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Biomedical subjects

H Valette

Publications and source records attributed to H Valette.

68 records · Page 4Linked to original sources
PubMed1983

Acute haemodynamic effects of a single intravenous dose of piretanide in congestive heart failure.

The haemodynamic effect of a single 12 mg intravenous dose of piretanide was assessed in 11 patients with congestive heart failure. It did not cause any change in cardiac output, heart rate or systemic vascular resistance, whereas the pulmonary wedge, mean pulmonary and right atrial pressures and pulmonary blood volume fell progressively, the difference from the control values being significant 5 minutes after the injection. The temporal evolution of the ratios pulmonary wedge pressure/total blood volume, pulmonary blood volume/total blood volume, right atrial pressure/total blood volume was chiefly determined by the numerator, which in all cases showed a more rapid decrease than total blood volume. Serum electrolytes remained unchanged 1 hour after the injection of the drug, except for potassium which fell from 4.9 to 4.1 mEq/l, while urinary sodium and potassium excretion were greatly increased. This high ceiling diuretic appears to have renal and venodilator properties close to those of furosemide.

Adult↗
PubMed1981

Cardiac function in chronic bronchitis: effects of pacing and plasma expansion.

1. We have investigated left ventricular function in 25 selected patients with chronic bronchitis by use of atrial pacing and plasma volume expansion. Nine subjects had a past history of acute respiratory failure. None had either clinical or electrocardiographic signs of coronary heart disease. Paradoxical pulse was absent, since the difference between the highest and lowest systolic arterial pressure throughout the respiratory cycle was 5.4 +/- 1.5 mmHg. 2. During atrial pacing, at a mean rate of 145 +/- 15, about 80% of the predicted maximal rate, none of the patients showed anginal pain or ventricular repolarization abnormality. Cardiac output remained unchanged compared with control values. 3. Plasma volume expansion was achieved by intravenous injection of 1 litre of gelatin over 30 min. Cardiac output, pulmonary wedge pressure and right atrial pressure rose as reported in literature for normal subjects. In four patients cardiac output did not increase although wedge pressure and right atrial pressure did; two of these four patients also had an overshoot in pulmonary wedge pressure just after atrial pacing, suggesting left ventricular dysfunction. Three out of 25 patients had high control right atrial pressures, probably in relation to impaired right ventricular function. No paradoxical pulse occurred during plasma volume expansion. Therefore competition for space in the pericardium between ventricles was unlikely. 4. Our data suggest that left ventricular dysfunction is rare in patients with chronic obstructive pulmonary disease. There was no significant difference between subjects with and without a past history of acute respiratory failure.

Adult↗
PubMed1981

[Ergometric study of a new vasodilator agent in angina: molsidomine. Value of combination with beta-blockaders].

Molsidomine, a new venous vasodilator, was studied in 40 cases of stable angina by ergometric stress testing. 1. In 10 patients, one hour after 2 mg molsidomine sublingually, the work inducing a 1 mm ST depression (WST 1) increased by 94% (p less than 0,05), the total work by 52% (p less than 0,005) and the maximum ST depression (ST max) fell by 45% (p less than 0,01). Resting heart rate was unchanged. There was a mild fall in systemic blood pressure. 2. Molsidomine had a significant synergic effect in 3 groups of 10 patients on betablocker therapy but with ischaemic changes on exercise: a) Molsidomine 1 mg sublingually increased WST 1 by 36% (p less than 0,05); at a 2 mg dosage, by 55% (p less than 0,001). ST max decreased from 2,4 +/- 0,4 mm to 1,3 +/- 0,3 (p less than 0,005) and 1,2 +/- 0,33 (p less than 0,001) respectively. The maximal effect was obtained with 1 mg in 5 out of 10 patients. b) One and three hours after 2 mg Molsidomine sublingually or orally: WST 1 increased from 97% to 110% (p less than 0,005): ST max decreased in similar proportions (p less than 0,005). c) 2 mg Molsidomine and 230 mg isosorbide dinitrate orally were compared after two hours: WST 1 increased by 130% after Molsidomine (p less than 0,005) and by 112% after isosorbide (p less than 0,005). ST max decreased in similar proportions (p less than 0,005). The blood pressure fell less with molsidomine. Molsidomine appeared to be better tolerated than isosorbide. (5 cases of mild headache in 40 patients compared to 4 cases out of 10 patients). The results of a preliminary clinical trial are reported. The association of molsidomine (2 mg per os three times daily) reduced the number of anginal attacks by over 50% in 16 out of 17 patients inadequately controlled by betablockade alone. 3 patients complained of headache at the onset of therapy. The efficacity was comparable and the tolerance better than in 28 patients with isosorbide dinitrate and betablockade, and in 10 patients with nifedipine and betablockade. In conclusion, molsidomine is a venous vasodilator with useful pharmacokinetic properties. It seems to be effective and well tolerated in the treatment of angina whether used alone or in association with betablockers.

Administration, Oral↗
PubMed1980

Comparison of hemodynamic effects of furosemide and piretanide in normovolemic patients.

The effects of furosemide and piretanide (Hoe 118) on the pulmonary hemodynamics in 20 patients recovering from uncomplicated myocardial infarctions were compared in a double-blind study. The diuretic effects and half-lives of the two drugs were not significantly different, so that their hemodynamic actions could be compared directly. Both drugs progressively reduced cardiac output and pressures in the pulmonary circulation, whereas systemic vascular resistance increased significantly. Both drugs slightly increased pulmonary blood volume but not significantly. Total blood volume decreased less rapidly than cardiac output, so that the ratio of cardiac output to total blood volume decreased with time. We conclude that both drugs increase venous compliance in normovolemic subjects and probably increase the compliance of pulmonary vessels.

Blood Pressure↗
PubMedDate not supplied

Iodine 123-labeled metaiodobenzylguanidine imaging in heart disease.

Scintigraphic images of myocardial iodine 123-labeled metaiodobenzylguanidine (MIBG) reflect the relative distribution of adrenergic neurodensity and function in the myocardium. In patients with hypertrophic cardiomyopathy or after infarction, MIBG uptake in hypertrophied myocardium and the infarct-related myocardium was found to be decreased in comparison to blood flow distribution, delineated with thallium 201. Most intriguingly, semiquantitative measurements in patients with congestive heart failure demonstrated reduced myocardial MIBG uptake. This reduction correlated directly with indexes of left ventricular function. Decreases in neuronal density, dysfunction of adrenergic neurons, or chronically elevated circulating norepinephrine levels may account for this diminished myocardial uptake, which, as demonstrated in a pilot study of 90 patients with congestive heart failure, was found to be of predictive value for survival.

3-Iodobenzylguanidine↗
PubMedDate not supplied

Effects of intravenous diltiazem on sinus node function and atrioventricular conduction in patients.

We studied the electrophysiologic effects of injectable diltiazem (dosage: bolus of 0.15 mg/kg, maintenance infusion of 0.3 mg/kg/h for 20 min) on sinus node function and atrioventricular function in 33 patients (22 men and 11 women, mean age 63.6 +/- 15.8 years). Seventeen patients had an electrophysiological exploration considered as normal, eight had sinus node dysfunction (corrected sinus recovery time greater than 525 ms), and eight had AV nodal block (PH greater than 160 ms and/or a Wenckebach point less than 125/min). Effects of the drug were assessed 20 min after the beginning of the infusion, which was continued until the end of examination. In normal subjects diltiazem lengthened corrected sinus node recovery time (305 +/- 115 ms leads to 451 +/- 283 ms) and slightly depressed AV nodal conduction (Wenckebach point: 163 +/- 23 leads to 147 +/- 25). In patients with sinus node dysfunction diltiazem provoked a bradycardia without significant changes in corrected sinus node recovery time or in estimated atrio-sino-atrial conduction time. In patients with AV nodal block diltiazem provoked a lowering of the Wenckebach point (137 +/- 47 leads to 122 +/- 38). There was no effect on hissian or infrahissian conduction, even when this was abnormal in the basal state. These data suggest that diltiazem must be utilized with caution in patients with sinus node dysfunction and AV nodal block.

Aged↗
PubMedDate not supplied

[Gamma function extrapolation of dilution curves for pulmonary blood volume determination in chronic bronchitis (author's transl)].

The risk of incorporating inapparent recirculation under the extrapolated downslope of dye dilution curves is greater with exponential than gamma function extrapolation since the latter makes use of ascending and early descending limbs of the curve. Extrapolation of a true gamma function is not affected by the level at which extrapolation begins. With curves obtained in eight normal subjects, cardiac output (phi) was comparable by exponential and gamma extrapolation if the latter began between 75 and 55% of the peak concentration (Cmax.). phi was underestimated or overestimated according to whether extrapolation began higher or lower than the above limits. Therefore, experimental curves were not true gamma functions. However, the level at which extrapolation began had little effect on pulmonary mean transit time and pulmonary blood volume (PBV) calculated by use of the double injection-single sampling method. Similar effects on phi of the level at which extrapolation by a gamma function begins were found with 24 chronic bronchitics. PBV calculated with a gamma function extrapolated from 0.75 X Cmax. downwards and with an exponential function averaged approximately 340 ml and did not differ from one another. The data suggest that the low values of PBV in chronic bronchitis are not an artifact due to the method of extrapolation.

Aged↗