Publications by authors named "Guerin F"

Many nocturnal cardiac arrhythmias and conduction defects have been reported in the adult sleep apnoea syndrome. The most original is the great variability of the heart rate which is cyclical and related to the apnoeic episodes, and easily differentiated from simple respiratory sinus arrhythmia. It is characterised by an initial bradycardia followed by rebound tachycardia.

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Myopathy may be associated with very variable cardiac involvement, the expression of which is related to the type of neuromuscular disease and also to the individual. This retrospective study, performed between 1986 and 1991, was undertaken to determine the prevalence of cardiac involvement in myopathy. A total of 216 subjects with an average age of 34 years were reviewed by clinical examination, ECG, echocardiography and Holter ECG monitoring.

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The authors report the rare case of a 12 year old child with an anomalous origin of the left pulmonary artery from the ascending aorta associated with Tetralogy of Fallot. This complex congenital malformation was treated surgically by a Deleval anastanosis between the right subclavian and right pulmonary arteries. The result was good with a 9 year follow-up, the patient having only Grade II effort duspnoea and cyanosis.

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A 59-year-old woman hospitalised because of dyspnea and a heart murmur in a context of pyrexia was found to have evidence of obstruction of the pulmonary arterial system, clearly defined by ultrasonography, catheterisation and angiography and Imatron scan. The particular feature of this fifth reported case of pulmonary artery leiomyosarcoma is its documentation by transesophageal ultrasonography and tumor biopsy during catheterisation. Surgery with partial excision of the tumor was followed by survival for 6 months, bearing in mind the absence of chemo- or radiosensitivity of this type of tumor.

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Whether or not atrial fibrillation is alone, if not idiopathic, is difficult to determine. The risk of embolization in lone atrial fibrillation is distinctly higher in healthy subjects over 60 years of age when the left atrium is dilated. In chronic atrial fibrillation this risk is higher than in paroxysmal fibrillation, especially within the year following the onset of the arrhythmia.

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Background: Bronchial hyperresponsiveness to cholinergic stimuli such as the inhalation of methacholine is common in patients with impaired left ventricular function. Such hyperresponsiveness is best explained by cholinergic vasodilation of blood vessels in the small airways, with extravasation of plasma due to high left ventricular filling pressure. Because this vasodilation may be prevented by the inhalation of the vasoconstrictor agent methoxamine, we studied the effect of methoxamine on exercise performance in patients with chronic left ventricular dysfunction.

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The improvement of our understanding of the pharmacology of nitrate derivatives has allowed rationalisation of their use in the treatment of coronary artery disease. The comprehension of the evolution of the sensitivity of the vessel wall to nitrate vasodilatation with time has enabled definition of a rhythm of administration which preserves therapeutic efficacy: a daily therapeutic window of 8 to 10 hours. The introduction of new galenic forms (slow release oral preparations and transdermal patches) facilitates the practical application of the "optimal" pharmacokinetic profile.

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Nitrate derivatives have to undergo metabolic activation in the smooth muscle cell or in the plasma with a sulflydryl radical. This transformation results in the formation of nitric oxide and/or S-nitrosothiols. These products stimulate an enzyme, the soluble guanylate cyclase in the sarcoplasm of the smooth muscle cell; giving rise to the formation of intracellular cyclic GMP from GTP.

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An eight-month-old was admitted for acute congestive heart failure with fever. The respective parts played by hypocalcemia (due to vitamin-D deficiency rickets) and acute Epstein-Barr virus infection are discussed. Hypocalcemia was sufficiently marked to induce heart failure per se but replenishment of calcium stores was followed by only partial improvement in cardiac manifestations.

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The eventuality of tolerance was assessed in 19 patients with unstable angina treated by continuous intravenous infusion of 50 micrograms/min of isosorbide trinitrate (ISDN) in association with heparin and betablocker therapy. The tolerance phenomenon was evaluated by the hypotension produced by the ISDN infusion and by the amplitude of fall in blood pressure produced by an intravenous bolus of 1 mg of glyceryl trinitrate (GTN) according to the principle of crossed tolerance to the two nitrate derivatives. Under these conditions of administration, the authors observed partial attenuation of the blood pressure response to continuous ISDN infusion and absence of cross tolerance between ISDN and intravenous GTN.

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Sinorphan is a powerful inhibitor of enkephalinases or endopeptidases 24-11, enzymes implicated in the degradation of the atrial natriuretic factor (ANF). In healthy volunteers, it increases plasma concentrations of endogenic ANF and increases diuresis and natriuresis. In order to study the tolerance and biological effects of pharmacological increase of plasma concentrations of endogenic ANF in severe congestive cardiac failure, 12 patients (in functional Classes III or IV of the NYHA classification) were given a single oral dose of 10, 20 or 40 mg of Sinorphan.

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Abnormalities of myocardial metabolism during acute rejection may be due to ischemia to primary metabolic changes related to rejection. An experimental study of heterotopic cardiac transplantation in the rat was undertaken to study myocardial mitochondrial oxidation during acute rejection. The receivers were Lewis rats and the donors Fischer (FL: allograft) or Lewis (LL: isograft) rats.

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There have been several reports of electromyographic and histological changes of striated skeletal muscle, especially of the type I oxidative fibres, in hypertrophic cardiomyopathy. In order to determine whether these anomalies also cause metabolic changes, a P-31 magnetic resonance spectroscopic study was undertaken at rest and on exercise in 5 pauci-symptomatic patients and 10 control subjects. The 5 patients had primary hypertrophic cardiomyopathy without alteration of systolic function or signs of congestive cardiac failure (Stages I or II).

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We assessed the effect of nifedipine on myocardial perfusion and metabolism in 9 patients with systemic sclerosis, using positron emission tomography with a perfusion tracer (potassium-38) and a metabolic tracer (18F-fluorodeoxyglucose [18FDG]). Nifedipine, 20 mg 3 times daily for 1 week, induced a significant increase in 38K myocardial uptake, a significant decrease in 18FDG myocardial uptake, and a significant increase in the myocardial 38K: 18FDG ratio. These results indicate that the increase in myocardial perfusion is associated with modifications in myocardial energy metabolism, which probably result from a beneficial anti-ischemic effect of nifedipine in patients with systemic sclerosis.

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NADH laser fluorimetry and mitochondrial oxigraphy were used to study myocardial oxidative energy metabolism during cardiac allograft rejection. Heterotopic cardiac transplantation was performed on Lewis rats; allografts (with Fischer rat donors) were compared with isografts (with Lewis rat donors). In vivo and in vitro assays were performed six days after transplantation.

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Two cases of dilated, hypokinetic cardiomyopathy complicated by cardiac failure, are reported in a 29 year old woman and a 55 year old man, with no etiological factors other than chronic major alcoholism (consumption of over 100 ml of alcohol per day for over 5 years). This was completely reversed 10 and 14 months after cessation of alcohol consumption. The isotopic left ventricular ejection fraction increased from 22 to 70 p.

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Many peripheral changes are observed in heart failure concerning regional blood flow, vasomotor tone and oxygen uptake by skeletal muscle. They contribute to the alteration of exercise capacity and have to be taken into consideration in adapting therapy. A regression of these peripheral abnormalities is often observed after prolonged treatment which implies evaluation of efficacy on effort tolerance after a sufficiently long period of administration.

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Noradrenergic sympathetic tone is always increased in chronic left ventricular failure of which it is one of the main compensatory mechanisms. Beta-1-adrenergic stimulation increases the heart rate and left ventricular contractility. However, the efficacy of this "compensatory" mechanism is limited on the one hand by the energetic cost of inotropic stimulation and, on the other hand, by the phenomenon of desensitisation and down-regulation of myocardial beta-1-receptors during intense and prolonged noradrenergic stimulation as observed in chronic cardiac failure.

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Hyperactivity of the noradrenergic sympathetic system is one of the essential "compensatory"mechanisms in chronic left ventricular failure. The ensuing stimulation of myocardial beta-adrenergic receptors results in an increase of heart rate and contractility which, to some extent, counterbalances the alteration of left ventricular function, but rapidly reaches its limits: the excessive shortening of diastoles and, mostly, the increase of myocardial oxygen demand neutralize the beneficial haemodynamic effect of beta-adrenergic stimulation, especially when ischaemia is the cause of the heart failure; the chronic exposure of adrenergic receptors to noradrenaline in high concentrations leads to desensitization, to a "down regulation" which primarily affects the beta 1 receptors and spares, at least partly, the myocardial beta 2 receptors which seem to play a quantitatively important inotropic role, particularly in chronic heart failure. These new data on the physiology of the cardiac noradrenergic system have major therapeutic consequences: in practice, the positively inotropic beta-stimulants can only be used for a short period in acute episodes of heart failure; - the use of beta-blockers in low doses is now considered in the treatment of some forms of heart failure; the mechanism of their therapeutic action remains controverted, and their long-term effectiveness in a large patient population is under study; - a new pharmacological class, beta-adrenoceptor partial agonists, seems to give satisfactory clinical and haemodynamic results in mode-rate heart failure, A wider clinical evaluation is needed to determine the therapeutic role of theses new pharmacodynamic agents.

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