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Biomedical subjects

M F Rousseau

Publications and source records attributed to M F Rousseau.

At least 91 records · Page 5Linked to original sources
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

Reassessment of the relation between QRS forces of the orthogonal electrocardiogram and left ventricular ejection fraction.

Previous studies have demonstrated the existence of a strong positive correlation between the amplitude of QRS forces of the orthogonal electrocardiogram and the angiographically determined left ventricular ejection fraction. In a large group of patients evaluated for chest pain, we examined the relationship between the arithmetic summation of RX + RY + QZ (sigma R), the maximal and mean spatial QRS vectors and the ejection fraction (EF). In a total of 252 patients, there was a statistically significant correlation between sigma R and EF but a low correlation coefficient value (r:0.22, P less than 0.001). This relationship was essentially due to the group of patients with coronary artery disease and myocardial infarction (r:0.24, P less than 0.015) whereas there was no correlation in the group of normal subjects or in patients with coronary artery disease without myocardial infarction. In the group with myocardial infarction, a significant correlation between sigma R and EF existed only in patients with anterior myocardial infarction (r:0.41, P less than 0.025). In conclusion, both ejection fraction and amplitude of QRS forces decrease in coronary artery disease especially when an anterior myocardial infarction is present. However, despite the positive association between these angiographic and electrocardiographic indices, the low value of the correlation coefficient indicates that it is not possible to predict ejection fraction from the value of sigma R in individual patients.

Cardiac Catheterization↗
PubMed1983

Bayesian analysis of stress thallium scintigraphy for the detection of multivessel coronary disease.

This study was performed in 224 men to determine the respective contribution of history and thallium-201 stress myocardial scintigraphic imaging in the non-invasive prediction of the severity of coronary disease. Myocardial scintigraphic imaging had the better diagnostic accuracy (80%) for the detection of multivessel disease but the results emphasize the importance of the history in predicting the extent of coronary artery disease. In patients with myocardial infarction, the diagnostic accuracy of the history (80%) was similar to the diagnostic accuracy of myocardial scintigraphic imaging (79%); in the subgroup of patients with residual angina pectoris after infarction, the accuracy of the history was even greater (87%) than that of myocardial scintigraphic imaging (78%). Thus, after myocardial infarction, scintigraphy was useful only in the small subgroup of patients without residual angina pectoris when it had a diagnostic accuracy of 79%, slightly but insignificantly superior to that of the history (62%). In patients without previous myocardial infarction, but with typical angina, myocardial scintigraphy was clearly superior to the simple history (diagnostic accuracy of 78% versus 53%; P less than 0.001). In patients without myocardial infarction and with atypical angina the prevalence of multivessel disease was low (17%) and the diagnostic accuracy of history (83%) was barely different from the diagnostic accuracy of myocardial scintigraphic imaging (90%). Thus, when the likelihood of multivessel disease is very high (angina pectoris post myocardial infarction), or very low (atypical angina), the contribution of exercise testing is very limited. Important additional information is provided by maximal exercise testing and myocardial scintigraphic imaging only in the groups with an intermediate prevalence of multivessel disease, namely in the asymptomatic patients after myocardial infarction and in the patients with typical angina but no previous myocardial infarction.

Angiography↗
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↗
PubMed1981

Hemodynamic effects of molsidomine at rest and during submaximal and maximal exercise in patients with coronary artery disease limited by exertional angina pectoris.

To analyze the mechanisms of action of molsidomine, a new antianginal drug, 10 patients with coronary artery disease and exertional angina pectoris were studied. Hemodynamic measurements were made at rest, during submaximal exercise and during angina-limited exercise before and 1 hour after intravenous administration of 2 mg of molsidomine. When angina pectoris was prevented after the drug was given (6 of 10 patients), the exercise intensity was increased until the recurrence of angina (3 patients) or until exhaustion (3 patients), and hemodynamic data were recorded at this higher exercise capacity. At rest and during submaximal exercise, molsidomine increased heart rate and decreased cardiac output and mean systemic and pulmonary arterial pressures. The prevention of angina pectoris was attended by lower mean systemic and pulmonary arterial pressures and pressure-rate product; cardiac output and heart rate were unchanged. The greater exercise capacity (+26 percent) after molsidomine was attended by increases in maximal cardiac output (+19 percent) and in arteriovenous oxygen difference (+6 percent); the maximal pressure-rate product was unchanged and systemic vascular resistance was lower. The mechanisms of action of molsidomine are very similar to those of nitrates and imply a decrease in venous and arterial tone. Molsidomine deserves further study in patients with angina or congestive heart failure.

Adult↗
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↗
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↗