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Biomedical subjects

S Adamopoulos

Publications and source records attributed to S Adamopoulos.

42 records · Page 3Linked to original sources
PubMed1991

Holter monitoring of ventricular arrhythmias in a randomised, controlled study of intravenous streptokinase in acute myocardial infarction.

The occurrence of ventricular arrhythmias attributed to streptokinase treatment in acute myocardial infarction is not well defined. Holter monitoring was performed for 24 hours in 81 patients with suspected acute myocardial infarction randomised in a ratio of 2:1 to intravenous streptokinase 1.5 x 10(6) IU (n = 55) or placebo infusion (n = 26) 6.7 hours (mean) after the onset of symptoms. No episodes of ventricular fibrillation were recorded. For the whole 24 hour period and during the first three hours after the start of treatment the incidence and frequency of ventricular arrhythmias were similar in the patients randomised to streptokinase and to placebo. But when the results in patients randomised "early" after the onset of symptoms of suspected acute myocardial infarction were analysed separately the frequency of abnormal complexes, pairs, runs, and repetitive arrhythmias seemed to be higher in patients allocated to streptokinase. This may reflect arrhythmias associated with reperfusion.

Arrhythmias, Cardiac↗
PubMed1991

Physical and pharmacological conditioning in chronic heart failure: a proposal for pulsed inotrope therapy.

There is good evidence that physical deconditioning may be playing an important role in the changes secondary to chronic heart failure, and that it may contribute to exercise intolerance. Physical training can improve the symptoms and exercise performance of patients in stable chronic heart failure and the possibility is discussed that pharmacological therapy may be able to stimulate some of these benefits. A protocol for pulsed inotrope therapy is proposed which may produce pharmacological conditioning whilst avoiding drug tolerance and beta-receptor down-regulation and lessening the incidence of arrhythmias.

Chronic Disease↗
PubMed1991

Peripheral abnormalities in chronic heart failure.

Exercise intolerance is a major cause of morbidity in chronic heart failure (CHF) and has traditionally been attributed to skeletal muscle hypoperfusion during exercise. However, intrinsic abnormalities in skeletal muscle biochemistry and histology may also play an important role in the pathophysiology of exertional fatigue in CHF. Studies using 31P nuclear magnetic resonance (NMR) spectroscopy have demonstrated early skeletal muscle metabolic changes during exercise including excessive acidification and phosphocreatine depletion. Patients with CHF show muscle fibre atrophy with transformation of type I to II fibres accompanied by a decrease in oxidative enzyme capacity. Most of the drugs currently used to treat patients with CHF do not improve oxygen availability within exercising muscle or exercise capacity although some of them increase blood flow to skeletal muscle or alter the pattern of blood flow distribution. Physical training programmes improve exercise performance, ventilation, autonomic function and symptomatic status in CHF. Training can also increase cardiac output and reduce peripheral vascular resistance with concomitant increases in blood flow to exercising muscle and reduced arterial and venous lactate. 31P-NMR studies in patients with CHF have demonstrated significantly less acidification and phosphocreatine depletion during exercise after physical training. Animal studies suggest that the NMR changes in skeletal muscle of CHF depend on both the severity of heart failure and physical deconditioning, whereas training may reverse or prevent these alterations.

Exercise↗
PubMed1990

Effects of physical training in chronic heart failure.

Eleven patients with chronic heart failure secondary to ischaemic heart disease (mean [SEM] age 63.0 [2.3] years; left ventricular ejection fraction 19 [8]% undertook 8 weeks of home-based bicycle exercise training and 8 weeks of activity restriction (rest) in a physician-blind, random-order, crossover trial. Training increased exercise duration from 14.2 (1.1) min to 16.8 (1.3) min and peak oxygen consumption from 14.3 (1.1) ml.min-1.kg-1 to 16.7 (1.3) ml.min-1.kg-1. Heart rates at submaximum workloads and rate-pressure products were significantly reduced by training, and there was also a significant improvement in patient-rated symptom scores. No adverse events occurred during the training phase. Thus home-based physical training programmes are feasible even in severe chronic heart failure and have a beneficial effect on exercise tolerance, peak oxygen consumption, and symptoms. The commonly held belief that rest is the mainstay of treatment of chronic heart failure should no longer be accepted.

Aged↗
PubMedDate not supplied

Pulsatility and resistance indices in intrarenal arteries of normal adults.

In order to establish the normal range of values of Pulsatility (PI) and Resistance (RI) Indices in the intrarenal vasculature, a study of 50 healthy volunteers (23 males, 27 females), divided into five groups of 10 according to age, was performed with Duplex Doppler ultrasound. Both kidneys were examined in all individuals and, in 12, indices were also compared between upper and lower poles of both kidneys. In addition, repeat examinations were performed in nine subjects on three different days, in order to assess the reproducibility of the method. No differences were found in the mean values of both indices between males and females, upper and lower poles, right and left kidneys. A statistically significant increase (p < 0.01, unpaired t-test) was demonstrated when the oldest age group (7th decade) was compared to the youngest age group (3rd decade). The method appeared remarkably reproducible for RI (4.2-7%), with wider variation in the PI (9.5-22.7%).

Adult↗