[Hemodynamic testing at rest and during exertion after mitral valve replacement with a St. Jude Medical prosthesis]. / Contrôle hémodynamique au repos et à l'effort après remplacement valvulaire mitral par prothèse St Jude Medical.

177 mitral valve replacements with the St Jude Medical prosthesis (SJM) were carried out from March 1979 to December 1983. 45 of these patients (22 men and 23 women) underwent right heart catheterisation 6 or 8 months after surgery. These patients were operated for pure mitral stenosis in 24 cases, mitral regurgitation in 10 cases and mixed mitral disease in 24 cases. There was associated aortic valve disease in 26 patients and valve replacement with a Björk prosthesis was carried out in 19 cases. Tricuspid valvuloplasty was performed in 6 patients. 37 patients were at Stage III or IV of the NYHA classification before surgery; one year later, only 1 patient remained at Stage III, 4 patients were at Stage II and 38 at Stage I. 2 patients died in the first postoperative year of extracardiac causes. Resting pulmonary capillary pressure (Pw) fell from 18 +/- 7 mmHg to 9 +/- 4 mmHg after surgery (p less than 0.001); cardiac index rose from 2.21 +/- 0.45 to 2.59 +/- 0.49 1/min/m2 (p less than 0.001). A capillary arteriolar obstruction observed in 16 patients before surgery was only found in 9 of these patients after surgery. The changes in pulmonary pressures and cardiac output during exercise were studied in 22 patients. Pw rose from 7.6 +/- 1.5 mmHg to 20 +/- 4 mmHg; cardiac index increased from 2.62 +/- 0.19 to 5.46 +/- 0.72 1/min/m2. When compared with theoretical results in a normal subject, pulmonary artery pressures were abnormally high in 13 subjects (59 p. 100), reflecting a stenosing effect of the prosthesis, unmasked by exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

[Hemodynamic data during muscular exercise after myocardial infarction. Correlations with coronaro-ventriculographic data]. / Données hémodynamiques recueilles au cours de l'exercice musculaire après infarctus du myocarde. Confrontation aux données coronaro-ventriculographiques.

Forty six patients aged 25 to 67 years (average : 52 years) underwent measurement of pulmonary arterial pressure (PAP), systemic pressure and cardiac output (Fick) at rest and during exercise in the recumbent position 12 +/- 3 weeks after uncomplicated myocardial infarction; the results were then compared with those of coronary angiography and right anterior oblique monoplane left ventriculography. The site of infarction was anterior in 18 cases and postero-diaphragmatic in 28 cases; it was non-transmural in 4 cases. Twenty patients (43%) had multivessel disease; this was equally common in anterior and inferior wall infarction. Regional wall abnormalities of 3 or more segments were observed in 14 cases. Mean PAP increased from 12,3 +/- 4,6 Torr at rest to 27,8 +/- 10,5 Torr on exercise. In 17 patients (Group A) PAP was normal at rest and during exercise (10 +/- 2 Torr and 18 +/- 3 Torr respectively); 25 patients (Group B) had normal resting PAP (12 +/- 3 Torr) but an abnormal rise on exercise (32 +/- 8 Torr); in 4 patients (Group C) PAP was abnormal at rest (24 +/- 4 Torr) and on exercise (44 +/- 7 Torr). The increase in PAP on exercise was inversely correlated to the ejection fraction (p less than 0.001) and related to the extent of left ventricular hypokinesia (p less than 0.001). Patients in Group A had higher ejection fractions (p less than 0.05), dp/dt/p index (p less than 0.01) and left ventricular compliance (p less than 0.01), lower resting (p less than 0.01) and exercise (p less than 0.05) systemic pressures and small regional wall abnormalities (p less than 0.01) than patients in Group B.(ABSTRACT TRUNCATED AT 250 WORDS)

Haemodynamic diversity and plasma renin activity in labile arterial hypertension.

Haemodynamic studies were made on 31 patients with labile hypertension at rest and during exercise. Plasma renin activity (PRA) was measured in 8 of them. Five haemodynamic types could be recognised and they could be arranged into two groups. The first was characterised by an increase of calculated peripheral resistance, sometimes permanent, sometimes revealed by effort, sometimes in relation to an increased cardiac output; this would appear to predict the development of permanent hypertension. The second group was characterised by normal systemic resistances, adapted to the cardiac output which was either normal or increased; the significance of labile hypertension in these cases was uncertain; from the haemodynamic studies one was unable to distinguish a transient emotive hypertension from potential permanent hypertension. The PRA was raised in the supine position and greatly increased by an orthostatic posture in the 8 patients tested, suggesting therefore an underlying neuro-adrenergic mechanism. In some patients with labile hypertension the haemodynamic tests were normal at rest and during effort. Others had different responses, which may be the result of varieties of hyper-sympathetic activity, either pure or predominantly beta-adrenergic (increased cardiac output, peripheral resistance adapted to the output) or combined beta and alpha (increased cardiac output with raised peripheral resistance) or mainly alpha-adrenergic (normal cardiac output, increased peripheral resistance).

[Labile arterial hypertension. Hemodynamic study with measurement of renin activity]. / Hypertension artérielle labile. Etude hémodynamique avec mesure de l'activité rénine

Plasma renin activity (PRA) was increased and highly sensitive to stimulation in eight cases of labile hypertension (HT), which were also studied haemodynamically. This increase in PRA would appear to result from neuro-adrenergic hyperactivity. The haemodynamic were characterised by a diversity which may be explained on the basis of differentiated sympathetic hyperactivity: exclusive or predominant beta-adrenergic activity causing a hyperkinetic cardiac state with moderate HT adapted to the increased cardiac output; A simultaneous alpha- and beta-adrenergic activity resulting in cardiac hyperkinesis with a relative or potential increase in peripheral resistance; isolated or predominant alpha-adrenergic hyperactivity causing a potential increase in peripheral resistance revealed or increased by effort, in the presence of a normal cardiac output. In certain cases of labile HT however, despite an increased PRA, haemodynamic findings were normal at rest and with effort, at the time of catheterisation.