PubMed Health⌕ Search

Biomedical subjects

B H Bulkley

Publications and source records attributed to B H Bulkley.

At least 109 records · Page 6Linked to original sources
PubMed1979

Infected saphenous vein coronary artery bypass graft with mycotic aneurysm. Fatal dehiscence of the proximal anastomosis.

A 33-year-old man underwent coronary artery bypass graft surgery for relief of angina pectoris. His postoperative course was complicated by hemorrhage and mediastinitis. Death, which occurred after severe hemorrhage from the operative site, was shown at autopsy to be caused by dehiscence of the proximal anastomosis of the right coronary artery graft. The same graft also had a mycotic aneurysm in its midportion. Graft disruption thus appears to be a potential complication of mediastinal infection in patients with saphenous vein bypass grafts.

Adult↗
PubMed1979

Papillary muscle rupture in fatal acute myocardial infarction: a potentially treatable form of cardiogenic shock.

Although cardiogenic shock in acute myocardial infarction is usually associated with a critical loss of myocardium, this may not be the case in papillary muscle rupture. During the past 21 years, 13 patients came to autopsy (11 died in cardiogenic shock) with a papillary muscle rupture complicating myocardial infarction. Rupture occurred from 2 to 7 (mean, 4) days after the infarct, and survival after rupture was usually brief (median, 3 days). The infarct involved between 1% and 50% (mean, 19%) of the left ventricle, and in 10 it was less than 25%. In all instances myocardium around the mitral annulus was not infarcted. Because papillary muscle rupture occurred mostly with first infarcts (eight), involved relatively small areas of necrosis, and spared the myocardium surrounding the annulus, early mitral valve replacement should make this cause of fatal acute myocardial infarction one of the most treatable forms of cardiogenic shock.

Acute Disease↗
PubMed1979

Potassium-induced cardioplegia during normothermic cardiac arrest. Morphologic study of the effect of varying concentrations of potassium on myocardial anoxic injury.

Most corrective procedures as well as myocardial revascularization require a period of cardiac arrest, and numerous methods have been proposed to protect the myocardium during this ischemic episode. Potassium-induced cardioplegia is one method that appears to be of benefit in this setting. Since it is recognized that myocardial necrosis may result at very high doses of potassium, we examined the effect of varying concentrations of potassium on myocardial anoxic injury. Using an isolated rat heart preparation, we evaluated anoxic injury occurring with cardioplegic solutions containing various concentrations of K+, ranging from 15 to 200 mEq. per liter, during a 50 minute normothermic arrest followed by 60 minutes of reperfusion. The transverse histologic sections of the left ventricular myocardium were analyzed for contraction band injury by morphometric and qualitative methods. Among the 62 animals studied the least severe anoxic injury was seen with K+ cardioplegia at concentrations of 25 and 30 mEq. per liter. At lower and higher concentrations there was little difference between the hearts exposed to anoxia with or without K+ cardioplegia. Potassium administered in very high doses, i.e., 100 or 200 mEq. of K+ per liter, led to contracture and extensive myocardial cell injury. This study suggests that potassium-induced cardioplegia is effective in reducing cell injury due to anoxia, and in this model an optimal concentration range was 25 to 30 mEq. per liter.

Animals↗
PubMed1978

Idiopathic familial myocardiopathy in three generations: a clinical and pathologic study.

A peculiar non-hypertrophic myocardiopathy is described which occurred in three and possibly five generations of a single family. Clinical features included systolic murmurs, electrocardiographic abnormalities, and sudden cardiac death with a paucity of symptoms of cardiac dysfunction. Pathological studies in three generations showed a striking similarity of cardiac findings including globular and dilated ventricles, endocardial fibroelastosis, and mitral valve thickening. Myocardium in two showed basophilic degeneration and fibrosis. A retrospective genealogic analysis and a prospective clinical evaluation of living family members suggested an autosomal dominant mode of inheritance with variable penetrance. The cause of this heritable myocardiopathy is presumably a mutant gene; the biochemical defect to which the mutant gene gives rise remains unknown.

Adolescent↗
PubMed1978

Angina pectoris, myocardial infarction and sudden cardiac death with normal coronary arteries: a clinicopathologic study of 9 patients with progressive systemic sclerosis.

The syndrome of angina pectoris or acute myocardial infarction without obstructive coronary artery disease has been the subject of much interest. We studied nine autopsied patients with progressive systemic sclerosis and evidence of ischemic heart disease but morphologically normal coronary arteries. Three patients had angina pectoris and three others chest pains of unknown etiology, six had ventricular arrhythmias, four had clinically suspected acute myocardial infarction, and eight had sudden cardiac death. At autopsy extensive focal myocardial necrosis was present in seven patients and myocardial scarring in all nine, but all patients had widely patent intramural and extramural coronary arteries. The finding of contraction band myocardial necrosis in seven of the eight patients who experienced sudden death suggests that the myocardial damage was a consequence of reperfusion of focally nonperfused myocardium, and thus due to a myocardial Raynaud's phenomenon. Patients with PSS may provide a model of spasm of intramyocardial vessels causing angina pectoris or myocardial infarction with morphologically normal coronary arteries.

Adolescent↗
PubMed1978

Acute postoperative graft phlebitis: a rare cause of saphenous vein-coronary artery bypass failure.

Most graft occlusions occurring early after saphenous vein coronary artery bypass procedures result from technical problems at the graft to coronary artery anastomosis site. This report describes an unusual cause of graft occlusion in a 67-year-old man who died three weeks after operation--a postoperative acute phlebitis of an implanted saphenous vein graft. Infection in the graft wall resulted in isolated graft thrombosis in the setting of a patent anastomosis. Graft phlebitis in this patient was associated with a purulent pericarditis and mediastinitis which failed to respond to surgical débridement and antibiotic therapy. Although mediastinitis is not infrequent, infection of an implanted saphenous vein coronary artery bypass graft in association with mediastinitis has never been reported. The findings in our case show that such graft infection may occur, and may result in graft thrombosis and occlusion.

Acute Disease↗
PubMed1978

Tortuosity as an index of the age and diameter increase of coronary collateral vessels in patients after acute myocardial infarction.

A possible correlation among increase in diameter, lengthening or tortuosity and age of bypassed obstruction was investigated in coronary arterial collateral vessels. In 35 autopsy patients with a myocardial infarct of known age, as determined from clinical history and pathologic demonstration of an infarct of consistent age in the distribution of an obstructed vessel, 140 collateral vessels were identified in postmortem arteriograms and measurements made of their diameter and tortuosity. Multivariable regression analyses showed that collateral diameter and tortuosity increase with greater time after the infarction. It is suggested that identification of tortuosity in a coronary vessel may provide an indication that it functions as a collateral channel and of the degree of its dilatation and the time it has been a collateral channel. The lengthening that produces tortuosity probably arises from the same relaxation of medial tension that induces dilatation as a result of increased blood flow.

Adult↗
PubMed1978

Anomalous left circumflex coronary artery: "normal" variant of uncertain clinical and pathologic significance.

Anomalous origin of the left circumflex artery from the aorta is generally viewed as a benign coronary arterial anomaly. Three such cases are reported in which the anomalous artery was totally occluded. Although coronary atherosclerosis was present in all three cases, the proximal segment of the anomalous circumflex vessel was particularly severely affected in each patient. Two patients had a myocardial infarct in the distribution of the aberrant vessel. Accurate angiographic diagnosis is needed before cardiac surgery is performed, whether for valve replacement or myocardial revascularization, because this variant may be less benign than one believed.

Aged↗
PubMed1978

Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia.

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".

Adolescent↗
PubMed1978

Association of left dominant coronary arterial system with congenital bicuspid aortic valve.

Clinical angiographic studies have documented an association of left dominance of the coronary arteries with aortic stenosis and congenital bicuspid aortic valve. The postmortem arteriograms of 973 autopsy patients were reviewed for pattern of coronary dominance and the hearts examined for the nature of any aortic valve disease. There were 673 hearts (70 percent) with a right dominant pattern, 198 (20 percent) with equal dominance and 102 (10 percent) with left dominance. Of 34 hearts with congenital bicuspid aortic valve, 10 (29 percent) had left dominance, a difference significant at the 0.005 level. Of 44 hearts with calcific aortic stenosis, an acquired valve lesion, 9 (20 percent) had left dominance. Rheumatic aortic valve disease (47 cases) and aortic regurgitation (27 cases) had no apparent relation to the coronary arterial pattern. The results confirm the association of left coronary arterial dominance with congenital bicuspid aortic valve. It is suggested that a left dominant coronary system may arise as a consequence of disproportionately decreased blood flow in the left heart chambers, one cause of which is aortic valve stenosis, during early cardiogenesis.

Adolescent↗
PubMed1978

Supravalvular aortic stenosis with parafollicular cell (C-cell) hyperplasia.

Autopsy examination of a patient with well-documented supravalvular aortic stenosis and other characteristic features of the idiopathic infantile hypercalcemia syndrome revealed previously unreported hyperplasia of parafollicular cells (C cells). Immunohistochemical analysis demonstrated up to 30 calcitonin-containing cells per high power field, whereas normal glands contain only 4 to 10 cells per low power field in areas of highest concentration. The parathyroid glands were found to be normal both grossly and microscopically, whereas the bones showed thickened trabeculas, normal Haversian canals and no apparent increase in osteoblast or osteoclast activity, suggesting normal parathyroid hormone, but increased thyrocalcitonin activity. We suggest that C-cell hyperplasia has occurred in response to a persistent, rather than transient, elevation in serum calcium levels and that thyrocalcitonin function is augmented, rather than impaired in this disorder. The primary biochemical defect promoting hypercalcemia remains to be clarified, as well as the role, if any, such a defect plays in producing significant pathology in the central nervous system and in the cardiovascular, renal and skeletal systems.

Adult↗
PubMed1978

Effect of potassium cardioplegia on myocardial ischemia and post arrest ventricular function.

To assess the effects of moderate potassium cardioplegia (37 mEq/l KCl) on the severity of myocardial ischemia during arrest and on post arrest ventricular function, 32 isolated, isovolumic feline hearts were studied before, during and 1 hour after ischemic arrest. Normothermia (37 degrees C) was maintained in the remaining 16 hearts, eight without KCl and eight with KCl. Hypothermia (27 degrees C) was maintained in the remaining 16 hearts, eight with KCl and eight without KCl. Myocardial oxygen (PmO2) and carbon dioxide tensions (PmCO2) were measured by mass spectrometry. Maximum developed intraventricular pressure (max DP) and max dP/dt were used as indices of performance. Compared with normothermic or hypothermic arrest alone, the addition of potassium cardioplegia resulted in a significant reduction in the peak PmCO2 measured during the arrest period. Hypothermia alone resulted in morphologic evidence of improved myocardial preservation and a significant reduction in peak PmCO2 compared with normothermia. Post arrest ventricular function was best with the combination of hypothermic arrest and potassium cardioplegia (max DP = 96 +/- 6% of control and max dP/dt = 99 +/- 5% of control). These data suggest that the beneficial effects of postassium cardioplegia and 27 degrees hypothermia are additive, and that reduction in myocardial ischemia as evidenced by a reduction in peak PmCO2 correlated with improvement in ventricular performance in the post arrest period and with preservation of myocardial structure.

Animals↗