late morphologic changes in human coronary arteries after percutaneous transluminal coronary angioplasty.

Certain clinical and morphologic observations are described in 6 men who had percutaneous transluminal coronary angioplasty (PTCA) of the left anterior descending (LAD) or right (R) coronary artery early (4 hours to 7 days) or late (80, 90, and 150 days) before coronary endarterectomy and aortocoronary bypass grafting or death. Histologically, each of the 3 early patients had the site of PTCA narrowed 76-95% in cross-sectional area by atherosclerotic plaque, and each had either coronary dissection or plaque hematoma or both at the site of PTCA. Each of the 3 late patients had a decrease in the mean trans-stenotic coronary gradient (17, 38, and 43 mmHg, respectively) and an angiographic increase in the LAD luminal diameter (55, 60, and 65%, respectively) at the time of PTCA. At necropsy, 80, 90, and 150 days later, the LAD coronary artery in the area of the PTCA in each patient was narrowed 76-95% in cross-sectional area by 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 late patient.

Adult↗
PubMed1983

Right ventricular infarction with cardiac rupture in an infant with pulmonary valve atresia with intact ventricular septum.

This report describes an 8 day old infant with pulmonary valve atresia, hypoplastic and hypertensive right ventricle and myocardial sinusoid-left anterior descending coronary artery connections. A large right ventricular sinusoid complex developed that was associated with transmural right ventricular necrosis and cardiac rupture. This is the first report to document transmural myocardial infarction and rupture in pulmonary valve atresia with intact septum, and this condition should be added to the causes of myocardial infarction in infancy. A reduced number of caliber of sinusoid-coronary artery channels may be responsible for right ventricular damage in this condition.

Coronary Vessel Anomalies↗
PubMed1983

Systolic anterior motion of the posterior mitral leaflet: a previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy.

Dynamic obstruction to left ventricular outflow in patients with hypertrophic cardiomyopathy usually occurs when the anterior mitral leaflet moves forward in systole and approaches or contacts the ventricular septum. However, we have recently identified, by M mode and two-dimensional echocardiography, 21 patients with hypertrophic cardiomyopathy who had a unique pattern of mitral valve motion characterized by abnormal mitral valve coaptation and systolic anterior motion of the posterior mitral leaflet. This abnormality of mitral valve motion was most reliably identified with two-dimensional echocardiography in views of the left ventricle obtained from the apex. At end-diastole the anterior and posterior mitral leaflets did not appear to coapt at their distal free margins. Rather, at mitral valve closure, the anterior mitral leaflet contacted the basal portion of posterior mitral leaflet. Subsequently, during systole the "residual" distal portion of posterior mitral leaflet approached or contacted the ventricular septum. Morphologic observations in nine other patients with hypertrophic cardiomyopathy suggested that systolic anterior motion of the posterior mitral leaflet is due to elongation of the middle scallop of the posterior leaflet, which probably comes into apposition with the ventricular septum during systole by passing through the space created by the normal pattern of chordal attachments onto the anterior mitral leaflet. Of the 16 patients who underwent cardiac catheterization, nine had basal subaortic gradients of 20 to 85 mm Hg, which were apparently due to moderate or marked systolic anterior motion of the posterior mitral leaflet. Ventricular septal myotomy-myectomies were performed in two patients and resulted in markedly diminished systolic anterior motion of the posterior mitral leaflet in each and abolition of subaortic gradient in the one patient who underwent postoperative cardiac catheterization. Hence, in patients with hypertrophic cardiomyopathy, systolic anterior motion of the posterior mitral leaflet (1) is not uncommon (identifiable in about 10% of a consecutively studied series of patients), (2) constitutes a previously undescribed mechanism for dynamic subaortic obstruction, and (3) is due to a malformation of the posterior mitral leaflet.

Adolescent↗