Profunda femoral arteriovenous fistula after percutaneous arterial and venous catheterization.
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Biomedical subjects
Publications and source records attributed to U Thadani.
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The role of epinephrine in eliciting myocardial ischemia was examined in patients with coronary artery disease. Objective signs of ischemia and factors increasing myocardial oxygen consumption were compared during epinephrine infusion and supine bicycle exercise. Both epinephrine and exercise produced myocardial ischemia as evidenced by ST segment depression and angina. However, the mechanisms of myocardial ischemia induced by epinephrine were significantly different from those of exercise. Exercise-induced myocardial ischemia was marked predominantly by increased heart rate and rate-pressure product with a minor contribution of end-diastolic volume, while epinephrine-induced ischemia was characterized by a marked increase in contractility and a less pronounced increase in heart rate and rate-pressure product. These findings indicate that ischemia produced by epinephrine, as may occur during states of emotional distress, has a mechanism distinct from that due to physical exertion.
Nisoldipine, a dihydropyridine calcium antagonist, has greater vascular selectivity than other calcium channel antagonists and does not depress the intact myocardium in vivo. It should be taken on an empty stomach. Both rapid-release and coat-core formulations are available for clinical use, but only the coat-core formulation extends antihypertensive, antiischemic, and antianginal effects throughout the dosing interval when given once daily. The coat-core formulation in daily doses of 10 to 40 mg does not cause the proischemic effects reported with the rapid-release formulation. When given as monotherapy, the coat-core formulation is highly effective in lowering blood pressure to a similar extent as other long-acting calcium channel blockers, diuretics, beta-blockers, or angiotensin-converting enzyme (ACE) inhibitors. The antihypertensive effects are potentiated when the coat-core formulation of nisoldipine is given in combination with lisinopril. In patients with stable angina pectoris nisoldipine coat-core increases exercise duration, reduces anginal frequency and myocardial ischemia, and is effective as monotherapy or in combination with a beta-blockers. In monotherapy the drug is as effective as other long-acting calcium channel blockers or a beta-blocker. The effects of nisoldipine coat-core in patients with heart failure are unclear at present.
Hemodynamic profiles at rest and during bicycle exercise are described in 50 normal male subjects. In nine of these, the hemodynamics at rest and during exercise in the supine position have been compared to those in the sitting position. In the supine position, the observed and derived hemodynamic parameters at rest and during exercise (mean +/- standard deviation) were: heart rate 77 +/- 11 vs 127 +/- 17 beats . min-1, brachial arterial mean pressure, 12.4 +/- 1.2 vs 15.0 +/- 1.6 kPa (93 +/- 9 vs 113 +/- 12 mmHg), pulmonary arterial mean pressure 1.9 +/- 0.5 vs 3.2 +/- 0.8 kPa (14 +/- 4 vs 24 +/- 6 mmHg), left ventricular end-diastolic pressure 1.2 +/- 0.4 vs 1.7 +/- 0.7 kPa (9 +/- 3 vs 13 +/- 5 mmHg), cardiac output 6.3 +/- 1.5 vs 12.0 +/- 3.0 1 . min-1, stroke volume 88 +/- 22 vs 95 +/- 23 cm3, and left ventricular stroke work 0.93 +/- 0.27 vs 1.26 +/- 0.34 J . beats-1. Comparison of hemodynamic data in the supine and sitting position showed that pulmonary capillary wedge pressure, left ventricular end-diastolic pressure, cardiac output, stroke volume, and left ventricular stroke work were lower and heart rate higher in the sitting position, while brachial arterial and pulmonary arterial mean pressures were similar in the two positions. During exercise, the absolute values of pulmonary capillary wedge pressure, left ventricular end-diastolic pressure and stroke volume were lower and heart rate higher in the sitting position, while cardiac output and left ventricular stroke work were similar in the two positions. Comparison of changes from rest to exercise in the supine and sitting postures revealed similar increases in heart rate, pulmonary capillary wedge pressure, left ventricular end-diastolic pressure, cardiac output, and stroke volume in the two positions.
As a result of recent advances in our understanding of the role of nitric oxide and endothelial-derived relaxing factor (EDRF) in vascular control, physicians now have the potential to overcome the loss of EDRF effect by administering nitrates. Nitrates are converted to nitric oxide, resulting in vasodilator effects that improve the myocardial oxygen supply-demand imbalance responsible for myocardial ischemia. This discovery has resulted in a renewed interest in the nitrates for the treatment of ischemic syndromes, particularly chronic stable angina pectoris. Over the past 2 years, an important new formulation of nitrate has become available--isosorbide-5-mononitrate. Three different mononitrate formulations are available in the United States: Ismo tablets in December 1992; followed over a year later by Monoket tablets, available since June 1993; and Imdur extended-release tablets, available since August 1993. Although the mononitrates share the same generic name, they are not similar in regard to their formulations, which suggests the need for future studies designed to explore any clinical differences.