[Absence of the effect of nitric oxide on pulmonary and systemic hypertension induced by sino-aortic denervation]. / Absence d'effet du monoxyde d'azote sur l'hypertension artérielle pulmonaire et systémique induite par la défrénation sino-aortique.

Inhaled nitric oxide, a selective pulmonary vasodilator, reverses hypoxic pulmonary vasoconstriction and is an effective treatment in some cases of human pulmonary hypertension. Localization of nitric oxide synthase had indicated a neural role for nitric oxide. Thus, we studied the interactions between inhaled nitric oxide and systemic and pulmonary vascular reactivity in acute neurogenic hypertension. In 6 male beagle dogs (mean weight: 15 +/- 1 kg), anesthetized by chloralose (8 cg/kg) and in spontaneous ventilation, the hemodynamic effects on systemic and pulmonary circulation of inhaled nitric oxide (12 ppm) were studied before and after acute sino-aortic denervation. The hemodynamic effects of intravenous propranolol (300 micrograms/kg) were studied after denervation. Mean arterial pressure (MAP), pulmonary capillary pressure (PCP), mean arterial pulmonary pressure (MAPP), cardiac input (CI) and oxygen venous saturation (SvO2) were measured. [table: see text] Sino-aortic denervation causes an acute and transitory pulmonary hypertension due to a double mechanism: a post-capillary hypertension (increase PCP) secondary to an increase left ventricular post-charge by systemic hypertension and a precapillary hypertension. In fact, vascular pulmonary resistances increase from 1.8 +/- 0.1 to 3.4 +/- 0.8 uW after denervation (p < 0.05). Change in pulmonary vascular reactivity induced by catecholamines is probably involved. Propranolol but not inhaled nitric oxide reverse pulmonary hypertension due to sino-aortic denervation.

[Myocardial infarction in non-menopausal women. Coronary lesions and prognosis]. / Infarctus du myocarde chez des femmes non ménopausées. Lésions coronaires et pronostic.

Between 1977 and 1990, 64 premenopausal women, under 50 years of age (42 +/- 5.6 years), were admitted for typical acute myocardial infarction with pathological Q waves. Twenty one patients had attempted myocardial revascularisation either by intravenous thrombolysis or primary angioplasty (n = 3). All patients underwent coronary angiography with selective left ventriculography during their hospital admission. This group of 64 women was characterised by the association of coronary risk factors (2.8 per patient): smoking (89%), hyperlipidaemia (67%), diabetes (45%) and oral contraception (35%). Coronary angiography showed single vessel occlusion in 86% of patients receiving oral contraception, multiple vessel disease in 36.5% and single or double vessel disease in 31.7% of the other patients. There were 3 deaths during the hospital period (4.6%), 12 cases of left ventricular failure, 2 ventricular aneurysms, 2 operated ischaemic mitral regurgitations and 9 recurrences of pain treated by angioplasty. During follow-up (36.5 +/- 4 months), 22 patients were readmitted to hospital and there were 3 further deaths, 12 cases of persistent cardiac failure, 10 cases of latent ventricular dysfunction and 9 ischaemic reoccurrences treated by angioplasty or surgery. The results in this group of patients suffering from myocardial infarction at an unusually early age for women showed that although the mortality was similar to that observed in men of the same age (9%) there was a very high morbidity and a high risk of cardiac failure. The prognosis of myocardial infarction in women, though better than 10 years ago, should improve with immediate revascularisation, the correction of cardiovascular risk factors and the rapid application of all techniques of modern cardiology.

[Inferior wall myocardial infarction and atrioventricular block; angiography and prognosis]. / Infarctus inférieurs et blocs auriculo-ventriculaires; données angiographiques et pronostic.

This study was based on 42 cases of 2nd or 3rd degree atrioventricular block out of 292 cases of inferior wall myocardial infarction. The criteria of selection were monitoring in the intensive care unit during the acute phase, selective coronary angiography in the first 48 hours to 5 days, and regular clinical follow-up during the first year after infarction. The conduction defect was either immediately recorded on the first ECG, delayed (between the 12th and 24th hour) or late (after the 3rd day). These 42 inferior wall infarcts with atrioventricular block (incomplete in 14 and complete in 28 cases) differed from inferior infarction without block by: - the severity of the clinical signs during the acute phase (35% with cardiac failure, 19% with cardiogenic shock); - the severity of the coronary lesions (71.4% with triple vessel disease in infarction with atrioventricular block compared with 32% in those without block, p < 0.02); - the prevalence of the association of > 70% stenosis of the right coronary and left anterior descending arteries; - the alteration of left ventricular function (53% patients with atrioventricular block had ejection fraction of under 30%); - the severity of these infarcts was not related to the atrioventricular block which regressed in 95% of cases but to the severity of the coronary disease, the left ventricular dysfunction and the advanced age of the patients (72.3 +/- 8 years).

[Left ventricular filling and left bundle branch block: an echocardiographic and radionuclide study]. / Remplissage ventriculaire gauche et bloc de branche gauche: étude échocardiographique et isotopique.

Left bundle branch block changes the activation and haemodynamics of the left ventricle. In order to evaluate its consequences on left ventricular filling, the duration of the isovolumic relaxation period, the velocities and the integrals of the rapid and slow filling waves were recorded by Doppler echocardiography and the ejection fraction, the peak filling rate and its time of apparition were measured by gamma angiocardiography in 18 patients aged 55 +/- 9 years and 18 control subjects aged 53 +/- 9 years. Left bundle branch block was associated with a prolonged isovolumic relaxation period (104 +/- 14 vs 88 +/- 11 ms) a delayed and reduced peak filling rate and an increased atrial filling velocity at a heart rate comparable to that of control subjects (69 +/- 9 vs 72 +/- 8 beats/mn). Despite these changes in left ventricular relaxation and filling and a reduced ejection fraction (55 +/- 7 vs 61 +/- 6%, p < 0.01) cardiac output was not significantly decreased in left bundle branch block (4.9 +/- 1 vs 5.2 +/- 0.9 l/mn). Therefore, left bundle branch block interferes with left ventricular filling and ejection fraction without decreasing the resting enddiastolic volume.

[Normal aging, hypertension and left ventricular filling]. / Vieillissement naturel, hypertension artérielle et remplissage ventriculaire gauche.

Because of discrepancy in interpretation of early diastolic filling indices in normal subjects and hypertensive, we studied the correlations between age and radionuclide angiographic peak filling rate (PFR), doppler echocardiographic early E and late A waves, left ventricular mass (LVM), blood pressure (BP) and ejection fraction (EF) in cautiously screened 30 untreated hypertensive and 30 age paired normal subjects (mean of age 52 +/- 17 ranging from 34 to 78 years). No patient had gross obesity nor coronary artery disease. Univariate analysis revealed strong correlations between LV filling and age in normal (r = -0.82 p less than 0.0001) and hypertensive (r = -0.61 p less than 0.001), with a very significant difference in y intercepts (t = 0.61 p = 10(-6)). LVM correlated poorly with age (r = 0.35 p less than 0.05) but with none of the LV filling indexes. BP correlated with PFR (r = 0.33 p less than 0.05) and A wave (r = 0.44 p less than 0.02) in hypertensive only. After multivariate analysis, significant dependencies of PFR, age, LV mass were more accurate if BP was in a higher range. The variability of the values of LV filling indexes was wider in hypertensive than in normotensive. Normotensive aging and hypertension have similar effects on the cardiovascular system. In the most aged people even without apparent cardiac disease, it is not possible to identify the specific effects of hypertension on diastolic function.