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Biomedical subjects

R Lebeau

Publications and source records attributed to R Lebeau.

35 records · Page 2Linked to original sources
PubMed1989

Sympatho-adrenal and cardiovascular responses during hand-grip in human hypertension.

Circulating norepinephrine and epinephrine levels were correlated with echocardiographic indices of cardiovascular function during isometric exercise (hand-grip at 30% of maximum force for 3 minutes) in 19 patients with mild essential hypertension and 9 normotensive subjects. At the end of the third minute of exercise, plasma norepinephrine and epinephrine, blood pressure and heart rate, increased significantly and similarly in both groups of patients. In contrast, peripheral resistance tended to increase in hypertensives but tended to decrease in normotensives. Moreover, indices of ventricular function increased in normotensives but decreased in hypertensives. At the end of the exercise, systolic and diastolic blood pressures were directly correlated with epinephrine levels in normotensives but were correlated only with norepinephrine levels in hypertensives. On the other hand, norepinephrine and epinephrine levels were inversely correlated with changes in indices of left ventricular performance in hypertensive patients only. These results demonstrate that during isometric exercise, the increase in blood pressure in normotensives is associated with a sympatho-adrenal activation of cardiac performance and contractility, while in hypertensives the increase in blood pressure results mainly from an increase in peripheral resistance associated with a reduction in cardiac performance and contractility, despite a similar sympatho-adrenal activation in both groups. These differences in the hemodynamic responses may be compatible with the hypothesis of beta-adrenoceptor desensitization or structural alterations of the cardiovascular system in hypertensive patients.

Adrenal Glands↗
PubMed1987

Abnormalities in the regulation of sympathetic activity in human hypertension.

Various biochemical, pharmacologic, and physiologic techniques were used to evaluate the sympathetic tone and reactivity in labile and sustained hypertension in humans. The results of these studies suggest the existence of an important subgroup of hypertensive patients characterized by increased basal sympathetic tone and reactivity to standing. Such abnormalities could be the result of various dysfunctions, involving the activity of central and peripheral cardiovascular sympathetic fibers, the presynaptic modulation of sympathetic fibers (including the interaction with the parasympathetic system), the inactivation of circulating norepinephrine, and the sensitivity of the efferent cells. The increase in circulating norepinephrine in a group of hypertensive patients seems to reflect a functional increase in the sympathetic tone as shown by the presence of hyperkinetic cardiac functions in hyperadrenergic patients (elevated catecholamine levels), while cardiac functions are normal in normoadrenergic patients (catecholamine levels within normal range). Moreover, the better hypotensive response, combined with normalization of the basal and reactive circulating norepinephrine levels following beta-blockade in hyperadrenergic hypertensive patients, strongly supports the participation of the sympathetic system in the maintenance of hypertension in those patients. The identification and characterization of this subpopulation of patients may be helpful in the development of more rational therapeutic approaches and could eventually permit us to devise better predictors of outcome in hypertension.

Blood Pressure↗
PubMed1986

Echocardiographic assessment of left ventricular performance before and after marathon running.

Echocardiography was used to indirectly assess the effects of marathon running on myocardial performance. Thirteen marathon runners (mean +/- SEM:30 +/- 1.6 years) were submitted to a resting echocardiographic examination before racing and during early recovery from marathon racing. Indices of left ventricular performance were computed from M-mode recordings of left ventricular dimensions and aortic valve motions. Comparison of basal and post-marathon indices of left ventricular performance showed no significant differences in either pre-ejection period (PEP), left ventricular ejection index (LVEI), fractional shortening (% delta D), ejection fraction (EF), or mean rate of circumferential fiber shortening (mVcf). Cardiac output (Qc) computed from left ventricular end-diastolic (LVEDV) and end-systolic volumes (LVESV) were significantly higher following marathon running (4.9 +/- 0.4 to 6.7 +/- 0.7 L/min) because of a marked increase in resting heart rate (HR) (58 +/- 3 to 76 +/- 3 bpm). A significant decrease in systolic blood pressure (118 +/- 4 to 108 +/- 3 mm Hg), associated with a slight reduction in calculated total peripheral resistance was also observed after the race. These circulatory adjustments probably reflect thermoregulatory activity that allows a greater blood flow to the skin for heat dissipation, as well as persistence of reactive muscle hyperemia. Echocardiographic evidence suggests that marathon running does not lead to marked impairments in left ventricular performance. However, the absence of change in the end-systolic volume, despite a marked reduction in cardiac afterload, may suggest a slight alteration in contractility that could not be detected with the use of echocardiography.

Adult↗
PubMed1982

Left ventricular dimensions following training in young and middle-aged men.

To document the effects of endurance training upon left ventricular dimensions, an echocardiographic examination was performed on 11 young (19 +/- 1 years) and 13 middle-aged (40 +/- 3 years) subjects before and after a 20-week endurance training program. The maximal working capacity was increased by 28% and 27% in young and in middle-aged subjects, respectively. Following training, the left ventricular posterior wall and septal thickness in diastole were unchanged both in young (10.1 +/- 0.2 mm and 9.0 +/- 0.2 mm, pre-; 10.1 +/- 0.2 mm and 9.3 +/- 0.3 mm, post-) and in middle-aged subjects (10.0 +/- 0.3 mm and 10.2 +/- 0.3 mm, pre-; 9.7 +/- 0.2 mm and 10.1 +/- 0.2 mm, post-); the left ventricular end-diastolic internal diameter was unchanged in middle-aged subjects (47.8 +/- 0.9 mm, pre-; 48.1 +/- 1.0 mm, post-) but was significantly increased in young subjects (47.8 +/- 1.0 mm, pre-; 49.9 +/- 1.0 mm, post-) (P less than 0.05). These data could suggest that the left ventricular adaptation to training decreases with age. However, the decrease in resting heart rate observed in young subjects (68 +/- 3 to 60 +/- 2 beats X min-1) (P less than 0.05) but not in middle-aged subjects (63 +/- 3 and 65 +/- 3 beats X min-1) could also increase diastolic filling time and explain the small left ventricular end-diastolic enlargement found in the young subjects.

Adult↗
PubMed1981

[Use of echocardiography in the diagnosis of pulmonary hypertension].

There are few data regarding the sensitivity and specificity of the pulmonic valve echogram in the detection of pulmonary hypertension (PHT). In the present study, simultaneous pulmonic echograms were evaluated in 40 patients with normal pulmonary artery pressure and 24 with PHT (mean pressure greater than 20 mmHg). The A wave depth (Amax) was 4.0 plus or minus 1 mm (2-6 mm) in normals but was (1.05 plus or minus 0.2 mm) (p less than 0,001) in PHT and was absent in 5 of 24 PHT patients with a mean pulmonary artery pressure (MPAP) greater than or equal to 35 mm. The ef slope in normals was 22 plus or minus 1.8 mm and 7.1 plus or minus 2 mm (p less than 0.01) in patients with PHT. A negative slope was observed in 4 patients with severe PHT (MPAP) greater than or equal to 40 mm, but never in normals or in patients with mild PHT. The opening velocity (OV) was significantly higher in PHT patients 363.2 plus or minus 19.3 verus 293 plus or minus 7.3 mm/sec (p less than 0.01). Normal values were found in patients with moderate to severe PHT but an OV greater than or equal to 450 mm/sec was not encountered within the normal group. A mid-systolic notch was observed in 10 patients with PHT of which 9 with a MPAP greater than or equal to 35 mmHg. The maximum systolic excursion of the pulmonary valve in both groups did not differ significantly (13.3 plus or minus 0.5 vs 12.8 plus or minus 0.3). Even less specific, the systolic intervals (PEP/ET), were raised greater than or equal to 0.30 in 12 out of 15 with PHT. In conclusion, the reduction or disappearance of Amax with sinus rhythm, a flattening or negativation of ef slope and the presence of a mid-systolic notch were found to be the 3 most reliable criteria to detect and quantify PHT.

Adolescent↗
PubMed1980

Electro- and echocardiographic study of the left ventricle in man after training.

Fourteen sedentary middle-aged men underwent a chest X-ray, a 12 lead ECG, a VCG, and an echocardiographic examination prior to and following 5 months of training a moderately severe intensity, on a cycle ergometer. No modification in the X-ray cardiac profile was observed following training. Some electrocardiographic (R wave amplitude in V5 and V6 and Sokolow index: SV1 + RV5 or V6) and vectorcardiographic (maximal QRS vector amplitude, maximal spatial QRS vector, and R wave amplitude) indices of left ventricular hypertrophy were slightly but significantly increased following training. The echocardiographic measurements in diastole (septal and posterior wall thickness, left ventricular internal diameter, and left ventricular mass) were unchanged after training. Results suggest that electrical changes may not provide adequate indications of left ventricular morphological modifications. The lack of echocardiographic evidences of left ventricular hypertrophy suggest that: (1) training does not necessarily induce left ventricular hypertrophy; (2) the large heart sometimes observed in athletes may be the result of a genetic factor or of a prolonged and very intensive training pursued since a very young age, over a number of years; and (3) left ventricular enlargement probably plays a minor role in the increase in aerobic capacity following training.

Echocardiography↗