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Biomedical subjects

H Pouleur

Publications and source records attributed to H Pouleur.

At least 109 records · Page 6Linked to original sources
PubMed1983

Force-velocity-length relations in hypertrophic cardiomyopathy: evidence of normal or depressed myocardial contractility.

To assess myocardial contractility in patients with hypertrophic cardiomyopathy (HC), force-velocity-length relations were analyzed during left ventricular (LV) ejection. LV pressure, volume and wall stress data in 15 patients with HC were analyzed and compared with values from 32 normal subjects. Patients with HC had a greater LV mass than did normal subjects (272 versus 96 g/m2, p less than 0.001), elevated LV end-diastolic pressure (17.5 versus 9.8 mm Hg, p less than 0.01) and impaired LV relaxation compared with those of normal subjects. Patients with HC also had a greater ejection fraction (84 +/- 7 versus 74 +/- 8%, p less than 0.01) and mean velocity of shortening than did normal subjects. However, in patients with HC, end-systolic stress (60 +/- 29 versus 187 +/- 61 kdyne/cm2, p less than 0.001) was significantly lower. End-systolic volume and stress data were linearly related in normal subjects (r = 0.88), and values from patients with HC fell either within the lowest part of the 95% confidence interval of this normal relation or outside it in the zone of depressed contractility (11 patients with HC). In addition, the slopes of the relations between end-systolic wall stress and ejection fraction or mean velocity of shortening were abnormal in patients with HC; the slope of the stress-volume trajectory during late ejection was also depressed in 12 patients with HC (average slope 2.6 versus 5.5 kdyne/cm5/m2, p less than 0.001). Thus, there is no evidence of a hypercontractile state in patients with HC; their high values of ejection phase indexes may be explained by a reduction in myocardial afterload.

Adolescent↗
PubMed1983

Effects of a cardioselective beta 1 partial agonist (corwin) on left ventricular function and myocardial metabolism in patients with previous myocardial infarction.

Corwin is a new selective beta 1 partial agonist, able to stabilize the beta 1 adrenoceptors at approximately 43% of their maximal activity. The aim of the study was to determine the effects of this agent in patients with coronary artery disease (CAD) and previous myocardial infarction (MI). In a first group of 14 patients, corwin increased significantly the peak (+)dP/dt (+35%; p less than 0.005), the global ejection fraction, and the ejection fraction of abnormally contracting segments (from 20 +/- 18 to 26 +/- 19%; p less than 0.02). Corwin also induced significant decreases in mean systolic (-8%; p less than 0.05) and mean diastolic (-38%; p less than 0.001) wall stress and accelerated the relaxation rate. In a second group of 11 patients, a metabolic study indicated that neither myocardial oxygen consumption (15 +/- 7 versus 15 +/- 7 ml/min; difference not significant) nor lactate extraction was modified by the drug. In this group, increases in peak (+)dP/dt, acceleration in ventricular relaxation (-8 ms in time constant of isovolumic pressure decrease; p less than 0.01), and decreases in left ventricular end-diastolic pressure also were noted after administration of corwin, both under basal conditions and during a cold pressor test. In conclusion, corwin is a positive inotrope which, in patients with CAD and left ventricular dysfunction, improves left ventricular systolic and diastolic function without inducing myocardial ischemia.

Adrenergic beta-Agonists↗
PubMed1983

Changes in plasma renin activity and haemodynamics during vasodilator therapy in conscious dogs with myocardial infarction or chronic volume overload.

The aim of the study was to compare the changes in plasma renin activity induced by a vasodilator in normal dogs and in dogs with an impaired cardiac reserve. In normal conscious dogs, a 60-min nitroprusside infusion increased plasma renin activity from 1.05 +/- 0.26 to 8.35 +/- 1.20 ng, angiotensin I ml-1 h-1 (P less than 0.002) and heart rate from 83 +/- 6 to 149 +/- 15 beats/min (P less than 0.002). In five dogs in which a aortocaval fistula had been created 4 weeks earlier, the same infusion still increased plasma renin activity but significantly less than in normal dogs (0.90 +/- 0.29 to 4.44 +/- 0.64 ng ml-1 h-1; P less than 0.01) and the heart rate was unchanged (134 +/- 4 to 139 +/- 7 beats/min; NS). Similarly, in five dogs with a previous myocardial infarction, the heart rats response to nitroprusside was blunted (108 to 107 beats/min;NS) and plasma renin activity increased less than in normal dogs. Plasma renin activity also increased acutely after hydralazine administration in dogs which myocardial infarction (1.05 +/- 0.26 to 8.99 +/- 0.79 ng ml-1 h-1; P less than 0.05); after 1 week of hydralazine, plasma volume had increased from 54.9 +/- 0.9 ml kg-1 to 74.5 +/- 4.9 ml kg-1 (P less than 0.05) and plasma renin activity remained higher than control (4.66 +/- 0.66 ng ml-1 h-1; P less than 0.01). In conclusion, vasodilator therapy rapidly activates vasoconstrictor forces and fluid retention even in dogs with limited cardiac reserve. Although the regulation of plasma renin secretion appears altered in these models of heart disease, the renin response remains sufficient to seriously limit the beneficial effects of vasodilator therapy.

Animals↗
PubMed1983

Effects of chronic volume overload on left ventricular response to tachycardia.

The aim of the study was to determine the effects of chronic volume overload on the inotropic response of the left ventricle to a change in frequency of stimulation. Ten normal dogs (normal) and eight dogs with a chronic left ventricular (LV) volume overload (aortocaval fistula) were studied by cardiac catheterization after sedation with morphine (1 mg/kg). In normal dogs, increasing heart rate from 122 to 172 beats/min produced insignificant changes in peak +dP/dt (+2%; NS) or (dP/dt)/DP40 (+6%; NS). In volume overload, these indexes increased by 16% (P less than 0.01) and 31% (P less than 0.01), respectively, when heart rate increased from 135 to 173 beats/min. Conversely, the poststimulation potentiation appeared greater in normal than in volume overload; (dP/dt)/DP40 increased by 40% in normal vs. 1% in volume overload (P less than 0.01). These differences between normal and volume overload persisted after propranolol (1 mg/kg) and atropine (0.25 mg) administration. In both groups, AR-L115 BS, a nonsympathomimetic positive inotrope with caffeinelike properties, reduced the inotropic response to tachycardia, thereby normalizing the peak +dP/dt changes in volume overload. We conclude that the positive inotropic effects of tachycardia are enhanced in LV volume overload. Changes in LV compliance or alterations in the cellular mechanisms responsible for the force-frequency phenomenon might explain these findings.

Animals↗
PubMed1982

Changes in control of renin release in congestive heart failure in dogs: response to acute and chronic vasodilator therapy.

Neural control of renin secretion is an important physiologic mechanism, but alterations in the central nervous system feedback and control of renin release in heart failure have not been investigated. Accordingly we studied conscious dogs after volume overload (arteriovenous fistula) or chronic myocardial infarction. Acute infusion of nitroprusside was used to test the renin response to arterial hypotension and decreased central blood volume. Hydralazine and prazosin administration were used to test the response to chronic vasodilator administration. After 4 weeks of volume overload or 3 weeks after myocardial infarction, the renin response to a graded hypotensive stimulus was blunted. After 7 days of hydralazine or prazosin administration, plasma renin activity remained elevated and blood volume increased from baseline values. Our results indicate a decrease in the neural feedback control of renin release after chronic volume overload or myocardial infarction. However, chronic vasodilator administration still resulted in sustained augmented renin secretion and an increase in blood volume.

Animals↗
PubMed1981

Relationship between changes in left ventricular inotropic state and relaxation in normal subjects and in patients with coronary artery disease.

The aim of the study was to examine the changes in left ventricular (LV) relaxation rate induced by variations in inotropic state. Eight normal subjects and 29 patients with coronary artery disease (CAD) were studied. First, we used interventions that increase myocardial calcium influx (atrial pacing or postpacing beat) or decrease it (intracoronary injection of nifedipine). Relaxation rate was estimated from the time constant (T1) of isovolumic LV pressure fall during the fist 40 msec after peak negative dP/dt. Under basal conditions, T1 was impaired in CAD patients (58 vs 43 msec; p less than 0.01), despite similar heart rate, LV pressures and peak positive dP/dt (1620 vs 1787 mm Hg/sec; NS). During atrial pacing at 135 +/- 7 beats/min, peak positive dP/dt increased to 2220 mm Hg/sec in 11 CAD patients and to 2256 mm Hg/sec in eight normal subjects. T1 decreased more in CAD patients than in normal subjects (17 vs 7 msec; p less than 0.01). T1 changes also differed in the postpacing beat between CAD patients and normal subjects (-6 vs 5 msec; p less than 0.01) or when nifedipine was injected during the pacing (4 vs 20 msec; p less than 0.01). Intravenous calcium injection during atrial pacing in another group of 18 CAD patients further improved peak positive dP/dt and T1 (-3 msec; p less than 0.05) and normalized the changes in relaxation during the postpacing heart. Our data indicate that a variable coupling between LV inotropic state and relaxation rate exists in man during changes in calcium influx and that this coupling is abnormal in CAD patients.

Adolescent↗
PubMed1981

[Kussmaul's paradoxical pulse. Etiopathogenic aspects].

Paradoxical pulse (reduction in systolic blood pressure during inspiration) is a sign common to many pathological conditions affecting the heart and lungs. The aim of this paper was to determine its mechanism on the basis of recent publications in the literature, supported by personal clinical cases. Three cases of pulmonary embolism with paradoxical pulses of over 30 mm Hg are reported. In all three cases, cardiac and pulmonary function were normal before the embolism. The significant findings were a marked elevation in inspiratory transmural RA pressure (average 10 mm Hg), contrasting in one case with normal LV inspiratory transmural pressures. Two factors seem to play a role in the genesis of a paradoxical pulse: firstly, increased left ventricular afterload due to negative intrathoracic pressure during inspiration, and, secondly, a reduction of left ventricular compliance during inspiration related to mechanical interference between the two ventricles. In the absence of increased central venous pressure, increased left ventricular afterload probably plays the major role in the inspiratory reduction of peak systolic pressure (e.g. "physiological" paradoxical pulse, hypovolaemia, asthma). On the other hand, when central venous pressure is increased, the phenomenon of mechanical interference related to improved right ventricular filling during inspiration, added to increased left ventricular afterload, may result in very considerable paradoxical pulses (e.g. pulmonary embolism, cf. the cases reported: paradoxical pulses of over 30 mm Hg). Finally, certain pathological entities are associated with the greater role of mechanical interference (e.g. tamponade, constrictive pericarditis) for the principal causes, especially pulmonary embolism and pericardial effusion.

Aged↗
PubMed1980

Free-wall shortening and relaxation during ejection in the canine right ventricle.

Relations between shortening, velocity of shortening, and relaxation of inflow and outflow segments of the right ventricular (RV) free wall (FW) were examined during ejection in 12 open-chest dogs after pharmacologic blockade by recording RV pressures, RVFW dimensions (piezoelectric crystals), and pulmonary blood flow. At heart rates of 113 +/0 8 (SD) beats/min, investigated segments remained isometric or even lengthened before the end of ejection. Tension-length data in the outflow tract converged at the time of peak systolic tension toward a common linear relation (average slope 65 +/- 10 cmH2O/mm, average intercept 5.9 +/- 0.9 mm), but markedly deviated from this line at the end of ejection. Consistent relations between peak tension and mean velocity of shortening were only observed during the first part of ejection. In addition the rate of segmental isometric relaxation, estimated from RV pressure fall was load dependent (e.g., +60% increase in relaxation rate when RVFW end-diastolic segment length increased from 12.9 +/- 0.8 to 13.5 +/- 0.8 mm). We conclude that under normal conditions, the tension-velocity-length relations of the RVFW are comparable to those of the left ventricle during the first part of ejection only. We also conclude that RV relaxation is load dependent and that a significant part of RV ejection occurs during RVFW relaxation.

Animals↗