Ventricular arrhythmias in hypertensive patients with mild left ventricular hypertrophy. A possible relationship with autonomic nervous system activity.
Mario MalerbaEnrico Agabiti RoseiDamiano RizzoniRoberto ZulliMaría Lorenza MuiesanM. BeschiMaurizio CastellanoG Muiesan
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Sympathetic nervous system
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It was established that left ventricular hypertrophy in patients with ischemic heart disease associated with hypertensive disease reflects a functionally more intact myocardium than similar hypertrophy in analogous patients without hypertensive disease. Hypertrophy of the left ventricle in patients with ischemic heart of different severity may be considered an index of myocardial lesion and this should be considered in the treatment tactics.
Hypertensive heart disease
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Hypertensive heart disease
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The aim of the study is to evaluate the effect of Valsartan on the autonomic heart regulation in hypertensive patients with left ventricular hypertrophy or diastolic dysfunction. Fourteen hypertensive patients (grade 1 or 2, according to WHO 1999), with echocardiographic criteria of left ventricular hypertrophy or diastolic dysfunction, participated in the study. After a period of 3 weeks of washout, the patients start to receive Valsartan 80mgr qd. Blood pressure (SBP, DBP) and echocardiographics parameters were take at the beginning of the study and after 3 month of follow-up. We observed important decrease in Blood pressure parameters: SBP: 156.42 ± 13.75 mm Hg vs 128.35 ± 9.10 mm Hg (p<0.001), and DBP: 97.42 ± 6.24 mm Hg vs 74.28 ± 7.4 mm Hg (p<0.001). We also observed decrease in the Left ventricular mass index (LVMI): basal 163.73 ± 44.50 g/mt2 vs 134.90 ± 19.51 g/mt2 (p=0.04), and in the rate of A/E: basal 0.67 ± 0.2 vs 1 ± 0.33 (p<0.001) at the end. In Basal conditions, Valsalva response was 1.4 ± 0.2 and heart rate variation with deep breath was 1.3 ± 0.2. After 3 months of treatment with Valsartan, Valsalva response was 1.5 ± 0.2 (p=n.s.) and heart rate variation with deep breath was 1.3 ± 0.2 (p=n.s.). We can conclude that Valsartan as monotherapy has no without affect in the autonomic heart regulation in hypertensive patients. Valsartan has efficiency in reducing Blood Pressure and left ventricular mass.
Basal (medicine)
Hypertensive heart disease
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In order to assess the involvement of the cardiopulmonary receptors in the regulation of the coronary circulation, changes in coronary resistance produced by the application of a -10 mmHg pressure to the lower body were studied in 6 healthy subjects and 6 patients with arterial hypertension and left ventricular hypertrophy. The results show that the inhibition of the ventricular receptors significantly increases coronary resistance and that this reflex response is eliminated in hypertensive patients with ventricular hypertrophy. The results show that the inhibition of the ventricular receptors significantly increases coronary resistance and that this reflex response is eliminated in hypertensive patients with ventricular hypertrophy.
Coronary circulation
Ventricular hypertrophy
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Hypertensive heart disease
Pathophysiology of hypertension
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Hypertensive heart disease
Pathophysiology
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The effects of long-term (mean 3–9 months) pharmacotherapy of hypertensive and normotensive hypertrophy (hypertensive heart disease, hypertrophic non-obstructive cardiomyopathy) as well as of advanced cardiac disease due to coronary artery disease and dilatative cardiomyopathy by large doses of nifedipine (mean 120 mg/day−1) were analyzed with regard to systolic blood pressure, to left ventricular function and to the hypertrophy degree of the ventricle, (a) Nifedipine, in addition to conventional and maintained antihyper tensive and cardiac therapy, lowers blood pressure in hypertensive patients, whereas hypotensive effects in the normotensive patients were absent, (b) Nifedipine enhances left ventricular function in all patient groups significantly, i.e. in normotensive hypertrophic non-obstructive cardiomyopathy, in hypertensive heart disease and especially in heart disease due to coronary artery disease and dilatative cardiomyopathy. (c) Significant regression of septal and of global hypertrophy was found in hypertrophic non-obstructive cardiomyopathy and in hypertensive heart disease. These results indicate, that long-term nifedipine treatment may be beneficial for left ventricular function in all patient groups and for hypertrophy regression in established left ventricular hypertrophy due to hypertrophic, non-obstructive cardiomyopathy and due to hypertensive left ventricular hypertrophy, It is concluded that long-term nifedipine treatment improves left ventricular function and leads to regression of established ventricular wall hypertrophy in hypertrophic non-obstructive cardiomyopathy and in hypertensive heart disease.
Hypertensive heart disease
Concentric hypertrophy
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