Left atrial myxoma with multicentric recurrence and evidence of metastases.
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Biomedical subjects
Publications and source records attributed to B F Waller.
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Despite recent renewed interest in the detection of tricuspid valve regurgitation by echocardiographic and Doppler techniques, little morphologic information is available on dysfunctioning tricuspid valves. This report describes 45 necropsy patients with clinical and morphologic evidence of pure (no element of stenosis) tricuspid regurgitation and provides morphometric observations (anular circumference, leaflet area) of the tricuspid valve useful in determining the etiology of pure tricuspid regurgitation. Of 45 patients, 24 (53%) had pure tricuspid regurgitation resulting from an anatomically abnormal valve (prolapse in 7, papillary muscle dysfunction in 6, rheumatic disease in 5, Ebstein's anomaly in 3, infective endocarditis in 2, carcinoid tumor in 1), and 21 (47%) had an anatomically normal valve with systolic pulmonary artery hypertension (cor pulmonale in 12, mitral stenosis in 9). Anular circumference was dilated (greater than 12 cm) in patients with various causes of pulmonary hypertension, floppy valve and Ebstein's tricuspid anomaly. Leaflet area was increased in floppy valve and Ebstein's anomaly. Of the 45 patients, 24 had pulmonary systolic artery pressure measurements available for correlation with tricuspid valve morphology. Pulmonary artery pressures accurately predicted morphologically normal from abnormal valves in 16 patients (89%). Morphologic overlap occurred in six patients with pulmonary pressures of 41 to 54 mm Hg. Of these six, the additional knowledge of normal or dilated anular circumference correctly separated valves with normal and abnormal leaflets.
Distal migration of occluding coronary thrombus during thrombolysis therapy for acute myocardial infarction rarely has been observed angiographically. Necropsy documentation of the final location of embolic fragments in this circumstance has not been reported previously. This report documents multiple occluded intramyocardial vessels with thrombus observed to have showered distally during thrombolysis therapy. Depending on size and number, fragments of dislodging proximal coronary embolus may produce additional myocardial necrosis.
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To assess the status of a saphenous vein (SV) excised for coronary artery bypass grafting (CABG), 3,394 cm of remnant SV from 402 patients who underwent CABG were examined. The SV remnants were 0.5 to 52 cm long (mean 8.4). They were sectioned into 5-mm-long segments, and the resulting 6,788 five-millimeter segments were examined histologically: 5,896 (87%) were narrowed 0 to 25% in cross-sectional area by fibrous tissue; 853 (12%) were narrowed 26 to 50%; 23 (0.6%), 51 to 75%, and 16 (0.4%) segments were narrowed 76 to 100%. Of the 16 segments severely narrowed, 7 (44%) were nearly totally occluded by fibrous tissue. In 17 patients who died within 24 hours of CABG, similar degrees of luminal narrowing were observed in remnant segments and in utilized segments of SV. Thus, significant preexisting luminal narrowing of SV used for CABG is infrequent. The intimal fibrous thickening is variable within the same vein when each 5-mm-long segment is analyzed; it is variable from 1 vein to another in the same patient, and it varies among patients.
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The histologic criteria for the diagnosis of myocarditis on an endomyocardial biopsy specimen are troubled by varying institutional criteria and interobserver differences. A comprehensive approach to tissue evaluation including quantitative assessment of mononuclear cell populations enhances the accuracy and the specificity of the morphologic diagnosis. Future efforts to characterize the infiltrating cell lines in inflammatory conditions of the heart will aid in the ultimate refinement of therapeutic efficacy.
Surgical intervention for critical aortic stenosis in neonates is associated with an appreciable risk. Refinements in the technique of aortic valvotomy have been developed in an attempt to lower the operative mortality. This case report summarizes our experience with transventricular balloon dilation of critical aortic stenosis in 2 neonates. Both patients survived operation with objective evidence of hemodynamic improvement.
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This report describes a previously unrecognized combination of congenital coronary artery abnormalities in the heart of a 30-year-old amateur athlete who died suddenly during a basketball game. Both right and left circumflex coronary arteries were half of their normal length (hypoplastic) decreasing posterior ventricular myocardial perfusion. In addition, the right coronary ostium rose 5 mm above the sinotubular junction (high takeoff position), which also contributed to decreased right coronary artery perfusion. This combination of congenital coronary arterial lesions should be added to the list of structural cardiac defects associated with exercise-related sudden death.
Morphologic observations following balloon angioplasty are summarized from adult patients undergoing coronary or saphenous vein bypass graft angioplasty and from infants undergoing aortic valve stenosis angioplasty. Possible mechanisms of dilation injury and complications of angioplasty balloon bursting are reviewed.
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Certain clinical and morphologic observations are described in 4 men who had PTCA of the left anterior descending coronary artery early (4 hours) or late (80, 90 and 150 days) before sudden death. Histologically, each of the 4 patients had the site of PTCA narrowed 76 to 95% in cross-sectional area by atherosclerotic plaque. The early PTCA patient had coronary artery dissection at the site of PTCA. Each of the 3 late PTCA patients had a decrease in the mean transstenotic coronary gradient (17, 38 and 43 mm Hg) and an angiographic increase in the left anterior descending coronary artery luminal diameter (55, 60 and 65%) 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 to 95% in cross-sectional area by plaques. No cracks in plaques or other lesions that may have resulted from PTCA were identified histologically in the left anterior descending coronary artery in any late PTCA patient.