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Biomedical subjects

L A Brasseur

Publications and source records attributed to L A Brasseur.

36 records · Page 2Linked to original sources
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↗
PubMed1978

Vectorcardiographic diagnosis of right ventricular hypertrophy in the presence of right bundle branch block in young subjects.

Two groups of young patients, one with right bundle branch block complicated by right ventricular hypertrophy due to congenital heart disease, the other with right bundle branch block and no right ventricular hypertrophy, could be separated on the basis of a few quantitative vectorcardiographic and electrocardiographic criteria. Vectorcardiographic criteria proved better than electrocardiographic criteria in detecting right ventricular hypertropy in individual patients with complete right bundle branch block. Criteria based on the configuration of the QRS loop were also specific but much less sensitive for the diagnosis of this association. In a similar population, that is, young patients with postoperative right bundle branch block, the existence of a residual right ventricular overload would be strongly suggested by the presence of any one of the following criteria: (1) a clockwise rotation of the QRS loop in the horizontal plane, (2) a ratio of the magnitude of the R wave to that of the S wave (R/S ratio) in lead X at less than 2.0, (3) a mean QRS vector in lead X more negative than--10 mv.msec, or (4) a maximal QRS vector located between 90 degrees and 270 degrees in the horizontal plane. In contrast, an R/S ratio in lead X that was equal or superior to 2.0 or an azimuth angle of the mean spatial QRS vector that was not between 90 degrees and 180 degrees would indicate that the right ventricular conduction defect is probably uncomplicated.

Adolescent↗
PubMed1978

Haemodynamics during maximal exercise after coronary bypass surgery.

Fifty patients underwent an objective measurement of physical working capacity by means of a multistage test of maximally tolerated exertion before and after coronary bypass surgery; 29 patients also had haemodynamic measurements during maximal exercise before and after coronary bypass surgery. The patients were divided into 3 groups according to the degree of revascularisation: adequate (n = 20), partial (n = 17), or none (n = 13). Adequate revascularisation induces a large increase in physical working capacity because of an increased maximal heart rate and maximal cardiac output; stroke volume during maximal exercise and ejection fraction at rest were not modified, suggesting no major changes in left ventricular function. After unsuccessful coronary bypass surgery, the physical working capacity was unchanged despite an increased maximal heart rate; maximal cardiac output was unchanged and stroke volume during maximal exercise was significantly lower. These undesirable results are often associated with perioperative myocardial infarction and are attended by a decreased ejection fraction at rest; these data suggest an impaired left ventricular function after unsuccessful coronary bypass surgery. The results of partial revascularisation are intermediate but appear to be determined by the incidence of partial graft failure which is also often associated with perioperative myocardial infarction. From individual changes in data collected during maximal exercise testing, it is often impossible to predict the degree of revascularisation.

Adult↗
PubMed1976

Hemodynamic effects of lidoflazine during graded levels of bicycle exercise in normal subjects.

The hemodynamic effects of lidoflazine were studied in 12 young healthy subjects who received the drug orally (240 mg daily) for 8 weeks. During exercise after lidoflazine, heart rate (-2.6%), mean arterial pressure (-3.1%), arterio-venous oxygen (A-V02) difference (-3.4%), pressure rate product (-6.2%), and systemic vascular resistance (-8.6%) were significantly lower, while cardiac output (+5.4%) and stroke volume (+8.3%) were significantly greater. The maximal heart rate was lower after lidoflazine (-6 beats/min) but the maximal oxygen intake (VO2max) was not affected by the drug. The major hemodynamic effects of lidoflazine appear to be, on the one hand, an unexplained decrease in heart rate, and on the other, a decrease in systemic vascular resistance; the latter, which was expected from a vasodilator, could account for the greater stroke volume and contributes to the decrease of the pressure rate product. Lidoflazine has another unexplained effect, i.e. a decrease of the A-VO2 difference, suggesting a decreased peripheral extraction of oxygen at rest as well as during submaximal and maximal exercise.

Adult↗
PubMed1975

Maximal exercise testing in patients with spontaneous angina pectoris associated with transiet ST segment elevation. Risks and electrocardiographic findings.

Six patients with spontaneous angina associated with transient ST segment elevation had a multistate maximal exercise (bicycle) test. In 5 patients, typical electrocardiographic changes were recorded during exercise, namely ST segment elevation often accompanied by an increase in the voltage of the R wave and a widening of the QRS complex. Four of these patients developed severe rhythm disturbances: ventricular tachycardia (2 cases) and ventricular flutter (1 case) were the reason for early interruption of the test in 3 patients, while 1 patient had a short run of ventricular tachycardia after exercise. These rhythm disturbances which spontaneously regressed in all cases were consistently preceded by obvious ST elevation and in 2 patients were attended by slight chest discomfort. Maximal exercise testing of patients suspected of variant angina provides important diagnostic information in many patients, but the risks of potentially lethal arrhythmias should be considered and resuscitation facilities should always be immediately available.

Adult↗
PubMed1975

Early hemodynamic adaptations to physical training in patients with healed myocardial infarction.

Seven patients with coronary heart disease (CHD) but no angina pectoris had hemodynamic studies at rest and during submaximal and maximal exercise levels 2 mth after an acute uncomplicated myocardial infarction. The hemodynamic study was repeated after 3 mth of regular physical training. Maximal oxygen intake (VO2max) increased by 16.1% after physical training while maximal heart rate unsignificantly decreased (minus 3.3%). Higher VO2max after training resulted from an increase in maximal cardiac output (+7%) and stroke volume (+9.2%) and from a widening of the maximal arterio-venous oxygen (A-VO2) difference (+7.3%). The fall in stroke volume observed from submaximal to maximal exercise level was not affected by training. During submaximal exercise, the lower heart rate after training was attended by both a greater stroke volume and a wider A-VO2 difference; the cardiac output slightly decreased. We conclude that the increase in VO2max observed with early physical training in CHD results on one hand from an increased stroke volume whose specificity is not established, and on the other hand from a wider maximal A-VO2 difference; the latter is entirely due to a greater extraction of oxygen from the blood by the working muscles during maximal exercise.

Adult↗
PubMed1970

Hemodynamic determinants of exercise ST-segment depression in coronary patients.

Eight patients with coronary heart disease were studied during two periods of exercise separated by 30 min of rest; workload was increased in a stepwise fashion every minute of exercise up to a level that produced limiting symptoms of angina, fatigue, or dyspnea. The magnitude of ST-segment depression and the central aortic pressure were measured during exercise and recovery periods, and myocardial oxygen requirements were estimated by the pressure-time index (systolic aortic pressure x heart rate x ejection time). Seven of the eight patients exhibited a close relationship (r ranged from 0.74 to 0.98) between magnitude of exercise ST-segment depression and indices expressing myocardial oxygen requirements; heart rate, blood pressure, and ejection time were also related to magnitude of exercise ST-segment depression. These relationships were reproducible during two consecutive exercises. Like onset of angina, magnitude of exercise ST-segment depression is usually related to hemodynamic factors influencing myocardial oxygen needs. Consequently, comparisons of exercise-induced ST depression before and after therapy (drugs, physical training, and surgery) are valid only if ECG findings are compared at the same level of myocardial oxygen requirements. In contrast, absence of such a relationship during recovery suggests an important difference in mechanisms of the post-exercise electrocardiogram.

Coronary Disease↗