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Biomedical subjects

A N Brest

Publications and source records attributed to A N Brest.

15 recordsLinked to original sources
PubMed1992

Congestive heart failure in the elderly.

Congestive heart failure is in large part a disease of patients with advancing age. As our population ages, the incidence and prevalence of this disorder will continue to rise. The etiology of CHF in the elderly is multifactorial and one must take into account normal changes associated with aging, the heterogeneity of the elderly population, and possible noncardiac as well as cardiac disorders. Therapy must be aimed at the primary pathophysiologic process affecting the heart. Despite a number of therapeutic advances with medical therapy, CHF usually signals a generally irreversible process with a high mortality, especially in those patients with advanced disease. Therefore preventive measures should assume a paramount role in this disorder. Modification of risk factors such as diabetes, smoking, obesity, sedentary life style, and hypercholesterolemia should be aggressively stressed and pursued in patients of all ages. These preventive measures may have a substantial impact on the incidence of CHF in the elderly.

Aged↗
PubMed1977

Pathophysiology and medical management of angina pectoris.

Myocardial oxygen demand is a function of the product of heart rate and blood pressure. Agents such as nitroglycerin not only produce coronary vasodilatation, which increases oxygen supply, but also reduce myocardial oxygen demand secondary to a reduction in both preload and afterload. Beta-adrenergic blockers are useful in angina because they reduce myocardial work and, hence, oxygen demand. A heart rate in the 50s does not preclude an increase in the dosage of propranolol when necessary.

Angina Pectoris↗
PubMed1976

Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases.

A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.

Adult↗
PubMed1975

Comparative hemodynamic effects of placebo and oral isosorbide dinitrate in patients with significant coronary artery disease.

Comparative hemodynamic effects of placebo and 10 mg of oral isosorbide dinitrate were studied in patients with significant coronary artery disease (larger than or equal to 75 per cent lumen narrowing) proved angiographically. Isosorbide dinitrate or placebo was given to eight and 10 patients, respectively, in a double-blind fashion. Cardiac performance at rest and during supine leg exercise was evaluated before and 60 minutes after drug administration. In the resting state, isosorbide dinitrate compared to placebo significantly reduced the left ventricualr (systolic and diastolic), mean pulmonary artery and mean aortic pressures, cardiac index, stroke index, left ventricular work index, stroke work index, and mean systolic ejection rate. Isosorbide dinitrate also significantly reduced left ventricular (systolic and diastolic and mean pulmonary artery pressures during exercise. This study indicates that 10 mg of isosorbide dinitrate has a significant influence on ischemic left ventricular dysfunction 60 minutes after its oral administration.

Adult↗
PubMed1975

Correlation of abnormal Q waves, coronary pathology, and ventricular contractility.

Four hundred and ninety-two patients with coronary artery disease underwent analysis of their electrocardiograms, coronary arteriograms, and ventriculograms. Significant Q-waves were correlated with critical coronary occlusions (greater than or equal 75 per cent obstruction) and ventricular contractility. It was found that Q-waves correlate equally well with ventriculographic abnormalities and critical coronary occlusions. The Q-wave correlation varied from 77 to 87 per cent, depending on the area of myocardium under consideration, except for true posterior myocardial infarction, which correlated 55 per cent with ventriculographic abnormalities and 55 per cent with critical coronary occlusions. Significant Q-waves in Leads II, III, and aVF are better indicators of ventriculographic abnormality than in Leads III and aVF alone, whereas Q-waves in the latter two leads are more definitive than in Lead III alone. Patients who have critical coronary occlusions and normal electrocardiograms have normal ventriculograms in 71 to 78 per cent of the cases, again depending on the area of the myocardium under consideration. Thus, the normal electrocardiogram correlates better with the ventriculogram than with coronary pathology. The abnormal electrocardiogram correlates equally well with both.

Coronary Angiography↗
PubMed1975

The various forms of pulmonary varices. Report of three cases and review of the literature.

Ture pulmonary varices are congenital local dilatations of a pulmonary vein or veins, with normal or collateral transpulmonary drainage into the left atrium. Pulmonary varices do not cause pulmonary venous hypertension, but existing varices can further become dilated by pulmonary venous hypertension due to mitral valve disease. Embryologically, pulmonary varices may represent residual primitive splanchnic venous components incorporated into the pulmonary venous system, or atresia of an individual pulmonary vein which occurred at a time that enable adoption of unobstructed transpulmonary collateral drainage into the left atrium. True pulmonary varices do not produce symptoms, do not change in diameter over the years, and, usually, do not require treatment.

Diagnosis, Differential↗
PubMed1975

Surgery for impending myocardial infarction, acute evolving myocardial infarction, and complications of myocardial infarction.

Post-infarction ventricular aneurysm, ventricular septal defect, and mitral insufficiency are all potentially amenable to surgical intervention. In each instance the results of operation and the prognosis following operation depend largely on the extent of infarction, the status of the residual myocardium, and the interval between infarction and operation. When the residual myocardium exhibits good contractility, the results are usually good. When early operation is performed in the face of a deteriorating clinical course and with poorly contracting residual myocardium, the mortality rates are extremely high. In an effort to increase the efficiency of the residual myocardium, concomitant coronary bypass surgery should be performed whenever possible. In this difficult group, more recent supportive measures such as the intra-aortic balloon pump may be particularly helpful when utilized both before and after operation. The surgical indications and results of coronary bypass surgery in impending or acute evolving myocardial infarction are not as well defined, but it is evident that myocardial revascularization may be useful in carefully selected patients.

Acute Disease↗
PubMed1975

Heart failure in acute myocardial infarction.

In recent years, our understnading of heart failure complicating acute myocardial infarction has expanded considerably. Although it is not always possible to control cardiac decompensation in this situation, rational therapy has evolved with the improved recognition of the hemodynamic alterations in heart failure and the factors contributing to ventricular performance. Furthermore, a more secure physiologic basis now exists for the early identification of such patients and the development of additional therapeutic techniques.

Heart Failure↗