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Biomedical subjects

B H Bulkley

Publications and source records attributed to B H Bulkley.

At least 55 records · Page 3Linked to original sources
PubMed1982

Nifedipine in unstable angina: a double-blind, randomized trial.

We assessed the efficacy of adding nifedipine to the conventional treatment of unstable angina in 138 patients in a prospective, double-blind, randomized, placebo-controlled trial. There was no difference between the two groups in the dose of conventional antianginal medication or in age, prior myocardial infarction, ejection fraction, or other risk factors. Failure of medical treatment (defined as sudden death, myocardial infarction, or bypass surgery within four months) occurred in 43 of 70 patients given placebo and in 30 of 68 given nifedipine. Kaplan-Meier survival-curve analysis of the number and time dependence of treatment failures demonstrated a benefit of nifedipine over placebo (P = 0.03). The benefit was particularly marked in patients with ST-segment elevation during angina (P = 0.02). Side effects (transient hypotension or diarrhea) required withdrawal of the drug from four patients given nifedipine and from one given placebo. We conclude that the addition of nifedipine to conventional therapy is safe and effective in unstable angina.

Adult↗
PubMed1982

Involvement of the heart by malignant lymphoma: a clinicopathologic study.

Although involvement of the heart by malignant lymphoma is relatively common, it is difficult to detect antemortem, and only a small number of studies discuss this subject in the literature. The authors reviewed the 150 patients with malignant lymphoma autopsied at this hospital and studied the 13 (8.7%) who were found to have metastases to the heart or parietal pericardium. Four patients had Hodgkin's disease, and nine non-Hodgkin's lymphoma. Cardiac or pericardial disease apparently resulted from retrograde lymphatic spread, hematogenous spread, and direct extension from other intrathoracic tumor masses. In two cases, lymphomatous involvement of the heart and pericardium was the immediate cause of death; in one of these, myocardial infiltration was detected during life. For the group as a whole, the signs and symptoms of cardiac dysfunction were typically absent or nonspecific, and electrocardiograms and thallium imaging were not effective screening tools for lymphoma metastases. The findings suggest, however, that the most destructive form of cardiac involvement is that associated with direct epicardial spread, and that this form appears with cardiac dysfunction, which should clinically suggest its presence.

Autopsy↗
PubMed1982

Aspergillus pericarditis: clinical and pathologic features in the immunocompromised patient.

There has been a proliferation of infectious complications due to Aspergillus in patients receiving chemotherapy for cancer and transplantation; however, aspergillus pericarditis has been rarely described. Reported here are the clinical and pathologic findings of Aspergillus pericarditis in six immunocomprised patients who came to autopsy in the past 11 years. Five had leukemia, one had received a renal transplant. All had pulmonary aspergillosis. Two had clinically overt pericarditis leading to cardiac tamponade and death. Pulmonary aspergillosis preceded development of pericardial signs. Chest radiographs, serial electrocardiograms, and echocardiograms showed abnormality but were nonspecific. Pericardiocentesis was performed in one patient but proved nondiagnostic and yielded only transient hemodynamic improvement; postmortem Gram stain of the spun sediment of that pericardial fluid revealed branched hyphae. Although five patients received Amphotericin B, whether it entered the pericardial space is uncertain. Postmortem examination revealed extensive pericardial involvement by Aspergillus associated with effusions as large as 1000 ml Aspergillus penetrated the pericardium by rupture of myocardial abscesses and invasion from contiguous pulmonary foci into the pericardial space. A clinical diagnosis of Aspergillus pericarditis was never established, and at least two died of their pericardial disease. Aspergillus pericarditis is a lethal cardiac infection, which is likely to increase in frequency, and should be considered in the hemodynamically unstable immunocompromised patient, especially when signs of pericarditis or pulmonary aspergillosis are present.

Adolescent↗
PubMed1982

Myocardial infarction before age 36 years in women: predominance of apparent nonatherosclerotic events.

To examine whether myocardial infarction (MI) in young women resulted from atherosclerosis, we studied 19 women aged 18 to 35 years who had documented MI at our institution from 1955 to 1979. They were compared to 20 similar men who were selected randomly. All 20 men had at least one major coronary risk factor; six of the women did not (p less than 0.01). The risk factors were up to four times more common in men. Coronary anatomy, defined in 13 women and 13 men, demonstrated patent vessels or single stenotic disease in 10 (77%) women but in only one (8%) man, and multilesion disease in only three (23%) women but in 12 (92%) men (p less than 0.005). All with patent coronaries were women. Thus atherosclerosis is more advanced and accounts for most myocardial infarcts in young men, but is less evident and accounts for only a minority of MI in young adult women, who have a greater preponderance of nonatherosclerotic related infarcts.

Adolescent↗
PubMed1982

Pathogenesis of left ventricular aneurysms: an experimental study in the rat model.

Left ventricular aneurysms, convex protrusions at sites of transmural scar, are clinically recognized late after myocardial infarction because of their hemodynamic or arrhythmic complications. Whether aneurysms develop from dilation of freshly infarcted myocardium early after myocardial infarction or from late dilation of scar is not known. To investigate this question, the time course of changes in shape of the left ventricle early and late after myocardial infarction was studied. One hundred forty-one myocardial infarcts were produced in rats by coronary ligation, and the animals were killed at time periods of up to 6 weeks. True aneurysms developed as early as 2 weeks and only in rats with a transmural infarct. The percent of rats that manifested "aneurysmal shape changes" (defined as a protrusion of the full thickness of the left ventricular wall) increased from day 1 to day 5, but did not change significantly thereafter. The extent of left ventricular dilation in hearts with early aneurysmal shape changes did not progress significantly up to day 42. Accordingly, in the rat, regional aneurysmal shape alterations are due not to late dilation of scare tissue, but rather to "expansion" of freshly necrotic myocardium within the first 5 days of infarction. Thus, early changes in shape appear to determine late aneurysm formation.

Animals↗
PubMed1982

Optimal myocardial protection with fluosol cardioplegia.

An oxygenated perfluorocarbon cardioplegic solution was examined, utilizing a blood-perfused canine model. Twenty-one animals were divided into three equal groups, and each animal received Fluosol cardioplegia at one of three infusion temperatures: 20 degrees C, or 4 degrees C. All hearts underwent 90 minutes of ischemia, during which time 150 ml of the cardioplegic solution was infused every 30 minutes. Myocardial oxygen and carbon dioxide tensions (PmO2 and PmCO2) were monitored continually using mass spectrometry, and myocardial oxygen consumption was calculated with each cardioplegic injection. The mean increase in PmO2 was 7.1 +/- 0.9 mm Hg with 20 degrees C Fluosol infusions, 31.1 +/- 4.7 mm Hg with 10 degrees C Fluosol injections, and 22.2 +/- 4.7 mm Hg with infusions of 4 degrees C Fluosol. Average myocardial oxygen consumptioN, expressed as cubic centimeters of oxygen per 100 gm of left ventricle (wet weight), was 21.2 +/- 0.5 with 20 degrees C Fluosol, 22.8 +/- 1.3 for 10 degrees C Fluosol, and 19.6 +/- 1.0 for 4 degrees C Fluosol. Mean myocardial temperatures with infusions of 20 degrees C, 10 degrees C, and 4 degrees C solutions were 21.4 +/- 0.1 degree C, 16.9 +/- 0.4 degree C, and 15.9 +/- 0.5 degree C, respectively. After 45 minutes of reperfusion, maximum rate of rise of left ventricular pressure, expressed as percentage of preischemic control, was 70.9 +/- 3.9% for 20 degrees C Fluosol, 90.9 +/- 3.2% for 10 degrees C Fluosol, and 90.4 +/- 2.3% for 4 degrees C Fluosol (p less than 0.005, 20 degrees C versus 10 degrees C, 4 degrees C Fluosol). In addition, the 10 degrees C and 4 degrees C Fluosol hearts had essentially normal structure by light and electron microscopy. These data demonstrate tht Fluosol cardioplegia results in near optimal myocardial protection when infused at cold temperatures (4 degrees C to 10 degree C). The increases intramyocardial oxygen and myocardial oxygen consumption with each injection demonstrate that there is enhanced oxygen delivery and utilization, which may account for the improved functional recovery observed in these hearts.

Animals↗
PubMed1982

Mechanisms of ischemic myocardial cell damage assessed by phosphorus-31 nuclear magnetic resonance.

Phosphorus-31 nuclear magnetic resonance (31P NMR) can estimate tissue intracellular pH as well as the content of high-energy phosphate metabolites in isolated perfused hearts. We used 31P NMR to examine mechanisms associated with the recovery of ventricular function in hearts subjected to global ischemia and reperfusion, with special emphasis on intracellular pH, a previously unreported variable. Single-dose and multiple-dose administration of a hyperkalemic cardioplegic solution were compared with hypothermia alone in 18 isolated perfused rabbit hearts. Hearts in group 1 were subjected to 24 degrees C hypothermia during 60 minutes of global ischemia; group 2 hearts received a single injection of 37-mM KCL cardioplegic solution at 10 degrees C at the onset of ischemia; and group 3 hearts received a similar initial cardioplegic injection followed by two subsequent 24 degrees C injections at 20-minute intervals during the ischemic period. Using an intraventricular balloon, maximal dP/dt provided a quantitative index of left ventricular performance before and after ischemia. Return of ventricular function expressed as a percentage of control was 54 +/- 11% for group 1, 84 +/- 6% for group 2, and 101 +/- 18% for group 3. Differences in the rate of development of intracellular acidosis were noted during the 60-minute ischemic period. Intracellular pH fell to 6.09 +/- 0.12 in group 1, 6.31 +/- 0.09 in group 2, an 6.79 +/- 0.03 in group 3. In all three groups intracellular pH returned to control (pH 7.20) within 10 minutes of reflow. The metabolic correlates of functional recovery appeared to be the tissue content of ATP at the end of ischemia and after reflow. ATP content at the end of ischemia was 22 +/- 2% of control in group 1 hearts, 31 +/- 4% in group 2 and 64 +/- 2% in group 3. After 45 minutes of reperfusion, ATP levels recovered to 33 +/- 9% of control in group 1, to 71 +/- 9% in group 2 and to 86 +/- 6% in group 3. Although there were no differences between groups in the content of creatine phosphate after 60 minutes of ischemia, the rates of creatine phosphate decline were dissimilar. Further, during the early reflow period, a marked overshoot in tissue creatine phosphate was detected, especially in groups 1 and 2. Histologic damage assessed by light microscopy correlated with the metabolic data, confirming that multidose cardioplegia provided the best preservation of cellular morphology. These results demonstrate that the magnitude of intracellular acidosis and the associated increase in inorganic phosphate correlate inversely with recovery of postischemic ventricular structure and function. ATP, but not creatine phosphate, content correlates with return of contractile performance after reperfusion. The overshoot in creatine phosphate during early reperfusion might impede optimal restoration of ATP content and, as a result, optimal recovery of cell functions.

Adenosine Triphosphate↗
PubMed1982

Expansion of acute myocardial infarction: an experimental study.

Expansion (regional dilatation and thinning) of acutely infarcted myocardium in man has been shown to correlate with overall cardiac dilatation and rupture. We studied gross and histopathologic features and the time course of expansion in rats. Infarcts were produced in 84 rats by ligation of the left coronary artery and studied at 1, 2, 3, 4, 5 and 7 days. All hearts were prepared by potassium diastolic arrest, gel distention and fixation. Expansion was graded 0 to 4+ : 1+, mild thinning of infarcted wall; 2+, mild thinning and dilatation; 3+, moderate thinning and dilatation; and 4+, marked thinning and dilatation. There were 80 transmural infarcts, and 66% showed expansion; 36 of 80 (45%) were graded 1-2+ and 17 of 80 (21%) 3-4+. None of the four exclusively nontransmural infarcts showed expansion. Expansion was present in 61% of transmural infarcts at 1-2 days, in 65% at 3-4 days and in 80% at 5-7 days. The percentage of rats with severe (3-4+) expansion increased markedly over this period, from 0% at 1-2 days to 23% at 3-4 days to 65% at 5-7 days. Histopathologic infarct evolution was roughly twice as rapid as that of humans; 5-7 day-old infarcts showed well-developed granulation tissue. Thus, expansion can be produced in an animal model. A critical infarct size of 17% appeared necessary for significant (greater than 1+) expansion, and the degree of expansion correlated with infarct size. Although this phenomenon begins early after infarction, its extent progresses over days, making interventions to interrupt its development feasible.

Animals↗
PubMed1982

Failure of blood cardioplegia to protect myocardium at lower temperatures.

To assess the effect of temperature, oxygenated blood and crystalloid cardioplegic solutions (CPs) at infusion temperatures of 20 degrees C, 10 degrees C and 4 degrees C were compared. The amount of potassium in each CP was 25 mEq/l. There were six study groups with seven canine hearts in each group, all of which were subjected to 90 minutes of global ischemia at 20 degrees C, 10 degrees C or 4 degrees C, followed by 45 minutes of normothermic reperfusion. During ischemia, either blood or crystalloid CP was given every 30 minutes. With each infusion, any change in myocardial oxygen tension was recorded using mass spectrometry, and oxygen consumption (MVO2) was calculated. Left ventricular (LV) function was assessed before and after ischemia in all hearts by measuring isovolumic developed pressure using an intraventricular balloon. Injection of 20 degrees C blood CP resulted in a mean increase in intramyocardial oxygen tension (PO2) of 7 mm Hg. At 10 degrees C or 4 degrees C, blood CP infusions did not cause a significant increase in intramyocardial PO2, while with crystalloid CP, intramyocardial PO2 did not increase at any of the three infusion temperatures. The mean MVO2 with each blood CP injection, expressed as ml O2/100 g LV wet weight, was 16.5 +/- 0.8 for 20 degrees C blood, 4.1 +/- 0.3 for 10 degrees C blood and 3.5 +/- 0.4 for 4 degrees C blood (p less than 0.001, 20 degrees C blood vs 10 degrees C and 4 degrees C blood). MVO2 with each crystalloid CP injection was 0.9 +/- 0.1 for 20 degrees C CP, 0.8 +/- 0.1 for 10 degrees C CP, and 0.7 +/- 0.1 for 4 degrees C CP. Recovery of developed pressure after 45 minutes of reperfusion, expressed as a percentage of preischemic control, was 76.0 +/- 3.4% or 20 degrees C blood CP, 65.6 +/- 2.3% for 10 degrees C blood CP, and 54.0 +/- 2.7% for 4 degrees C blood CP (p less than 0.05, 20 degrees C blood CP vs 10 degrees C and 4 degrees C blood CP). Recovery of developed pressure, also expressed as a percentage of preischemic control, was 56.6 +/- 1.4% for 20 degrees C crystalloid CP, 72.9 +/- 3.0% for 10 degrees C crystalloid CP, and 72.0 +/- 2.3% for 4 degrees C crystalloid CP (p less than 0.05, 20 degrees C crystalloid CP vs 10 degrees C and 4 degrees C crystalloid CP). These data show that blood CP is most effective when infused at 20 degrees C. The use of 10 degrees C blood CP enhanced myocardial cooling, but was of no additional benefit, presumably because there was little oxygen delivery. Blood CP at 4 degrees C resulted in significantly poorer preservation of LV function. Crystalloid CP infused at either 4 degrees C or 10 degrees C was as effective as 20 degrees C blood CP, despite the absence of oxygen use by hearts treated with crystalloid CP.

Animals↗
PubMed1982

Constrictive epicarditis as a cause of delayed or absent response to pericardiectomy: a clinicopathological study.

It is widely held that constrictive pericarditis is curable by pericardiectomy, and failure to respond reflects an underlying myocardial disease. Fibrous epicarditis could account for residual cardiac constriction, and delayed hemodynamic response in some patients is an alternative explanation. To examine this, we studied the 12 consecutive patients with otherwise normal hearts treated with extensive pericardiectomy for constrictive pericarditis over the past 7 years. Three hemodynamic responses to pericardiectomy were observed: (1) rapid response, where central venous pressure (CVP) fell below 10 cm H2O by 24 hours in two patients; (2) delayed response, where CVP fell below 10 cm H2O by 48 hours in six patients; and (3) no response of CVP in four patients. The CVPs remained critically elevated (greater than 25 cm H2O) in three patients with delayed response until a sclerotic epicardial peel was resected. Another patient whose CVP of 30 cm H2O showed no change after parietal pericardiectomy was thought to have amyloid cardiomyopathy but instead at autopsy had constrictive epicardial sclerosis not recognized at parietal pericardiectomy. Histologic features of parietal pericardium had no correlation with hemodynamic response, whereas epicardial histology did correlate with hemodynamic response in four patients. The data showed a spectrum of postpericardiectomy delayed hemodynamic responses, which in some patients may be due to a slowly resolving or fixed component of fibrous epicarditis that may be clinically misconstrued as a cardiomyopathy. Interruption of visceral pericardial tissue may be as important as resection of the parietal pericardium in patients with epicardial sclerosis.

Adolescent↗
PubMed1982

Acute adriamycin cardiotoxicity: morphologic alterations in isolated perfused rabbit heart.

Adriamycin is an antitumor agent whose use is limited by cardiac toxicity resulting in a late congestive cardiomyopathy. The time course of the cardiac changes and whether they are due to direct effect of the drug on the myocyte is unknown. The purpose of this study was to determine the very early changes in subcellular structure caused by adriamycin in an isolated, perfused, working heart. Eighteen rabbit hearts were perfused with oxygenated Krebs-Ringer-bicarbonate buffer at 39 degrees C. containing either 1, 2, 4, or 8 mg. per liter of adriamycin for periods of 30 to 150 minutes; 10 controls were perfused with buffer only. Light microscopic study of sections through both ventricles revealed no differences between treated and control hearts. Electron microscopy showed a striking and distinctive central clumping of nuclear chromatin in all 18 hearts exposed to adriamycin, but in no controls; this nuclear change was more marked with increasing dose of drug, but not with longer durations of perfusion. In 15 of 18 hearts sarcomeres and mitochondria were normal, and in 15 of 18 mild cytoplasmic vacuolization was present. In contrast, of 10 control hearts nuclei in seven were normal, and three showed some focal peripheral clumping of chromatin; seven had normal sarcomeres and mitochondria, and three showed mild cytoplasmic vacuolization. Thus, exposure of the isolated rabbit heart to adriamycin results in acute and distinctive nuclear alterations, with associated mild cytoplasmic changes. To what extent these nuclear effects mediate subsequent myocyte degeneration or dysfunction remains to be determined.

Animals↗
PubMed1981

Early post-infarction angina. Ischemia at a distance and ischemia in the infarct zone.

We studied two forms of post-infarction angina: ischemia at a distance (angina with new electrocardiographic changes distant from the acute infarct) and ischemia in the infarct zone (angina with new electrocardiographic changes limited to the leads originally involved by the acute infarct). Seventy patients with early post-infarction angina were followed for an average of six months; 43 had ischemia at a distance, and 27 had ischemia in the infarct zone. Mortality in the entire group was 56 per cent, but it was 72 per cent (31 of 43 patients) among those with ischemia at a distance and 33 per cent (nine of 27) among those with ischemia in the infarct zone (P less than 0.005). Post-infarction angina identifies patients with high mortality; among such patients, ischemia at a distance may represent an especially high-risk subset of patients with large areas of viable but jeopardized myocardium who could benefit from aggressive intervention.

Aged↗
PubMed1981

Thallium imaging in cardiac lymphoma.

A clinicopathologic correlation was made of thallium-201 myocardial perfusion imaging in two patients with massive myocardial invasion by malignant lymphoma. Despite extensive tumor involvement, the thallium scintigram was normal in one patient, while the other had only a modest-sized region of reduced tracer uptake. The discrepancy between the results of thallium scans and postmortem observations in these patients is probably related to uptake of thallium by tumor cells. The ability of any cellular and well-perfused tissue to absorb potassium, and potassium analogs such as thallium, suggest that thallium-201 scintigraphy may not be a useful method to screen for cardiac involvement in patients with known malignant neoplasms.

Adult↗
PubMed1981

Ischemic ventricular fibrillation: the importance of being spontaneous.

Although the energy level required to defibrillate normal myocardium is low and constant, as determined from studies of induced ventricular fibrillation, little is known of the specific energy requirements in regionally ischemic hearts for spontaneous or induced ventricular fibrillation. In this study the lowest energy threshold for defibrillation was determined in 10 open chest dogs with reversible 10 minute coronary occlusions at various sites for each of 44 events of ventricular fibrillation, using apical and superior vena caval electrodes with a generator providing variable output of 1 to 30 watt seconds. The ischemic mass, quantitated from postmortem angiographic and planimetric data, was 52 +/- 9 percent (mean +/- standard deviation) of the left ventricle in dogs with induced ventricular fibrillation (Group I), 52 +/- 12 percent in dogs with spontaneous ventricular fibrillation after occlusion (Group II) and 54 +/- 9 percent in dogs with spontaneous ventricular fibrillation after reperfusion (Group III). Defibrillation thresholds in watt seconds were 9 +/- 7 in Group I (n = 12), 19 +/- 10 in Group II (n = 13) and 18 +/- 10 in Group II (n = 19). (Group I versus Groups II and III, probability [p] less than 0.025). In nonischemic hearts, the defibrillation threshold was 3 +/- 2 (n = 32) (p less than 0.001 compared with values in Group I, II or III). Thus, despite similar masses of ischemia, twice as much energy was required for defibrillation of spontaneous ventricular fibrillation (whether after occlusion or reperfusion) as for induced ventricular fibrillation, suggesting that these conditions are caused by different metabolic or pathologic derangements. Such differences should be considered in assessing interventions such as drug therapy designed to inhibit the repetitive ventricular response and in design of implantable defibrillators.

Animals↗