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Biomedical subjects

H Pouleur

Publications and source records attributed to H Pouleur.

At least 127 records · Page 7Linked to original sources
PubMed1980

Impaired early left ventricular relaxation in coronary artery disease: effects of intracornary nifedipine.

It has been shown that the maximal rate of left ventricular (LV) relaxation is impaired in patients with coronary artery disease (CAD) under basal conditions. To test the hypothesis that this impaired LV relaxation could be related to viable but metabolically abnormal myocardium, we studied the time course of isovolumic LV pressure fall in 21 patients with CAD and in 13 control subjects under basal conditions. This study was repeated after intracoronary injection of the calcium antagonist nifedipine (N) in 11 patients with CAD and in eight controls. Our data showed that isovolumic pressure fall was biexponential in 20 of 21 CAD patients and in six of 13 controls. Moreover, the time constant of isovolumic pressure fall during the first 40 msec after peak (negative) dP/dt (T1) was significantly greater in CAD patients than in controls (62 +/- 3 vs 44 +/- 1 msec, p < 0.002); the time constant of pressure fall during the 40-80 msec after peak (negative) dP/dt (T2) was similar in both groups ( 42 +/- 2 vs 39 +/- 2 msec, NS). Thirty seconds after injection of nifedipine, T1 and T2, were significantly prolonged in patients with CAD (14 msec and 16 msec, respectively, p < 0.005) and in controls 12 msec and 14 msec, respectively, p < 0.05), and a negative inotropic effect was observed in both groups (peak (positive) dP/dt - 16% in controls and -23% in CAD patients, p < 0.01). At rest, impairment of isovolumic relaxation in CAD patients is mainly limited to the first 40 msec after peak (negative) dP/dt, suggesting a dyssynchronous wall motion. This impairment of LV relaxation is better identified by T1 than by peak (negative) dP/dt in individual patients, and cannot be improved by administration of a calcium antagonist.

Adult↗
PubMed1980

Left ventricular wall stress and aortic input impedance.

The systolic load faced by the left ventricle has been approached from several different aspects over the past decade. One major approach relates instantaneous levels of ventricular wall stress to ventricular systolic load. This approach, based on a large body of information on in vitro performance of muscle, has provided substantial insight into factors influencing ventricular performance. Another equally useful approach to describing ventricular load has been to assess the hydraulic load faced by the ventricle as arterial input impedance or by pulse transmission wave theory. The studies reviewed and the data presented in this article clearly show that in the intact, but open-chest anesthetized preparation, alterations in characteristic impedance are indeed reflected by alterations in ventricular performance, but these alterations are also reflected by alterations in ventricular wall stress that more adequately predict alterations in ventricular shortening associated with changes in load. Moreover, changes in input impedance do not, in themselves, appear to influence the force-velocity-length framework for examining ventricular function.

Animals↗
PubMed1978

Significance of pulmonary input impedance in right ventricular performance.

Right ventricular adaptation to changes in pulmonary input impedance was studied in open-chest dogs. When identical increases in pulmonary vascular resistance are imposed by two different manoeuvres (lung inflation and clamping of the left pulmonary artery), external power and pressure-time integral of the right ventricle at similar filling pressure are always greater during clamping than during inflation. Further studies demonstrate that, at equal increases in pulmonary input impedance modulus at 0 Hz, the clamping produces a greater change in the sum of the first three harmonics of impedance than the inflation (respectively +77% and -10% vs control modulus; -82% and +8% vs control phase). These impedance changes could explain the different behaviour of the right ventricle either by better matching of the ventricular internal impedance or by functional modification of the outflow tract.

Animals↗
PubMed1977

Effects of disopyramide and aprindine on arrhythmias after acute myocardial infarction.

The incidence of ventricular arrhythmias after myocardial infarction was compared in a double blind study of disopyramide (33 patients), aprindine (34 patients) and placebo (31 patients). Total ventricular arrhythmias were less frequent in the aprindine group than in the disopyramide group (P less than 0.05) or than in the combined disopyramide and placebo groups (P less than 0.05). The incidence of life-threatening arrhythmias and of ventricular arrhythmias in high risk patients was also reduced by aprindine compared to disopyramide (P less than 0.001) or placebo (P less than 0.001). It is concluded that aprindine is effective in reducing ventricular arrhythmias and that further investigations on its preventive use after the onset of myocardial infarction are justified.

Acute Disease↗
PubMed1975

Cardiac function early after repair of tetralogy of Fallot.

Hemodynamics of 12 patients with tetralogy of Fallot were monitored during the first 72 hours after surgical repair. Total immediate repair in 5 patients was followed after 24 hours by a greater decrease in cardiac index than that observed in the group of 4 patients with previous palliative shunt (minus 25 plus or minus 6 vs. minus 1 plus or minus 7 per cent, p smaller than 0.025). This difference disappeared after 48 hours, and the short-term follow-up periods of these two groups were equally smooth. Six patients with pulmonary stenosis requiring the placement of an outflow patch had higher right ventricular filling pressures (after 24 hours 13.8 vs. 10.8 mm. Hg, p smaller than 0.025; 2 to 4 weeks later 9.6 vs. 5.5 mm. Hg, p smaller than 0.05), suggestive of a persistent right ventricular depression. This ventricular depression must be attributed to the induced pulmonary insufficiency and to the presence of akinetic areas. Both these factors should therefore be carefully minimized during the surgical procedure.

Adolescent↗
PubMed1974

Circulatory effects of deep inspirations, blocked expirations and positive pressure inflations at equal transpulmonary pressures in conscious dogs.

1. Circulatory effects of deep inspirations, blocked expirations and constant endotracheal positive pressure inflations were studied in six conscious dogs under comparable geometries of the pulmonary vascular bed, i.e. at equal transpulmonary pressures (around 10.2 cm H(2)O) and similar lung volumes.2. In order to characterize these effects, we measured beat-by-beat left and right ventricular ejections, pulmonary arterial, left atrial and aortic mean transmural pressures, and concomitant intrathoracic and tracheal pressures. Changes in pulmonary-left heart blood volume were also computed.3. During inspiration when intrathoracic pressure became more negative, there was a slight increase in right ventricular output (+15%; P < 0.1) and always a net decrease in left ventricular output (-25%; P < 0.01) despite a significant increase in mean transmural left atrial pressure (+3 cm H(2)O, i.e. +40%; P < 0.005). It is concluded that the more negative intrathoracic pressure increases the left ventricular outflow impedance and that an inspiratory increase in pulmonary vascular capacity cannot explain the observed reduction in left ventricular output since this reduction occurs together with an increase in left ventricular filling pressure.4. During blocked expiration when intrathoracic pressure was positive, decreases in right ventricular output (-17%; P < 0.05) and in pulmonary-left heart blood volume (-12 ml.; P < 0.05) were observed while right ventricular outflow impedance increased. After an initial augmentation in left ventricular output (despite a concomitant progressive decrease in mean transmural left atrial pressure), left ventricular output also decreased (-17%; P < 0.05). Such circulatory changes were similar but less marked than those observed under constant positive pressure inflations. These observations suggest that the decrease in venous return (and consequently in right ventricular output) following the increase in intrathoracic pressure is the leading factor which overshadows the augmentation in left ventricular output associated with the simultaneous decrease in left ventricular outflow impedance.5. Similar experiments performed on two additional dogs in acute conditions showed the same circulatory effects before and after pharmacological blockade. These observations therefore confirm that mechanical factors play a leading part during these respiratory manoeuvres.

Animals↗
PubMedDate not supplied

Cardiovascular effects of AR-L115 BS in conscious dogs with and without chronic congestive heart failure.

AR-L115 BS is a phenyl-imidazo-pyridine derivative that combines positive inotropic and vasodilator properties. To analyze the mechanisms of action of AR-L115 in the presence or absence of heart failure, we administered it intravenously to conscious dogs (seven normals and eight with a volume-overload heart failure). In normals, at a plasma level around 1,000 ng/ml, AR-L115 BS increased left ventricular (LV) peak (+) dP/dt (+48%; p less than 0.02) and heart rate (+29 beats/min; p less than 0.05) without altering significantly cardiac filling pressures or cardiac output. The mean aortic pressure and the systemic vascular resistances (-20%; p less than 0.02) were reduced, but plasma renin activity (PRA) was unchanged. In heart failure, the same plasma level increased peak (+) dP/dt by 36% (p less than 0.01), but heart rate stayed unchanged. Mean aortic pressure, systemic vascular resistances (-20%; p less than 0.01), and LV end-diastolic pressure (-9.1 mm Hg; p less than 0.01) all dropped significantly, while cardiac output increased slightly; PRA did not rise significantly. After beta-blockade, the increases in peak (+) dP/dt and the changes in systemic vascular resistances were markedly reduced. In conclusion, AR-L115 BS has strong positive inotropic and vasodilator effects, both of which are partially dependent on the level of the sympathetic tone in the intact animal. These combined properties improve hemodynamics in heart failure; this improvement is already significant at relatively low plasma levels, at which deleterious changes in heart rate or PRA are absent.

Adrenergic beta-Antagonists↗