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Biomedical subjects

B H Bulkley

Publications and source records attributed to B H Bulkley.

At least 73 records · Page 4Linked to original sources
PubMed1981

Exercise thallium-201 myocardial imaging in left main coronary artery disease: sensitive but not specific.

To determine the usefulness of thallium-201 scintigraphy for identifying left main coronary artery disease, the results of scintigraphy at rest and during exercise were compared in 24 patients with 50 percent or greater narrowing of the left main coronary artery and 80 patients with 50 percent or greater narrowing of one or more of the major coronary arteries but without left main coronary involvement. By segmental analysis of the scintigrams, perfusion defects were assigned to the left anterior descending, left circumflex or right coronary artery, singly or in combination, and the pattern of simultaneous left anterior descending and circumflex arterial defects was used to identify left main coronary artery disease. Of the 24 patients with left main coronary artery disease, 22 (92 percent) had abnormal exercise scintigrams. Despite this high sensitivity, the pattern of perfusion defects was not specific; the "left main pattern" was found in 3 patients (13 percent) with left main coronary artery disease but also in 3 (33 percent) of 9 patients with combined left anterior descending and left circumflex arterial disease, 4 (19 percent) of 21 patients with three vessel disease and 3 (6 percent) of 50 patients with one or two vessel disease but excluding the group with left anterior descending plus left circumflex arterial disease. The pattern of perfusion defects in the patients with left main coronary artery disease was determined by the location and severity of narrowings in the coronary arteries downstream from the left main arterial lesion. Concomitant lesions in other arteries were found in all patients with left main coronary disease (one vessel in 1 patient, two vessels in 7 patients and three vessels in 16). For this reason, it is unlikely that even with improvements in radiopharmaceutical agents and imaging techniques, myocardial perfusion scintigraphy will be sufficiently specific for definitive identification of left main coronary artery disease.

Coronary Circulation↗
PubMed1981

Cardiac hypertrophy in idiopathic dilated congestive cardiomyopathy: a clinicopathologic study.

Although clinical studies indicate that patients with idiopathic dilated congestive cardiomyopathy who develop electrocardiographic or angiographic signs of left ventricular (LV) hypertrophy may survive longer, there is little morphologic evidence for such anatomic favorable of unfavorable prognostic groups. We studied 30 autopsied patients who died of dilated cardiomyopathy; of these, 15 died within 1 year of the first symptom of their disease (short-term survivors) and 15 patients died 1-14 years after initial symptoms (long-term survivors). There were no significant differences in sex, race, clinical presentation or cause of death between the groups, but there were significant morphologic differences. In the short-term survivors, average heart weight was 540 g and LV wall thickness was 1.0 cm, whereas in the long-term survivors, the average heart weight was 759 g and LV wall thickness was 1.3 cm (p less than 0.001). LV cavity dilatation as measured by maximal transverse diameter from the postmortem angiograms did not differ between the two groups. These patients were compared with 10 autopsied patients with normal hearts and no clinical cardiac disease and 10 autopsied patients with volume overload secondary to valvular regurgitation. An LV hypertrophy/dilatation index (thickness/diameter) was 0.17 +/- 0.07 for the short-term survivors, 0.21 +/- 0.07 for the long-term survivors, 0.38 +/- 0.07 for volume overload patients, and 0.48 +/- 0.19 for normal subjects (F = 20.24, p less than 0.001). Thus, in patients with hypertrophy due to volume overload, wall thickening increased with dilatation, returning the ratio of wall thickness to cavity size toward normal. In contrast, among the idiopathic congestive cardiomyopathies, dilatation was disproportionate to hypertrophy and the difference was most marked for short-term survivors.

Adult↗
PubMed1981

Beneficial effects of adding propranolol to multidose potassium cardioplegia.

The use of propranolol with multidose potassium cardioplegia was studied in 32 in situ canine hearts subjected to 90 minutes of global ischemia at 15 degrees C and 60 minutes of reperfusion at 37 degrees C. All hearts received potassium (37 mEq/l) every 30 minutes during ischemia. There were four groups of equal size: group 1 received no propranolol, group 2 received low-dose propranolol and group 3 received high-dose propranolol. Group 4 received high-dose propranolol only with the initial potassium infusion. Myocardial CO2 (PmCO2) was monitored by mass spectrometry as an indicator of metabolic activity. An intraventricular balloon was used to measure isovolumic developed pressure, maximal dP/dt and end-diastolic pressure (EDP) before and after ischemia. During ischemia, peak PmCO2 was significantly higher in group 1 (45.6 +/- 2.8 mm Hg) than in groups 2, 3 and 4 (35.2 +/- 2.8 mm Hg, 33.4 +/- 2.8 mm Hg and 30.4 +/0 2.8 mm Hg, respectively) (p less than 0.05). There were no differences between the four groups in systolic ventricular function assessed by developed pressure and dP/dt. Hearts that received high-dose propranolol had significantly lower EDP after 60 minutes of reperfusion (group 3 13.3 +/- 1.5 mm Hg, group 4 10.4 +/0 1.5 mm Hg) compared with group 1 hearts (25.3 +/- 3.8 mm Hg, p less than 0.05). Hearts in groups 3 and 4 exhibited less ischemic injury as assessed by electron microscopy than hearts in groups 1 and 2. These data show that propranolol added to multidose potassium cardioplegia reduced metabolic activity during ischemia and improved ventricular compliance during reperfusion without depressing systolic function. Because left ventricular compliance and morphologic preservation were similar in groups 3 and 4, it appears that a single high dose of propranolol is sufficient and that subsequent doses do not further enhance the beneficial effects.

Animals↗
PubMed1980

Constituents of the human ventricular myocardium: connective tissue hyperplasia accompanying muscular hypertrophy.

Left-sided congestive heart failure may be secondary to decreased left ventricular myocardial compliance in some patients. To investigate the anatomic basis for altered wall stiffness, morphometric determinations of muscle cell nuclear density and percent of myocardium consisting of muscle cells were made for right and left ventricular free wall and septum in 127 hearts with normal coronary arteries. The hearts were normal (33 patients), had left ventricular hypertrophy (28 patients), right ventricular hypertrophy (25 patients), or chronic dilatation (41 patients). With cardiac enlargement, the average percent of myocardium consisting of muscle did not change from the approximately 75% value characteristic of normal hearts. In contrast, muscle cell nuclear density decreased proportionate to cardiac enlargement, demonstrating that muscle cell hypertrophy, not hyperplasia, is the basis for weight increase. Some hearts with marked longstanding dilatation also had perivascular and interstitital "striae" of connective tissue differing from replacement fibrosis. An increase in epicardial coronary artery caliber commensurate with increased heart weight suggests that ischemia is not the basis of connective tissue increase. The results show that cardiac muscle cell hypertrophy is accompanied by commensurate increase in interstitial connective tissues. This pattern of myocardial growth with cardiac enlargement may produce increased myocardial stiffness simply as a result of increased wall thickness, and may lead to left-sided congestive heart failure.

Adolescent↗
PubMed1980

Multiple coronary thromboses in previously normal coronary arteries: a rare cause of acute myocardial infarction.

This report describes an unusual form of myocardial infarction in a 44-year-old woman who was found to have two proximal coronary artery thrombi with otherwise normal coronary arteries. An interesting feature of her history was that the coronary events occurred in association with thrombocytopenia and heparin treatment. Two other clinical reports of patients who developed thrombocytopenia and myocardial infarction while receiving heparin have been identified, and the possibility that these thrombi were secondary to a coagulation abnormality associated with heparin is considered.

Adult↗