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Biomedical subjects

L C Becker

Publications and source records attributed to L C Becker.

At least 163 records · Page 9Linked 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

Collateral circulation in patients with unstable angina.

Coronary collaterals were evaluated in 218 consecutive catheterized patients with unstable angina (defined as ischemic cardiac pain at rest associated with transient electrocardiographic changes). Collaterals were present in 106 patients (49 percent). The presence of collaterals correlated with the extent and severity of the coronary artery disease but not with age, sex, or risk factors. Among patients with comparable severity of narrowings, the presence of collaterals did not appear to protect against abnormal wall motion or pathologic Q waves on the ECG. In patients with single vessel disease, collaterals also did not appear to protect against transient ST segment evaluation during ischemia.

Age Factors↗
PubMed1982

Pathogenesis of angina pectoris.

There are two broad classes of angina pectoris, related to two fundamentally different pathogenetic mechanisms: in classic angina, atherosclerotic narrowings limit the ability of the coronary arteries to augment myocardial blood flow in response to increases in demand, and in variant angina, a primary reduction in coronary blood flow occurs, unrelated to changes in demand. Over the last decade, major advances have been made in our understanding of the factors that control coronary blood flow and how they interact in each of the major classes of angina. The present review examines these advances, as well as their relation to the syndromes of rest angina, postprandial angina, and exertional coronary artery spasm. Current knowledge about the mechanisms by which myocardial ischemia produces the sensation of angina is discussed, along with the application of pathogenetic principles to medical therapy.

Angina Pectoris↗
PubMed1981

Prostaglandin inhibition and myocardial infarct size.

In parallel with experimental research into methods for salvage of ischemic myocardium after acute myocardial infarction (AMI) over the last decade, there has been a growing interest in prostaglandins (PG) and their inhibition by aspirin-like drugs or nonsteroidal anti-inflammatory drugs (NSAID). The finding of enhanced PG release during myocardial ischemia and its blockade by the NSAID indomethacin led to the hypothesis that PG might influence the infarction process. Because PG differ in vasoactive, cellular, and metabolic properties, and PG inhibitors also differ in their ability to inhibit synthesis of different PG and their metabolites, some PG inhibitors might be expected to reduce myocardial ischemic injury and infarct size. In addition, the NSAID may directly modify cellular events during infarction. Experiments with NSAID in the anesthetized and conscious animals have demonstrated a reduction of myocardial infarct size with ibuprofen, but an increase in infarct size with indomethacin. The opposite effects of these agents on infarct size might have been related to the different doses used, different degrees of inhibition of PG and their metabolites, and different effects on factors influencing myocardial oxygen supply and demand, metabolic and cellular events during infarction. It has recently been suggested that some of these agents might also influence the healing process after AMI and, therefore, late complications.

Acute Disease↗
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

Stress thallium-201 myocardial scintigraphy for the detection of individual coronary arterial lesions in patients with and without previous myocardial infarction.

The value of stress thallium-201 scintigraphy for detecting individual coronary arterial stenoses was analyzed in 141 patients with angiographically proved coronary artery disease, 101 with and 40 without a previous myocardial infarction. In patients without infarction, the sensitivity for detecting greater than 50 percent narrowing in the left anterior descending, the right and the left circumflex coronary artery was 66, 53 and 24 percent, respectively. In those with a previous infarction, the sensitivity for demonstrating disease in the artery corresponding to the site of infarction was 100 percent for the left anterior descending, 79 percent for the right and 63 percent for the left circumflex coronary artery. In patients with a prior anterior infarction, concomitant right or left circumflex coronary arterial lesions were detected in only 1 of 12 cases, whereas in those with previous inferior or inferolateral infarction, the sensitivity for left anterior descending coronary artery disease was 69 percent. Because of the reasonably high sensitivity for detecting left anterior descending arterial disease, irrespective of the presence and location of previous infarction, myocardial scintigraphy was useful in identifying multivessel disease in patients with a previous inferior infarction. However, because of its relative insensitivity for right or left circumflex coronary artery disease, scintigraphy proved to be a poor predictor of multivessel disease in patients with a prior anterior infarction and in patients without previous myocardial infarction.

Adult↗
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

Clinical recognition of giant left ventricular aneurysm.

The noninvasive diagnosis of left ventricular aneurysm has markedly improved with gated blood pool scintigraphy. However, in patients with giant anterior ventricular aneurysms, the gated blood pool scintigram performed in two standard views (anterior and 40 degree left anterior oblique) may incorrectly suggest ischemic cardiomyopathy. We retrospectively identified five patients who underwent resection of a ventricular aneurysm over a 2 1/2 year period and who had preoperative scintigraphic studies that appeared to show severe diffuse left ventricular dysfunction. contrast ventriculography demonstrated preserved wall motion in septal, inferior and lateral segments not seen by gated blood pool scintigraphy and showed extraordinarily large anterior aneurysms. M-mode or two-dimensional echocardiograms showed intact posterior wall function in all patients, suggesting severe regional myocardial disease rather than global dysfunction. Two-dimensional echocardiography showed additional segments with preserved function as well as discrete aneurysms in all patients. We conclude that gated blood pool scintigraphy, when performed in two standard views, may fail to correctly diagnose some patients with very large anterior wall aneurysms. M-mode echocardiography, two-dimensional echocardiography and additional scintigraphic views that visualize the posterior portions of the left ventricle improve noninvasive diagnosis of patients with resectable giant left ventricular aneurysms.

Aged↗
PubMed1981

Salvage of ischemic myocardium by dipyridamole in the conscious dog.

We investigated the effect of i.v. dipyridamole, a potent small-vessel coronary vasodilator, on myocardial infarct size in conscious dogs. Dipyridamole, 7-9.7 microgram/kg; 15 dogs) or saline (15 dogs) was infused for 6 hours beginning 10 minutes after acute permanent occlusion of the mid-circumflex coronary artery. After sacrifice, 48 hours after occlusion, stereoscopic postmortem angiography was used to define the mass of the occluded coronary bed. Infarct size was determined by planimetry of weighed, unstained left ventricular slices. Dipyridamole produced a striking reduction in mean infarct mass compared with control (3.1 g vs 13.2 g, p less than 0.001), while mean occluded bed mass was similar (30.3 g vs 32.7 g, NS). As a percentage of the occluded bed, mean infarct size was reduced from 36.8% to 8.6% ( p less than 0.001). Mean arterial blood pressure declined approximately 10% after dipyridamole. Heart rate and left atrial pressure did not change significantly. Collateral blood flow, measured with 8- mu radioactive microspheres, increased in all regions during dipyridamole infusion. The infarct center and border regions had sustained increases over 6 hours of 23-80%, while nonischemic regions demonstrated a diminishing response over time, with a large (98-125%) increase 10 minutes after infusion and a smaller (22-25%) increase 6 hours later. Although antiplatelet or local metabolic effects cannot be excluded, the myocardial salvage produced by dipyridamole was most likely due to the increase in collateral blood flow.

Animals↗
PubMed1981

Combined administration of nitroglycerin and propranolol to patients with acute myocardial infarction.

Hemodynamic effects of combined nitroglycerin and propranolol administration were investigated in patients with acute myocardial infarction. After nitroglycerin infusion decreased the mean arterial pressure by 20 mm Hg for one hour, nitroglycerin was continued, and patients were given 0.033 mg/kg of propranolol every five minutes for a total dose of 0.1 mg/kg, or until there was a decrease in heart rate to less than 60 beats/min, an increase in left ventricular filling pressure (LVFP) to greater than 15 mm Hg, or a decrease in systolic arterial pressure to less than 85 mm Hg. Seven of eight patients with initial LVFP less than or equal to 15 mm Hg and three of seven with initial LVFP greater than 15 mm Hg received 0.1 mg/kg of propranolol. Propranolol significantly decreased heart rate. Although pressure time/minute decreased significantly, the magnitude of its decrease was small, suggesting only a minimal effect on myocardial oxygen demands. The LVFP increased after giving propranolol but remained less than the control value. Simultaneous administration of nitroglycerin likely prevented further increases, since LVFP increased after cessation of nitroglycerin infusion, and three patients subsequently had pulmonary edema. Propranolol administration resulted in a significant increase in peripheral vascular resistance and a decrease in cardiac output.

Blood Pressure↗
PubMed1980

Cardiac catheterization in patients with unstable angina. Recent onset vs crescendo pattern.

Among patients with unstable angina pectoris, those with crescendo angina seem to be at high risk for death and myocardial infarction. We reviewed the clinical, arteriographic, and hemodynamic findings in 218 consecutive catheterized patients with unstable angina. Unstable angina was defined as ischemic cardiac pain at rest associated with transient ECG changes but no evidence for acute myocardial infarction. Patients were divided into two groups according to the duration of symptoms: 134 patients with crescendo angina (new, or increasing, rest pain with previous ischemic symptoms present for more than three months) and 84 with recent onset angina (symptoms present for less than three months). Compared with patients with recent onset symptoms, patients with crescendo angina had more extensive coronary disease and lower ejection fractions, which may explain their poor prognosis.

Angina Pectoris↗