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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The treatment of coronary atherosclerosis risk factors is an essential part of secondary prevention of myocardial infarction. This should be started during the acute phase. Hypercholesterolemia is the principal causal factor and the occurrence of an infarct does not change the relative cardiovascular risk attributable to this factor. The absolute risk, positively correlated to total and LDL cholesterol and negatively to HDL cholesterol, is increased after myocardial infarction because of the higher prevalence of lethal or non-lethal ischemic cardiac events. The benefits of cholesterol reduction on cardiovascular mortality have been clearly established. They are greater with cholesterol-lowering drugs than with diet alone, and all the more significant when the initial cholesterol levels are high, but they are present at every value. A 1% reduction in total cholesterol is associated with a 2.5% reduction in coronary mortality both in secondary and primary prevention. After infarction, the cardiovascular benefits greatly exceed the risk of overmortality from other causes. Therapeutic effects may also be demonstrated by non-progression or regression of stenotic coronary lesions. The benefits of hypertension control are not as evident. Diastolic blood pressures inferior to 85 mmHg are associated with an increased coronary risk. While waiting for the results of specific therapeutic trials, reduction of high blood pressure without excessive lowering of the diastolic pressure is recommended. Stopping smoking is a measure of primary prevention which reduces the number of acute coronary events and of sudden deaths. However, the correlation with atherosclerosis is not remarkable. Treating diabetes, sedentarity and psychological behaviour seems to be useful. An evaluation of a personalized multifactorial approach to individual risk should be performed.
Arch Mal Coeur Vaiss 1992 Nov
PMID:[Treatment of risk factors of coronary atherosclerosis]. 130 42

The usefulness of salt restriction in essential hypertension is still now disputed. This study was designed to test the influence of a diet with and without salt restriction in 19 untreated essential hypertensives (12 with and 7 without family history of hypertension) and free of cardiovascular and renal complications. Each patient was examined after a placebo period, after 1 month of salt restriction, and after 1 month of salt supplementation. Weight, blood pressure, 24 hours urinary sodium excretion and red blood cell ionic fluxes were measured. In patients with hypertensive heredity, the blood pressure did not change. The intracellular sodium concentration, the cotransport and the countertransport remained stable. The ouabain sensitive sodium pump slightly increased during salt restriction and remained stable after salt supplementation. In patients without such hypertensive heredity (who were older and heavier), sodium restriction period was characterized by significant decrease in blood pressure, weight, intracellular sodium concentration and increase in sodium pump activity. When salt was increased, all the parameters remained stable. A more balanced diet with sodium restriction decreases the blood pressure in relation to age, weight and the blood pressure level. Hypertensive heredity does not seem to be a parameter of salt sensitivity. The blood pressure decrease is also related to the quantitative importance of sodium restriction. The ouabain sensitive pump activity changes during diet especially in relation to weight loss and decreasing salt intake.
Arch Mal Coeur Vaiss 1992 Aug
PMID:[Effect of dietary sodium in hypertension not treated with drugs]. 133 57

The results of epidemiologic studies on the efficacy of different strategies of prevention or improvement of the prognosis of coronary artery disease are generally expressed in terms of percentage reduction of risk; for example, the treatment of hypercholesterolaemia reduces the risk of coronary death by 21%. In order to improve the assessment of the efficacy of these approaches the authors propose to take into account the number of subjects which needs to be treated each year to prevent one cardiovascular event more than the control group (for example, in hypercholesterolaemia, 1,736 patients). This number depends on the reduction of risk and also on the incidence of complications in the control group. Using this method, the authors classified different therapeutic strategies in order of their efficacy: thrombolytic therapy in the acute phase of myocardial infarction, then aortocoronary bypass grafting of left main coronary or triple vessel disease, secondary prevention with stopping smoking, and betablocker therapy. Finally, primary prevention with anti-smoking campaigns, treatment of hypertension and hypercholesterolemia. Based on this figure and knowing the annual cost of patient treatment, it is possible to calculate a cost-effectiveness ratio for each of these therapeutic interventions.
Arch Mal Coeur Vaiss 1992 Feb
PMID:[How to evaluate the cost/effectiveness ratio of different therapies of coronary disease]. 134 16

Several authors have discussed an alteration of adrenergic receptivity in arterial hypertension. De Champlain (Hypertension 1990; 8: S77-S85) suggested that postsynaptic alpha 1-adrenergic functions became dominant while beta-adrenergic functions are attenuated in arterial hypertension. However, the status of presynaptic alpha 2-adrenoceptors remains unknown. The present study investigates presynaptic alpha 2-adrenoceptors in hypertension through the measurement of plasma levels of noradrenaline after administration of yohimbine, an alpha 2-adrenoceptor antagonist, in essential hypertension. Yohimbine (0.2 mg/kg per os) induced a 73% increase of plasma levels of noradrenaline in hypertensive patients (n = 12) and a 178% one in normotensive subjects (n = 6, p < 0.05). A similar significant difference was found in experimental neurogenic hypertension observed in awake dogs 3 weeks after sinoaortic denervation: the increase in plasma concentrations of noradrenaline after yohimbine (0.5 mg/kg i.v.) was +279% in hypertensive versus +642% in normotensive dogs (p < 0.05). The results show that the magnitude of the yohimbine-induced sympathetic activation is lower in hypertensives than in normotensives. They suggest the existence of a presynaptic alpha 2-adrenoceptor desensitization in arterial hypertension. The abnormality of this presynaptic inhibitory mechanism can increase the sympathetic tone and help to develop and maintain arterial hypertension.
Arch Mal Coeur Vaiss 1992 Aug
PMID:[Is there any desensitization of presynaptic alpha 2-adrenergic receptors in hypertension? Experimental and clinical studies]. 136 44

Cardiac involvement in Takayasu's disease is well documented. This is often the result of severe hypertension. However, severe clinical manifestations of aortic regurgitation and coronary insufficiency are much less common. The authors report a case in which post-infarction angina and severe left ventricular failure led to a double valve replacement and an aorto-right coronary bypass graft procedure. The diagnosis of Takayasu's disease was suspected before surgery and was confirmed by histological examination.
Arch Mal Coeur Vaiss 1992 Dec
PMID:[Heart valvular and coronary manifestations of Takayasu disease. Apropos of a surgically-treated case]. 136 95

Previous studies have shown that essential hypertension is frequently associated with insulin resistance and hyperinsulinism. Because insulin may exert a direct positive inotropic as well as chronotropic effect and controlled the initiation of peptide chains in the heart, we tested the hypothesis that insulin may be a determinant of myocardial hypertrophy and contractility. The relation between glucose metabolism (assessed by the oral glucose tolerance test) and left ventricular (LV) mass and function (assessed by echocardiography) was explored in 47 never-treated lean essential hypertensive patients (EH) of short duration and 19 normotensive subjects (NT). A greater number of EH versus NT (23 vs 5%) had an abnormal glucose tolerance. The fasting insulin-to-glucose ratio was significantly higher in EH as compared to NT. Fasting as well as integrated serum insulin to glucose values ratio were positively correlated with heart rate (r = 0.35, p < 0.05, r = 0.38, p < 0.05) and the LV end-systolic stress to volume ratio (r = 0.48, p < 0.001, r = 0.54, p < 0.001) but not with LV mass (r = 0.02, r = 0.02) in EH. When EH were divided into those with normal (n = 36) and supernormal (n = 11) LV contractility based on the relationship between LV fractional shortening and LV end-systolic stress, integrated insulin level and fasting insulin to glucose ratio were markedly higher in patients with supernormal LV contractility, whereas arterial pressure, heart rate, urinary sodium excretion, and plasma renin activity were similar in the two groups. We concluded that hyperinsulinemia and LV hypercontractility are associated in patients with hypertension of short duration. If chronic hyperinsulinemia is to be causally related to hypertension, one would have to postulate that the effects (inotropism and chronotropism) of insulin on the heart can be dissociated from the resistance to the glucose-lowering action of insulin.
Arch Mal Coeur Vaiss 1992 Aug
PMID:[Left systolic ventricular function and metabolic disorders in untreated hypertensive patients]. 148 35

We measured by thoracic bioimpedance (BoMed, NCCOM3-R7) non invasive cardiac index (CI), stroke index (SI) and systemic vascular resistance index (SVRI) in 48 hypertensive patients (OMS) compared to 30 normotensive. The mean arterial pressure (MAP) and the SVRI were significantly higher in the hypertensive group while the CI are significantly lower, as that was shown in previous invasive studies. We found an inverse correlation between age and CI (r = -.30, p < or = .05) in relation with a negative correlation between SI and age (r = -.35, p < or = .05) and no correlation between heart rate and age. Furthermore we divided normotensive and hypertensive patients in three groups of CI (low CI < 2.8 l/min/m2, 2.8 < or = normal CI < or = 4.2 l/min/m2, high CI > 4.2 l/min/m2) and in three groups of SVRI (low SVRI < 1660 Flohms/m2, 1660 < or = normal SVRI < or = 2580 Flohms/m2, high SVRI > 2580 Flohms/m2). Despite CI diminution in hypertension, high CI percentage's was the same in normotensive and hypertensive patients. In conclusion, these results confirm previous studies by using a simple, easy, non invasive and reproducible method.
Arch Mal Coeur Vaiss 1992 Aug
PMID:[Cardiac output studied by a non invasive method in hypertensive patients]. 148 36

The purpose of the study was to interpret the acute improvement in left ventricular (LV) filling induced by a new calcium channel blocker (SR 33 557) using Doppler echocardiography. Thirteen patients, 29 to 68 years old (mean 52) with mild to moderate hypertension were examined by Doppler echocardiography before and 4 hours after treatment (SR 33 557: 300 mg). The LV filling parameters, E, A, A/E, VTIM, VTIA, VTIA/VTIM, pressure half time (PHT) and isovolumic relaxation time (IRT) were measured. An index of left atrial pressure was obtained by measuring the mean pulmonary arterial pressure (PAP). The following hemodynamic parameters were also obtained: systolic blood pressure (SBP), heart rate (HR), PR interval (PR), stroke volume (SV) at aortic origin, total systemic resistances (TSR), pulse wave velocity (PWV) at thoracic descending aorta, LV end systolic stress (ESS), LV geometry (thickness/radius: th/r) and systolic function indices: mean VCF and contractility (mean VCF-ESS relationship). Following acute treatment, E and VTIM increased, A, VTIA and PHT did not change, and A/E, VTIA/VTIM ans IRT decreased, both significantly (p < 0.05). PAP did not change, HR, SBP, TSR, PWV, ESS decreased and PR increased both significantly (p < 0.05). LV geometry and systolic function did not change. No significant relationship was found between LV filling changes and changes in hemodynamic parameters. In conclusion, the acute increase in early LV filling induced by the calcium blocker treatment may be interpreted as the consequence of the improvement in LV relaxation in the absence of any change in left atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1992 Aug
PMID:[Apropos of acute changes in left ventricular filling induced by antihypertensive treatment]. 148 37

The sympathetic nervous system seems to be a non hemodynamic factor involved in the development of hypertension and in left ventricular hypertrophy determinism. The aim of this study was to estimate the myocardial norepinephrine content in essential hypertensive patients, using a reliable radio-iodinated marker of norepinephrine: the 123I-meta-iodobenzylguanidine (123I-meta-iodobenzylguanidine). Eight male and female hypertensive patients with left ventricular hypertrophy and average age of 52 +/- 9 years underwent a resting, ambulatory and effort blood pressure measure. Echocardiographic parameters allowed measure of left ventricular mass index (according to Devereux, and we considered left ventricular hypertrophy as left ventricular mass index greater than 120g/m2. Plasma norepinephrine is measured at rest. Cardiac and mediastinal radioactivity is detected 4 h after a 4mCi i.v. injection of 123I-meta-iodobenzylguanidine and meta-iodobenzylguanidine myocardial uptake is definite as the cardiac/mediastinal ratio (N:1.78 +/- 0.19). Meta-iodobenzylguanidine-myocardial uptake average value of hypertensive patients was 1.89 +/- 0.19 (1.63 to 2.25) without statistical difference to control subjects. We found a significative correlation between meta-iodobenzylguanidine myocardial uptake and effort systolic blood pressure variation in one hand, and with heart rate increase with effort in the other hand. There is no correlation between meta-iodobenzylguanidine-myocardial uptake and left ventricular mass index or ambulatory blood pressure. In hypertensive patients with left ventricular hypertrophy, meta-iodobenzylguanidine myocardial uptake is normal or high, in agreement with experimental data in SHRs, model of human essential hypertension. Therefore myocardial scintigraphy with 123I-meta-iodobenzylguanidine can appreciate cardiac norepinephrine content in humans.
Arch Mal Coeur Vaiss 1992 Aug
PMID:[Evaluation of norepinephrine content in the myocardium in hypertensive patients with left ventricular hypertrophy]. 148 41

The release of catecholamines and their co-neurotransmitter neuropeptide Y was investigated in conscious dogs with neurogenic arterial hypertension elicited by sinoaortic denervation. One month after denervation, an elevation of catecholamine levels (measured by HPLC) without elevation of neuropeptide Y levels in plasma (evaluated by RIA) has been found. This dissociation could be explained by a transient release of neuropeptide Y during the first weeks after surgery; a depletion of neuronal neuropeptide Y due to the permanent sympathetic stimulation; or an insufficient increase in sympathetic tone. To test these three hypotheses, we investigated the time courses of catecholamine and neuropeptide Y levels in arterial plasma during the first five weeks after sinoaortic denervation; and the responses to yohimbine (an alpha 2 antagonist which enhances transmitter release). Resting neuropeptide Y levels in plasma remained normal during the first five weeks after sinoaortic denervation. In normal dogs, a high dose of yohimbine (0.5 mg/kg i.v.) elevated both catecholamine (6-fold) and neuropeptide Y levels (1.5-fold), whereas a lower dose (0.05 mg/kg i.v.) induced a two fold elevation of catecholamine levels without changing neuropeptide Y concentrations. In sinoaortically denervated dogs, yohimbine elicited elevation of both catecholamines and neuropeptide Y whatever the dose used. Thus, neurogenic arterial hypertension in dogs seams to involve catecholamines but not neuropeptide Y. Moreover, the present work suggests that a high level of sympathetic stimulation is required for a co-release of catecholamines and neuropeptide Y.
Arch Mal Coeur Vaiss 1992 Aug
PMID:[Differential regulation of the release of norepinephrine and neuropeptide Y]. 148 47


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