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Biomedical subjects

B Mettauer

Publications and source records attributed to B Mettauer.

52 records · Page 3Linked to original sources
PubMed1993

Role of cardiac innervation in atrial natriuretic peptide secretion in transplanted heart recipients.

To investigate whether cardiac innervation modulates atrial natriuretic peptide (ANP) secretion, we performed acute volume expansion on eight normal and eight matched (age, weight, and total blood volume) transplanted denervated heart patients (Htx), while monitoring fluid-regulating hormone, systemic blood pressure, and echocardiographic atrial area changes. At rest, plasma ANP and guanosine 3',5'-cyclic monophosphate (cGMP) were lower in control subjects than in Htx (45 +/- 16 vs. 103 +/- 35 pg/l and 0.9 +/- 0.3 vs. 3.5 +/- 1.4 pM, respectively; P < 0.001). Plasma active renin, aldosterone, and catecholamines did not differ significantly in the two populations, whereas arginine vasopressin and cortisol were higher in controls (P < 0.01 and P < 0.005). Although volume expansion (+15%) and atrial stretch were similar in the two groups, plasma ANP and cGMP increased significantly only in the Htx group (103 +/- 35 to 189 +/- 69 pg/l and 3.5 +/- 1.4 to 5.8 +/- 1.4 pM, respectively; P < 0.001). The decrease observed for the other hormones was not significant except for arginine vasopressin and cortisol (P < 0.05 and P < 0.001) in the control group. These results support the hypothesis of an inhibitory role of cardiac innervation in biologically active ANP secretion in humans, at rest and after acute volume expansion.

Adult↗
PubMed1986

Modulation of plasma and platelet vasopressin by cardiac function in patients with heart failure.

Two groups of patients with congestive heart failure were studied, one with elevated (Group I) and another (Group II) with suppressed plasma concentrations of vasopressin. The mean plasma arginine vasopressin (AVP) concentration in the 17 patients in group I was 3.1 +/- 0.4 pg/mliter whereas the eight patients in group II had plasma concentration less than 0.5 pg/mliter. Platelet AVP concentrations were also higher in the Group I than Group II patients (7.8 +/- 1.5 vs. 2.2 +/- 0.7 pg/mliter, P less than 0.001). Plasma effective osmolality (262 vs. 268 mOsm/kg H2O, P less than 0.05) and plasma sodium concentration (134 vs. 137 mEq/liter, P less than 0.05) were lower in Group I. The Group I patients had a lower cardiac index (CI, 1.9 vs. 2.5 liter/min/m2, P less than 0.05) and higher pulmonary capillary wedge pressure (PCWP, 30 vs. 22 mm Hg, P less than 0.02), plasma renin activity (4.4 vs. 2.0 ng/mliter/hr, P less than 0.01), and plasma aldosterone (74 vs. 10 ng/dliter, P less than 0.001) than the Group II patients. The Group I patients also excreted a smaller percentage of a 15 mliter/kg waterload (31 vs. 57%, P less than 0.005). Group I patients then were treated with agents to decrease cardiac afterload, either captopril or prazosin. CI increased (1.9 to 2.1 liter/min/m2, P less than 0.001) and PCWP decreased (30 to 27 mm Hg, P less than 0.001). This improved cardiac performance was associated with enhanced water excretion (31 vs. 52%, P less than 0.001) and decreased minimal urinary osmolality (375 vs. 208 mOsm/kg H2O, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Differential long-term intrarenal and neurohormonal effects of captopril and prazosin in patients with chronic congestive heart failure: importance of initial plasma renin activity.

Fifty patients with congestive heart failure received, by infusion, 15 ml/kg body weight water load, and systemic hemodynamic, renal function, and neurohumoral parameters values were measured before, 2 days, and 1 month after randomly allocating patients to prazosin or captopril therapy. Both prazosin and captopril caused similar and persistent hemodynamic changes, but important differences existed between their renal and neurohumoral effects. After 1 month of continuous therapy, captopril increased creatinine clearance from 71 to 84 ml/min/1.73(2) (p less than .05), increased the water load excreted in 5 hr from 50% to 71% (p less than .005), and increased 5 hr sodium excreted from 6.8 to 14.7 meq (p less than .005), Captopril also caused a decrease in plasma norepinephrine from 568 to 448 pg/ml (p less than .005), in plasma epinephrine from 94 to 73 pg/ml (p less than .05), and in plasma aldosterone from 57 to 28 ng/dl (p less than .005), without changing plasma vasopressin. These beneficial effects were greater after 1 month of therapy than after 2 days. The only beneficial effect of prazosin was to increase water excretion from 49% to 59% (p less than .05). The long-term response to captopril was similar in patients with higher (greater than 2.5 ng/ml/hr) and lower renin levels. However, in patients with lower renin levels, prazosin decreased pulmonary capillary wedge pressure (24.8 to 21.8 mm Hg, p less than .05), decreased plasma arginine vasopressin (1.16 to 0.75 pg/ml, p less than .05), increased water excretion (62% to 85%, p less than .005), and decreased plasma epinephrine (81 to 46 pg/ml, p less than .05), while in patients with higher renin levels none of these beneficial effects were noted. We conclude that captopril produces long-term beneficial renal and neurohumoral effects that prazosin does not despite similar hemodynamic changes with the two drugs, that these effects are at least partially dependent on the initial neurohumoral and hemodynamic status of the patient, and that through hemodynamic improvement vasodilators may chronically interrupt vasopressin overstimulation.

Captopril↗
PubMed1986

Sodium and water excretion abnormalities in congestive heart failure. Determinant factors and clinical implications.

The renal hemodynamic and neurohumoral determinants of sodium and water excretion abnormalities were studied in 66 patients with severe chronic congestive heart failure. Abnormalities were not closely related to any one variable but were the result of the convergence of a number of determinants. The most important determinants for sodium excretion were activation of the renin-angiotensin system and ventricular function; and the most important for water excretion were plasma vasopressin, plasma norepinephrine, and renal and ventricular functions. In a subgroup of patients, neurohumoral overactivation led to severe sodium and water excretion abnormalities and to increased furosemide requirements. A 17-month follow-up of all 66 patients showed a less favorable clinical course for this subgroup even when compared with hemodynamically matched patients.

Aged↗
PubMed1986

The effect of captopril on the coronary circulation and myocardial metabolism of patients with coronary artery disease.

The acute effects of captopril in three groups of patients with coronary artery disease were studied: 25 patients with congestive heart failure; 8 patients with hypertension; and 14 normotensive patients with angina, and systolic arterial pressure greater than 120 mmHg, but no evidence of heart failure. Systemic haemodynamics were assessed by balloon-tipped thermodilution catheter and coronary haemodynamics were assessed by thermodilution catheter in the coronary sinus. Despite significantly different baseline haemodynamic values, captopril decrease systolic arterial pressure without increasing heart rate in all three groups, thereby decreasing double-product, a major determinant of myocardial work. Coronary blood flow and myocardial oxygen consumption decreased similarly in all groups and decreased in parallel to double-product, while coronary vascular resistance and transmyocardial oxygen difference did not change except for a slight decrease in transmyocardial oxygen difference in those patients with congestive heart failure. Transmyocardial lactate extraction increased insignificantly. These findings suggest that captopril may improve metabolic balance in various types of patients with coronary artery disease and that it does this by decreasing myocardial oxygen demand.

Adult↗
PubMed1985

Detrimental arrhythmogenic and sustained beneficial hemodynamic effects of oral salbutamol in patients with chronic congestive heart failure.

The long-term efficacy and potential side effects of oral sympathomimetic amines in the treatment of advanced congestive heart failure remain controversial. We studied the acute and chronic hemodynamic and arrhythmogenic effects of the beta-2 agonist, salbutamol, 6 mg by mouth four times/day, in 20 patients with NYHA classes III to IV congestive heart failure. Acutely, salbutamol increased the cardiac index (1.9 to 2.3 L/min/m2, p less than 0.01) and heart rate (92 to 97 bpm, p less than 0.01) while it decreased pulmonary capillary wedge pressure (35 to 31 mm Hg, p less than 0.01). Salbutamol increased the number of patients having episodes of ventricular tachycardia from two to six and increased the number of episodes of ventricular tachycardia from 2 to 27. Once salbutamol was discontinued, no further episodes of ventricular tachycardia occurred in these six patients. Six patients did not have long-term hemodynamic studies because of serious arrhythmias and two died. In the 12 patients who had long-term studies, the initial beneficial hemodynamic effects of salbutamol were maintained. Thus, although salbutamol may have beneficial long-term hemodynamic effects, it may cause serious arrhythmias in patients predisposed to develop arrhythmias.

Aged↗
PubMed1985

Lack of reflex increase in myocardial sympathetic tone after captopril: potential antianginal effect.

Many vasodilators have been tried as antianginal agents, but the reflex increase in sympathetic tone produced by these drugs necessitate their use with caution in patients with angina. In the first part of this study, captopril was given to 14 patients with angina and systolic arterial pressures of greater than 120 mm Hg. Over the short term, captopril decreased arterial blood pressure (from 110 +/- 18 to 98 +/- 18 mm Hg, p less than .01) without increasing heart rate (75 +/- 15 vs 74 +/- 15 beats/min), arterial concentrations of epinephrine (0.38 +/- 0.28 vs 0.34 +/- 0.25 nM) or norepinephrine (2.7 +/- 2.1 vs 2.8 +/- 2.1 nM), or transmyocardial norepinephrine balance (216 +/- 254 vs 146 +/- 170 p mol/min). Captopril decreased average myocardial oxygen consumption (9.7 +/- 4.1 to 8.2 +/- 2.7 ml/min, p less than .01). Given over the long term (mean 5.5 months), captopril decreased the severity of angina from NYHA classification 3.0 +/- 0.8 to 1.6 +/- 0.8. In the second part of this study, captopril was given in a prospective, randomized, double-blind, placebo-controlled study to 21 patients with stable exercise-induced angina and systolic arterial pressures greater than 120 mm Hg. Captopril increased exercise time (309 +/- 137 vs 374 +/- 142 sec, p less than .05) without changing anginal threshold (rate-pressure product 17.0 +/- 6.0 vs 17.1 +/- 5.6 X 10(-3)). We conclude that captopril decreases mean arterial pressure without causing a reflex increase in myocardial sympathetic tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Prediction of the left ventricular ejection fraction response to doxorubicin using a multiple linear regression model.

The aim of this study was to develop a model for predicting clinically significant deterioration in the left ventricular ejection fraction due to chronic doxorubicin administration. Twenty-six patients were monitored during their courses of doxorubicin chemotherapy with serial gated equilibrium radionuclide angiography. Multiple linear regression analysis was used to derived the best combination of clinical and radionuclide angiographic predictors of resting left ventricular ejection fraction at any point during the course of chemotherapy. The final model consisted of five variables: left ventricular ejection fraction at the previous monitoring point; cumulative dose of doxorubicin achieved at the previous monitoring point; increment in dose from the previous monitoring point; age of the patient; and time to peak left ventricular emptying at the previous monitoring point. The cumulative dose, the ejection fraction at the previous monitoring point and the final model, respectively, explained 11%, 33% and 53% of the variability in ejection fraction determinations during the 26 patient courses. The final model also forecast a potentially very low resting left ventricular ejection fraction (less than 35%) at the cumulative doses of doxorubicin which provoked serious clinical cardiotoxicity in two patients. A multivariate model is a useful aid in timing discontinuation of doxorubicin prior to the development of a clinically significant deterioration in left ventricular ejection fraction.

Computer Simulation↗
PubMedDate not supplied

[The role of beta-2 stimulators in cardiac insufficiency].

Beta-2 adrenergic stimulators, a class of drugs which has been used for a long time in the treatment of bronchial asthma and in tocolysis, have recently become part of the therapeutic arsenal for congestive heart failure. Their action seems to be essentially vasodilator, although they do have a mild positive inotropic effect. In the short term, they improve the cardiac output and they decrease the peripheral vascular resistance. Their long term haemodynamic effects are still controversial. However, their are some arguments in favour of the persistence of the beneficial effects observed in the short term. They have a contradictory action on the capacity for exercise; one study states that they improve exercise capacity and another study finds that they do not. Their action on the length of survival is still unknown. Some reports suggest that they may aggravate ventricular arrhythmias. At the moment, then, this class of drugs is only used experimentally in congestive heart failure. We need to wait for the results of larger studies on the long-term benefits, the exercise capacity and the survival. Possible side effects also need to be studied in more detail.

Adrenergic beta-Agonists↗