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Biomedical subjects

H Pouleur

Publications and source records attributed to H Pouleur.

At least 91 records · Page 5Linked to original sources
PubMed1987

Myocardial protection by intracoronary nicardipine administration during percutaneous transluminal coronary angioplasty.

To determine if the calcium antagonist nicardipine protects the myocardium against ischemia, myocardial lactate, hypoxanthine and prostanoid function was studied in 12 patients during percutaneous transluminal coronary angioplasty (PTCA). Values were obtained before balloon inflation and during 4 minutes after deflation. Intracoronary injection of 0.2 mg of nicardipine distal to the stenosis was done randomly before the first or second inflation; the other inflation served as a control. One minute after deflation, coronary sinus flow levels were similar during the nicardipine and control procedure (161 +/- 61 vs 159 +/- 72 ml/min); lactate (-9 +/- 21% vs -17 +/- 21%, p less than 0.025) and hypoxanthine production (-107 +/- 85% vs -218 +/- 153%, p less than 0.05) were less severe after nicardipine pretreatment than after control. All patients reverted to lactate extraction 4 minutes after inflation plus nicardipine infusion, whereas lactate was still produced 4 minutes after control inflation. No significant changes in thromboxane B2 or prostacyclin levels were observed in the coronary sinus 1 minute after inflation, but higher arterial thromboxane B2 values were observed after control inflation than after inflation with nicardipine infusion (median values 169 vs 78 pg/ml, p less than 0.05). In conclusion, intracoronary infusion of nicardipine reduced signs of ischemia and alterations in prostanoid handling after coronary occlusion. The mechanisms of myocardial protection appeared unrelated to coronary sinus blood flow changes or to a systemic effect of nicardipine.

Angina Pectoris↗
PubMed1987

Ejection fraction response to upright exercise in hypertension: relation to loading conditions and to contractility.

The respective roles of peripheral and myocardial determinants of exercise ventricular performance were studied in 10 normal volunteers and in 9 mildly hypertensive patients without evidence of coronary disease. Hemodynamic measurements and equilibrium blood pool scintigraphy were simultaneously performed at rest and during maximal upright exercise. In hypertensive patients, mean systolic and diastolic blood pressure were, respectively, 199 +/- 23 and 102 +/- 12 mm Hg at rest, and 271 +/- 28 and 113 +/- 8 mm Hg at peak exercise. Ejection fraction response to exercise was normal (increase by more than 5%) in 4 hypertensive patients (normal hypertensive group: 63 +/- 4 to 77 +/- 6%) and in volunteers (65 +/- 3 to 78 +/- 4%) and abnormal in 5 hypertensive patients (abnormal hypertensive group: 66 +/- 6 to 58 +/- 10% at peak exercise). The abnormal response in the abnormal hypertensive group was not due to an inadequate decrease in systemic vascular resistance during exercise. By contrast, the ratio systolic blood pressure/end-systolic volume, an index of contractility, decreased by 2.3 +/- 4.9 in the abnormal hypertensive group, whereas it increased by 9.8 +/- 9.1 in the normal hypertensive group and by 7.3 +/- 2 in volunteers. Thus, abnormal exercise ejection fraction response in mild hypertension was not related to increased afterload but rather to intrinsic myocardial factors.

Adult↗
PubMed1987

Left ventricular sensitivity to beta-adrenoceptor-stimulating drugs in patients with ischemic heart disease and varying degrees of ventricular dysfunction.

The left ventricular sensitivity to sympathomimetic amines was assessed in 47 patients with ischemic heart disease and varying degrees of left ventricular dysfunction. Patients were divided into 3 subgroups according to their basal ejection fraction (less than or equal to 35%, between 36 and 54%, and greater than or equal to 55%). After injection of a bolus of isoproterenol (2 micrograms), the isovolumic indexes of inotropic state increased significantly less in patients with an ejection fraction less than or equal to 35% than in other patients, but the heart rate changes and the acceleration in the rate of isovolumic pressure fall were comparable in all subgroups. The dose-response curves to cumulative doses of xamoterol, a beta 1-adrenoceptor partial agonist, confirmed that the magnitude of the inotropic response was reduced during beta 1-stimulation in patients with an ejection fraction less than or equal to 35% when compared with patients with a greater ejection fraction. However, the dose of xamoterol necessary to produce 50% of the maximal inotropic response was not increased in patients with an ejection fraction less than or equal to 35% (range, 1.5-5.2 micrograms/kg; median 2.5 vs. median values of 2.3 and 3.3 micrograms/kg in the other subgroups; NS), and there was no shift to the right of the dose-response curve. It is concluded that in moderate ischemic heart failure, the magnitude of the inotropic response to isoproterenol or xamoterol is reduced. The absence of shift to the right of the dose-response curve to a beta 1-partial agonist suggests that this alteration in myocardial performance is not primarily caused by a decrease in beta-adrenoceptor responsiveness.

Aged↗
PubMed1986

Alterations in myocardial metabolism and function at rest in stable angina pectoris: relations with the amount of exercise-induced thallium-201 perfusion defect.

The relation between the amount of exercise-induced ischemia and alterations in left ventricular (LV) function and metabolism at rest was studied in 18 coronary patients with stable angina pectoris. An ischemic defect area score was computed from quantitative exercise thallium-201 (Tl-201) scintigraphy; this estimation of the amount of ischemic myocardium was used to classify the patients in group I (n = 8; score less than 15%, mean 6.7 +/- 2.5%) and II (n = 10; score greater than 15%; mean 27.2 +/- 8.9%). Hemodynamics and metabolism were studied in basal state. No patient had anginal pain during the study, and the extent of angiographic coronary artery disease (CAD) was comparable in the two groups. Heart rate, aortic pressure, coronary blood flow, and myocardial oxygen uptake were also similar in both groups. However, ejection fraction was reduced in group II (51 +/- 13 vs 63 +/- 5%; p less than 0.01) and LV relaxation was impaired as shown by the increase in time-constant of isovolumic pressure fall (55 +/- 16 vs 44 +/- 6 ms in group I; p less than 0.05); the LV end-diastolic pressure was also increased in group II (19 +/- 8 vs 10 +/- 4 mmHg in group l; p less than 0.05). Furthermore, in group II, myocardial lactate uptake was reduced (4 +/- 19 vs 30 +/- 29 mumole/min in group I; p less than 0.01) and the productions of alanine and glutamine were augmented (-7.5 +/- 4.4 vs -4.6 +/- 1.6 mumole/min in group I; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Impaired regional diastolic distensibility in coronary artery disease: relations with dynamic left ventricular compliance.

The regional left ventricular distensibility and its relations with the dynamic left ventricular chamber compliance were studied in 11 normal subjects and in 30 patients with coronary artery disease. The regional peak filling rates were calculated from angiographic data in eight ventricular segments and used as an index of regional distensibility. A depressed global peak filling rate was observed in only 30% of the patients with angina pectoris, but regional abnormalities in peak filling rate were detected in 75% of these patients. A relation between alterations in regional peak filling rate and left ventricular compliance was evident in these patients. Despite comparable end diastolic volume and pressure (10 +/- 2 mm Hg vs. 10 +/- 3 in normal subjects; not significant), the patients with angina pectoris, whose ventricle had at least three segments with a reduced peak filling rate, had indeed significant increases in mean left ventricular filling pressure (14 +/- 4 mm Hg vs. 8 +/- 3 in normal subjects; p less than 0.01) and upward shifts of their left ventricular pressure-volume relation during rapid filling. Conversely, an increase in regional peak filling rate produced by intravenous administration of the calcium antagonist nicardipine in a subgroup of patients with poor diastolic function was accompanied by a reduction in mean left ventricular filling pressure and by a downward shift of the early diastolic left ventricular pressure-volume relation. It is concluded that even in the absence of clinical signs of ischemia and of a previous myocardial infarction, large areas with impaired distensibility are frequently present in patients with angina pectoris.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Effects of atriopeptin III on renal function, regional blood flows and left ventricular function in conscious dogs in presence or absence of hypovolaemia.

The effects of atriopeptin III (AP III) on the left ventricular and renal functions were studied in thirteen chronically instrumented conscious dogs and compared to those of the solvent (saline). In the normovolaemic state, an AP III infusion (1 microgram kg-1 min-1 i.v.) had no effects on heart rate, on mean arterial or left ventricular pressure, on (dP/dt) Max (2989 +/- 119 vs. 3007 +/- 155 mmHg s-1; NS) or on the relaxation rate. The left ventricular endocardial and epicardial coronary blood flows (radioactive microspheres) and the renal flow in the outer cortex (707-683 ml (min-1 100 g-1); NS) or in the inner cortex (563-570; NS) were also insignificantly affected by AP III infusion. However, AP III increased urinary flow from 24 +/- 6 to 36 +/- 7 ml h-1 (P less than 0.025) and the Na+ and Cl- excretions by 92 and 98%, respectively, (P less than 0.025 and P less than 0.01 vs. saline group) without altering significantly K+, urea and creatinine eliminations. In the moderately hypovolaemic state (mean reduction in renal flow: outer cortex - 15%; P less than 0.05, inner cortex - 5%; NS), AP III infusion at two doses (1 and 3 micrograms kg-1 min-1) still had no effects on arterial pressure and on the indexes of left ventricular inotropic state and relaxation but in this setting, the diuretic effect of AP III became variable. Five dogs markedly increased their excretion of water, Na+ and Cl- whereas no change was noted in the seven remaining dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Changes in myocardial metabolism during therapy in patients with chronic stable angina: a comparison of long-term dosing with propranolol and nicardipine.

The long-term effects of antianginal therapy on coronary blood flow and myocardial metabolism were studied in 35 patients with chronic stable angina. Arterial and coronary sinus blood samples and coronary blood flow measurements were obtained before and after 1 month of oral administration of propranolol or of the calcium antagonist nicardipine. When the data obtained at a fixed heart rate (10% to 15% above the pretreatment sinus rhythm) were compared, no significant differences were evidenced between the propranolol and the nicardipine groups. Coronary blood flow and myocardial oxygen uptake were unchanged with both drugs. Myocardial lactate uptake increased in 11 patients of the propranolol group (from -2 +/- 42 to 66 +/- 47 mumol/min, p less than .001) and in 11 patients of the nicardipine group (from 0 +/- 36 to 31 +/- 29 mumol/min, p less than .001). In these 22 patients, the increase in lactate uptake was accompanied by reductions in uptake of free fatty acids and by a decrease in the coronary sinus concentration of thromboxane B2 from 131 +/- 87 to 61 +/- 32 pg/ml (p less than .01), whereas the transcardiac release of prostacyclin increased. None of these changes in free fatty acids or in prostanoid handling were observed in the nine patients (five in the propranolol and four in the nicardipine group) in whom lactate uptake was not augmented. During pacing-induced tachycardia, the metabolic effects of the two drugs appeared different. Myocardial lactate uptake decreased more in the patients receiving propranolol than in those receiving nicardipine and the combined productions of alanine and glutamine rose by 3.2 +/- 5.8 mumol/min in the propranolol group while it decreased by 3.1 +/- 8.2 mumol/min in the nicardipine group (p less than .025 propranolol vs nicardipine). In conclusion, long-term antianginal therapy with propranolol or nicardipine improved several markers of myocardial ischemia in approximately two-thirds of the patients. Although the changes observed at low heart rates were similar with the two drugs, the data also suggest that better metabolic protection is provided by the calcium antagonist during pacing-induced tachycardia.

Adult↗
PubMed1985

[Limitations of the clinical assessment of myocardial contractility].

The mechanical performance of the myocardium depends upon factors intrinsic to the myofibrils ("contractility") and upon the physicochemical conditions surrounding the cells ("inotropic state"). A precise description of cardiac muscle performance requires a knowledge of 4 variables: length, force, velocity and time. In vivo the problem is further complicated by the presence in the ventricle of spatio-temporal nonuniformities (activation sequence, fiber orientation) and by the fact that major determinants of the inotropic state, such as sympathetic tone, are hard to verify. The indices expected to reflect the tension-velocity-length relation of the myofibrils, either during isovolumic contraction (peak(+)dP/dt) or during ejection (end-systolic relations between pressure or stress and volume, relations between ejection fraction and stress) can generally detect acute changes in inotropic state. Up to now, however, none of these indices has been shown to be very sensitive in detecting basal alterations in contractility. Considering the practical and theoretical limitations on study of an intact ventricle, it would appear indispensable, if we want greater precision in detecting functional alterations of the myocardium, to supplement study of ventricular mechanics by biochemical and morphological analysis of the myocardium.

Animals↗
PubMed1985

Effects of nicardipine on coronary blood flow, left ventricular inotropic state and myocardial metabolism in patients with angina pectoris.

The effects of intravenous nicardipine (2.5 mg) on the left ventricular (LV) inotropic state, LV metabolism, and coronary haemodynamics were analysed in 22 patients with angina pectoris. Measurements were made at fixed heart rate (atrial pacing), under basal state, and during a cold pressor test. After nicardipine, coronary blood flow and oxygen content in the coronary sinus increased significantly. The indices of inotropic state increased slightly, and the rate of isovolumic LV pressure fall improved. Myocardial oxygen consumption was unchanged despite the significant reduction in pressure-rate product, but LV lactate uptake increased, particularly during the cold pressor test. When nicardipine was administered after propranolol, the indices of inotropic state were unaffected. The lack of direct effect of nicardipine on LV inotropic state was further confirmed by intracoronary injection of 0.1 and 0.2 mg in a separate group of 10 patients. It is concluded that the nicardipine-induced coronary dilatation seems to improve perfusion and aerobic metabolism in areas with chronic ischaemia, resulting in reduced lactate production and augmented oxygen consumption.

Adrenergic beta-Antagonists↗
PubMed1985

[Role of adrenergic beta receptor partial agonists in left ventricular failure of ischemic origin. Value of xamoterol (ICI 118,587, Corwin)].

The ideal sympathomimetic derivative should possess the positive inotropic and relaxing effects of catecholamines whilst remaining free of their side-effects. Theoretically, such properties could be present in beta 1-adrenoceptor partial agonists. Xamoterol (ICI 118,587, Corwin; ISA 43 p. 100) seems to be the most promising beta 1 partial agonist. The aim of the study was to determine if the beneficial effects of Xamoterol were maintained during long term administration. Xamoterol (200 mg twice dialy) was administered to 14 patients with anterior myocardial infarction and moderate heart failure (class II-III NYHA). After 3 months' therapy, left ventricular function improved as indicated by reduction in left ventricular (LV) end-diastolic pressure (23 +/- 5 to 16 +/- 5 mm Hg; P less than 0.0005), LV end-diastolic volume (153 to 140 ml/m2; P less than 0.05) and in LV end-systolic volume especially in 11 patients with a control end-systolic volume less than 100 ml/m2 (- 15 p. 100; P less than 0.05). LV inotropic state was also enhanced as indicated by 21 p. 100 increases in EMax, the maximal LV pressure/volume ratio (P less than 0.02) and 20 p. 100 increases in the ratio end-systolic stress/ end-systolic volume (P less than 0.02). Myocardial oxygen consumption was unchanged, global lactate extraction fraction increased from 20 +/- 18 to 33 +/- 14 p. 100 (P less than 0.05) and LV alanine release was reduced (-1.7 to -0.2 muMol/min; P less than 0.05). The rate of LV pressure fall accelerated from 57 to 52 ms (P less than 0.05) and the mean diastolic wall stress was reduced by 35 p. 100 (P less than 0.05), reflecting the improvement in LV relaxation and diastolic function. Thus, the beneficial effects of Xamoterol were maintained after prolonged therapy particularly in patients with class II-III heart failure; patients in class IV benefited less from this therapy. No tachyphylaxis or side-effects were observed.

Administration, Oral↗
PubMed1984

Effects of nicardipine and nisoldipine on myocardial metabolism, coronary blood flow and oxygen supply in angina pectoris.

The effects of the calcium antagonists nicardipine and nisoldipine on left ventricular (LV) metabolism were analyzed in 32 patients with angina pectoris. Measurements were made at a fixed heart rate under the basal state and during a cold pressor test (CPT). After administration of the drugs, coronary blood flow increased significantly and the mean aortic pressure decreased by 10% (p less than 0.01) in the basal state and by 11% (p less than 0.01) during CPT. Despite the reduction in pressure-rate product, myocardial oxygen consumption was unchanged in the basal state (18 +/- 4 vs 19 +/- 4 ml/min, difference not significant) and during CPT (21 +/- 5 vs 21 +/- 5 ml/min, difference not significant); this discrepancy between a reduced pressure-rate product and an unchanged oxygen consumption was also noted when nicardipine was given after propranolol (0.1 mg/kg; 12 patients). Both agents also increased LV lactate uptake, particularly during CPT (+13 mumol/min, p less than 0.05 vs control CPT) and reduced LV glutamine production. In 10 patients in whom 14C-lactate was infused, the chemical LV lactate extraction ratio increased more than the 14C-lactate extraction ratio after administration of the drugs, indicating a reduction in LV lactate production. The data are consistent with the hypothesis that nicardipine and nisoldipine improve perfusion and aerobic metabolism in chronically ischemic areas, resulting in an augmented oxygen consumption and in a reduced lactate production.

Aged↗
PubMed1984

Early changes in sodium and water balances in patients with acute myocardial infarction: relationship to haemodynamics and creatine kinase.

The changes in sodium and water balances during the first 4 days after an uncomplicated transmural myocardial infarction (MI) were determined in forty patients. The sodium balance was positive 4 days after MI in 80% of the patients but negative in 20%. Neither in anterior (n = 23) nor in inferior (n = 17) MI were rank correlations found between the haemodynamic parameters (cardiac index, mean arterial pressure, mean right atrial or pulmonary capillary pressures, right or left ventricular work indices) and sodium balance. However, the sodium balances correlated with the total creatine kinase (CK) release in anterior MI after 1 day (r = 0.60; P less than 0.002) and after 4 days (r = 0.65; P less than 0.001) but not in inferior MI. Furthermore, in anterior and inferior MI matched for their CK release, the sodium handling was different both after 1 day (-70 in anterior v. +44 mmol (24 h)-1 in inferior MI; P less than 0.001) and after 4 days (-36 v. +147 mmol (72 h)-1; P less than 0.01), a difference unexplained by differences in medical management or in sodium intake. Finally, sodium balance correlated with the changes in left ventricular stroke work index (LVSWI) observed during this period (r = 0.48, P less than 0.001), LVSWI being more stable when sodium balance was more positive. In conclusion, sodium balance after uncomplicated acute MI is related to MI location, to the size of anterior MI, and cannot be predicted from initial haemodynamics. Finally, the relation between LVSWI stability and positive sodium balance suggests that arbitrary sodium restrictions or diuretics might be deleterious to the haemodynamics after uncomplicated myocardial infarction.

Adult↗
PubMed1984

Assessment of regional left ventricular relaxation in patients with coronary artery disease: importance of geometric factors and changes in wall thickness.

To assess local myocardial relaxation abnormalities in patients with coronary artery disease, local myocardial left ventricular wall stress was computed in nine normal subjects and in 22 patients with coronary artery disease. In normal left ventricles, the rate of decrease in isovolumic local stress was not significantly different from the rate of decrease in isovolumic pressure, and the residual wall stress at the end of isovolumic relaxation was uniformly low. In patients with coronary artery disease, the residual wall stress was increased both in infarcted areas and in non-infarcted areas perfused by stenosed arteries (43 +/- 31 and 30 +/- 19 kdyne/cm2, respectively, vs 9 +/- 5 kdyne/cm2 in normal areas; p less than .001). The rate of decrease in local stress in infarcted areas paralleled the rate of decrease in pressure (48 vs 49 msec; NS), but in ischemic areas the rate of decrease in stress was significantly slower than the rate of decrease in pressure (69 +/- 35 vs 48 +/- 15 msec; p less than .05). It is concluded that in patients with coronary artery disease, indexes based only on the analysis of decreases in isovolumic pressure underestimate the severity of local impairments in relaxation rate and cannot be used to predict the level of residual diastolic wall stress.

Adult↗
PubMed1984

[Effects of a partial agonist of beta 1 adrenergic receptors (ICI 118,587) on left ventricular performance and metabolism in coronary disease].

ICI 118/587 is a partial agonist of beta 1 adrenergic receptors, a partial agonist being an agent which has both agonist and antagonist properties. The agonist properties of ICI 118/587 stabilise 43 p. 100 of the maximal activity of the beta 1 receptors whilst preventing a resulting increase in sympathetic stimulation. The aim of this study was to evaluate the effects of this new inotropic agent on left ventricular function and metabolism in patients with chronic myocardial infarction and left ventricular dysfunction. The study of LV function was performed in an initial group of 14 patients. After control left ventriculography, the injection of 0,1 mg/kg of ICI 118/587 increased the peak dP/dt by 35 p. 100 (p less than 0,005), reduced mean systolic parietal stress by 8 p. 100 (p less than 0,05) and LV end systolic volume from 58 to 53 ml/m2 (p less than 0,05). The global ejection fraction rose slightly, largely due to increases in the regional ejection fractions of abnormal segments (from 20 +/- 5 p. 100 to 26 +/- 5 p. 100, p less than 0,02). Left ventricular diastolic function also improved as shown by a 38 p. 100 fall (p less than 0,001) in mean diastolic stress and an increase in the time constant of isovolumic relaxation. The metabolic effects of ICI 118/587 were assessed in a second group of 11 patients with anterior myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1984

Effects of nicardipine or nifedipine added to propranolol in patients with coronary artery disease.

To assess the added effects of nicardipine and beta-blockers on the left ventricular (LV) function, 2.5 mg of i.v. nicardipine was given to 9 patients with coronary artery disease, pretreated with propranolol (0.1 mg/kg, i.v.). The changes in LV function observed after nicardipine were compared with those induced by nifedipine (20-30 mg sublingually), in 8 comparable patients also pretreated with propranolol. Nicardipine normalized the cardiac output and the rate of LV relaxation, both depressed by propranolol, without changes in LV filling pressure. After nicardipine, end-systolic volume (52 to 42 ml/m2; P less than 0.01) and ejection fraction (59 +/- 8 to 66 +/- 9%; P less than 0.01) improved; the mean systolic and diastolic wall stresses decreased respectively by 19% (P less than 0.01) and 21% (P less than 0.01) whereas the maximal LV pressure/volume ratio (Emax), an index of LV inotropic state, was unchanged (+4%; NS). Further, although nicardipine and nifedipine produced identical changes in LV systolic pressure (-25 vs -26 mmHg; NS nicardipine vs nifedipine) and in heart rate, the changes in end-systolic volume (-9 +/- 4 vs -3 +/- 9 ml/m2; P less than 0.005), in Emax (+0.14 +/- 0.31 vs -0.20 +/- 0.22 mmHg/ml/m2; P less than 0.025) and in ejection fraction (+7 +/- 4 vs +2 +/- 4%; P less than 0.025) were significantly greater after nicardipine than after nifedipine. In conclusion, nicardipine administered after propranolol improves LV pump function and has no negative inotropic effects as indicated by the lack of dP/dt Max and Emax changes. These additive effects of nicardipine after propranolol were greater than those of nifedipine administered at an equipotent vasodilator dosage.

Adult↗