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Biomedical subjects

M F Rousseau

Publications and source records attributed to M F Rousseau.

At least 73 records · Page 4Linked to original sources
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

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

Prognostic value of symptom limited exercise testing in men with a high prevalence of coronary artery disease.

In order to evaluate the independent prognostic information provided by exercise testing in populations with a high prevalence of coronary artery disease, survival rates were calculated with the life table method in 372 men, mean age 48 years, referred for coronary arteriography. The prevalence of angiographic coronary artery disease was 82%. During a mean follow-up of 29 months (1 to 8 years), 32 patients died and 27 patients had a nonfatal event (acute infarction or hospitalization for disabling angina). Both the history (presence or absence of typical angina pectoris or of a previous myocardial infarction) and the exercise test results (abnormal if angina and/or ST segment changes greater or equal to 0.1 mV occurred) had a significant prognostic value for the 5 year survival rate (P less than 0.001). In patients with a positive history, the 5 year cumulative survival rate was 76% if the exercise test was abnormal versus 94% if it was normal (P less than 0.001). The following 8 noninvasive and 2 invasive variables were submitted to a Cox regression analysis: age, typical angina pectoris, previous myocardial infarction, maximal heart rate and workload, maximal ST segment depression and elevation, angina pectoris during exercise testing, number of diseased vessels, and wall motion score on contrast ventriculography. By univariate analysis, the age and the maximal workload reached during exercise were the only noninvasive predictive variables for survival or cardiac events (P less than 0.05). By multivariate analysis, and combining all noninvasive and invasive variables, survival was predicted by the wall motion score, the presence or absence of 3 vessel disease, and age.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Diagnostic value of computerized exercise testing in men without previous myocardial infarction. A multivariate, compartmental and probabilistic approach.

The value of exercise testing for the diagnosis of coronary artery disease is disputed but very few studies have taken advantage of all recent improvements, namely computer averaging of the ECG signals, multivariate analysis of the data, a compartmental diagnostic approach and probabilistic interpretation of the results. These methods were tested in a group of 387 men who had a computer-assisted multistage maximal exercise test; none had a history of myocardial infarction. In 284 symptomatic patients, the diagnosis was made by arteriography; 103 ostensibly healthy men were also included. The computer-averaged ECG signals (X, Y, Z) recorded at maximal exercise, maximal heart rate, blood pressure and workload, and the onset of angina pectoris during exercise were submitted to a multivariate stepwise discriminant analysis. The pretest likelihood for CAD was calculated from age and history; the post-test likelihood was calculated from Bayes' theorem and the average information content of several diagnostic methods was assessed in categorical and compartmental models. By multivariate analysis, 5 variables collected at maximal exercise were selected, namely the heart-rate, the ST60 segment level, the onset of angina during the test, the workload and the slope of the ST segment in lead X. The average information content of the analysis using 5 variables was 44% in a categorical model versus 55% in a compartmental model (P less than 0.001). For comparison, the information content of the analysis using the ST60 segment level alone was only 16% in the categorical model and 27% in the compartmental model. The clinical value of these diagnostic methods (categorical versus compartmental, univariate versus multivariate) was assessed by a probabilistic classification of the patients. The classification provided by the analysis of the ST60 segment changes was barely better than that one provided by the simple history. The probabilistic use of a multivariate and compartmental analysis of the data led to a significantly better and more accurate classification of the patients (83% of correct classification).

Adult↗
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

Antianginal effects of corwin, a new beta-adrenoceptor partial agonist.

The hemodynamic effects of corwin were evaluated in 9 patients with coronary artery disease and without clinical signs of heart failure at rest, during submaximal exercise and during exercise-induced angina pectoris before and after administration of corwin. Angina pectoris was always prevented after the drug was given and the exercise intensity was increased until recurrence of angina pectoris; hemodynamic data were also recorded at this higher exercise capacity (+16%: p less than 0.001). At rest, corwin increased heart rate (from 80 to 84 beats/min) and pressure-rate product. During submaximal exercise, heart rate decreased from 105 to 96 beats/min, and pressure-rate product and ST-segment depression also decreased after corwin. The prevention of angina pectoris in all patients was accompanied by a lower heart rate (from 132 to 117 beats/min), pressure-rate product and ST-segment depression. At rest and during exercise, the cardiac output was unchanged and the pulmonary capillary wedge pressure was slightly decreased after corwin (from 12.5 to 10 mm Hg; p less than 0.001). At the 16% greater exercise capacity after corwin, angina pectoris recurred at the same values of cardiac output, pulmonary wedge pressure and ST-segment depression; maximal heart rate decreased from 132 to 124 beats/min, and the pressure-rate product was lower. Thus, corwin is an active antianginal drug. Its effects are likely due to a decrease in pressure-rate product and myocardial oxygen requirements during exercise. In contrast to beta-antagonists devoid of partial agonist activity, corwin does not depress left ventricular function either at rest or during exercise.

Adrenergic beta-Agonists↗
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↗
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↗