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F Thandroyen

Publications and source records attributed to F Thandroyen.

6 recordsLinked to original sources
PubMed1990

Potentiation of reperfusion-associated ventricular fibrillation by left ventricular hypertrophy.

Important electrophysiological alterations that may predispose hearts to arrhythmias have been described for hypertrophied myocytes, and hypertrophy coupled with ischemia has been associated with an increased incidence of sudden death; however, an influence of hypertrophy on reperfusion arrhythmias has not been previously described. We hypothesized that reperfusion-associated arrhythmias would be potentiated by left ventricular hypertrophy. After induction of renovascular hypertension, 37 awake, unsedated dogs (17 with left ventricular hypertrophy and 20 without hypertrophy) underwent 15 minutes of coronary artery occlusion and reperfusion. All dogs were pretreated with lidocaine bolus injections and with lidocaine by continuous infusion during coronary occlusion and reperfusion. Reperfusion-associated ventricular fibrillation occurred in seven of 17 dogs with left ventricular hypertrophy versus one of 18 dogs without hypertrophy (p less than or equal to 0.05). The presence of hypertension was not significantly associated with an increased incidence of reflow ventricular arrhythmias. Neither QT interval nor area-at-risk was different between the dogs with and without reperfusion ventricular fibrillation; however, increased heart rate just before reperfusion did correlate with an increased incidence of ventricular fibrillation at reperfusion. Thus, 1) left ventricular hypertrophy was associated with a significantly increased incidence of reperfusion-induced ventricular fibrillation after 15 minutes of ischemia, 2) this increased incidence was independent of the presence of hypertension, and 3) lidocaine protected control and hypertrophied hearts against ventricular fibrillation during ischemia but was ineffective in protecting hypertrophied hearts against reperfusion-induced ventricular fibrillation.

Animals↗
PubMed1989

Comparison of atenolol and nifedipine in chronic stable angina pectoris.

The antiangina effects of atenolol, 50 to 200 mg once daily, or nifedipine, 10 to 30 mg 3 times daily, were evaluated in a multicenter, randomized, double-blind, parallel study of 39 patients with known symptomatic coronary artery disease. Treatment was titrated to produce at least a 30% increase in treadmill exercise duration over placebo baseline and then maintained at that dosage for an additional 3 weeks. Both treatments produced significant (p less than 0.001) increases in duration of exercise, total work and exercise capacity when compared with placebo baseline. These improvements in exercise performance were obtained with significant (p less than 0.001) reductions in both ST-segment depression and rate-pressure product for atenolol compared with nifedipine. Furthermore, the total angina attack rate and rate at rest were significantly (p less than 0.01) less frequent with atenolol than with nifedipine. Hence, the antiischemic effects of atenolol exceeded those of nifedipine, based on ST-segment depression and rate-pressure product at comparable workloads.

Aged↗
PubMed1985

Serotonin and the heart: effects of ketanserin on myocardial function, heart rate, and arrhythmias.

Serotonergic receptors have been identified in the blood vessels of the heart and in myocardial tissue. We indirectly examined the potential significance of these receptors by studying the properties of ketanserin, an S2-serotonergic antagonist. In an isolated rat heart preparation, ketanserin at 10(-6) M slowed the heart rate, whereas at 10(-5) M it also decreased the cardiac output. Because the stroke volume rose, a negative inotropic effect could be excluded. Electrophysiologically, ketanserin (10(-7) M or more) increased the action potential duration of the superfused guinea-pig papillary muscle preparation. This Class III effect may account for the antiarrhythmic action of ketanserin (5 X 10(-6) M-10(-5) M) in an ischemic-reperfused rat heart preparation. The possibility of nonspecific effects of ketanserin such as an interaction with alpha 1-adrenergic receptors merits careful evaluation, but in the case of the Class III effect, ketanserin was approximately 100 times more active than prazosin in widening the action potential duration. These data suggest that even high concentrations of ketanserin are unlikely to have harmful effects on the myocardium and might, on the contrary, have beneficial effects in the context of myocardial ischemia.

Action Potentials↗
PubMed1980

Diabetic heart disease.

The fact that a significant proportion of diabetics die of heart disease has led to the belief that the excess mortality is due to coronary athersclerosis, yet many risk factors for the latter are common to diabetics and non-diabetics. In fact, heart disease in diabetes is not synonymous with coronary heart disease. There is evidence that heart disease in diabetes includes a variable combination of coronary atheroma, cardiomyopathy, micro-angiopathy and autonomioc neuropathy.

Coronary Disease↗