Archives des maladies du coeur et des vaisseaux
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Arch Mal Coeur Vaiss · Sep 1990
Comparative Study Clinical Trial Controlled Clinical Trial[Enoximone, vasodilator and/or inotropic agent in congestive cardiac insufficiency? Hemodynamic and ventriculographic study of 20 cases].
The aim of this study was to document the effects of enoximone in congestive cardiac failure. The haemodynamic data (aortic pressure, pulmonary pressures, left ventricular pressure, cardiac output, isovolumic contractility index: Vmax) and left ventricular kinetics of 20 patients with dilated cardiomyopathy (11 ischemic and 9 idiopathic in Stages III or IV of the NYHA Classification before recompensation) were recorded under basal conditions, after 30 minutes infusion of dobutamine (10 micrograms/kg/mn) and after 3 hours infusion of enoximone (total dose: 3.6 mg/kg). The two drugs had an equivalent inotropic effect: ejection fraction + 4 +/- 22% with dobutamine and + 16 +/- 39% with enoximone; Vmax increased from 1.53 +/- 0.5 c/sec to 2.49 +/- 0.8 c/sec with dobutamine and to 1.82 +/- 0.5 c/sec with enoximone. ⋯ Enoximone was less effective than dobutamine in increasing cardiac output (+ 46 +/- 42% with dobutamine and 16 +/- 33% with enoximone) and stroke volume (+ 23 +/- 47% with dobutamine and + 2 +/- 41% with enoximone). This difference in efficacy may be explained by the major reduction in ventricular preload which enoximone induced after that observed with dobutamine. "Responders" (12 patients) had basal cardiac outputs of less than 2.3 l/mn/m2; the peripheral vasodilatation caused by enoximone was greater. Finally, the reduction in left ventricular end diastolic pressure and the increase in Vmax were significantly less in the 11 patients with ischemic cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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Arch Mal Coeur Vaiss · Sep 1990
Clinical Trial[Treatment of chronic cardiac insufficiency with intravenous bolus enoximone. Study of a pharmacokinetic-hemodynamic relation].
The aim of this study was to evaluate the efficacy and pharmacokinetics of enoximone administered as an intravenous bolus in 12 patients (mean age 62 years) with severe chronic congestive cardiac failure (Stage IV of the NYHA) due to ischemic (N = 6) or idiopathic (N = 6) cardiomyopathy. The haemodynamic parameters and plasma concentrations of enoximone and its metabolite were measured 15, 30, 60, 90, 120 minutes, 4 and 6 hours, after IV bolus of enoximone 1 mg/kg in 10 minutes. Enoximone increased the cardiac index by an average of 37 p. 100 (1.92 +/- 0.3 to 2.63 +/- 0.35 l/mn/m2; p less than 0.001); pulmonary artery diastolic pressures fell by 33 p. 100 (p less than 0.01). ⋯ There was a significant correlation between the percentage increase in cardiac index and peak enoximone concentration (r = 0.91; p less than 0.001). In conclusion, an IV bolus of enoximone is an effective treatment for chronic cardiac failure. The haemodynamic response was related to the peak enoximone plasma concentration.
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Arch Mal Coeur Vaiss · Sep 1990
[Left ventricular dysfunction while weaning from mechanical ventilation. Contribution of enoximone].
Mechanical ventilation is a valuable therapeutic option in left ventricular failure because of its effect on ventricular load. However, weaning cardiac patients form mechanical ventilation may result in severe pulmonary oedema, especially if it is not properly prepared. Some of the factors which contribute to pulmonary oedema are: 1) increased venous return due to the inversion ot the regime of inthrathoracic pressures and the release of catecholamines commonly observed during weaning, 2) reduction of left ventricular compliance due to myocardial ischemia, compression of the cardiac chambers by the lungs, ventricular interdependence in some cases and left ventricular dilatation in others, 3) increased left ventricular afterload due to negative intrathoracic pressures and increased systolic blood pressure. ⋯ The authors report six cases of pulmonary oedema in coronary patients after discontinuing mechanical ventilation. The administration I. V. enoximone, a phosphodiesterase inhibitor, prevented acute left ventricular dysfunction in 5 of the 6 cases and enabled successful and definitive weaning from mechanical ventilation.
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Arch Mal Coeur Vaiss · Jul 1990
[Comparison of pro-edematous effects of 2 calcium antagonists in bilaterally nephrectomized rats].
Chronic treatment with dihydropyridines and to a lesser extent other calcium antagonists often cause peripheral edema without fluid retention. To test the possibility that calcium antagonists affect extracellular fluid partition between plasma and interstitium, we compared the effects of a benzothiazepine derivate diltiazem, a dihydropyridine derivate nicardipine and vehicle in binephrectomized anesthetized rats by measuring changes in hematocrit and plasma protein concentration. Forty minutes infusion of low dose of nicardipine and diltiazem (0.1 and 10 micrograms/kg/min respectively) had no significant effect on blood pressure (-2 +/- 2 and -4 +/- 3% respectively); nicardipine increased hematocrit by 5.6 +/- 0.5% (p less than 0.05); while diltiazem had no significant effect as compared to the vehicle (+1.5 +/- 0.3 and +1.5 +/- 0.3% respectively). ⋯ To document and localize an alteration in vascular leak of proteins induced by the drugs, albumin-bound Evans Blue (EB) extravasation was measured spectrophotometrically in different tissues after extraction by formamide. Nicardipine but not diltiazem increased vascular permeation of EB-albumin in skeletal and cardiac muscle. No change was observed in brain, liver, spleen as compared to rats receiving the vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)
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The overall cardiovascular mortality in patients with chronic renal failure is about 30 per cent of which 10 per cent is attributed to myocardial infarction. This prevalence led some workers to propose a hypothesis of "accelerated atherosclerosis" due to the hyperlipidaemia observed in 30 to 70 per cent of patients. However, the concept of accelerated atherosclerosis, which was based essentially on clinical studies, has been questioned. ⋯ Left ventricular hypertrophy and fibrosis may give rise to ventricular arrhythmias which could explain some of the cases of sudden death observed in patients with renal failure and often wrongly attributed to ischemic heart disease. Another form of myocardial disease which is observed later is characterised by an alteration of systolic function with left ventricular dilatation and hypokinesia and increased end diastolic pressures without an increase in left ventricular wall thickness. Valvular heart disease may also result from renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)