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

In systemic hypertension, a certain degree of impairment of left ventricular diastolic function is often detectable, and is the consequence of two factors: elevated afterload and left ventricular hypertrophy. The goal of improving diastolic dysfunction can thus be achieved by lowering blood pressure and by inducing a regression in left ventricular hypertrophy. A reduction in blood pressure by intravenous administration of verapamil has proved capable of enhancing left ventricular filling properties in patients with hypertension. This finding has not been corroborated, however, in midterm protocols using an array of drugs (beta-blockers, dihydropyridines, diltiazem, and diuretics). Reduction in left ventricular mass can be achieved by several categories of drugs, and it has been shown that a decrease in mass is accompanied by an improvement in the early diastolic filling pattern. The kind of drug used to accomplish mass reduction seems to be irrelevant as far as the improvement in diastolic function is concerned. The pattern of left ventricular hypertrophy, however, might play a role in influencing the outcome on diastolic mechanics of left ventricular mass decrease.
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PMID:Effects of antihypertensive therapy on diastolic dysfunction in left ventricular hypertrophy. 138 87

The determinants of cardiac output were investigated in 161 patients with essential hypertension World Health Organization (WHO) stages I and II. In multiple regression analysis, cardiac output was inversely and independently related to blood pressure and to age. In patients with more severe hypertension, the lower cardiac output was associated with a lower stroke volume and a higher peripheral oxygen extraction. When age and blood pressure were taken into account, cardiac output was not a significant predictor of total mortality and of future cardiovascular events. Clinic and casual blood pressure explain only up to about 30% of the variability of echocardiographic left ventricular mass. The relationship of electrocardiographic voltages with blood pressure at various levels of bicycle exercise was highly significant in 169 patients with essential hypertension (r = 0.29-0.38; p less than 0.001) but the relationship was not better than with pressure at rest (r = 0.39). Ambulatory blood pressure, however, may be better related to left ventricular mass than clinic pressure. Several studies indicate that left ventricular hypertrophy is a significant risk factor for future cardiovascular events, independent of age and blood pressure. Left ventricular systolic function is usually normal in established hypertension, but diastolic function is frequently impaired, which could explain the reduced peak oxygen uptake in patients with more severe hypertension.
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PMID:Hypertensive heart disease: pathophysiology and clinical and prognostic consequences. 138 96

Left ventricular hypertrophy in systemic arterial hypertension is associated with an increased risk of morbidity and mortality due to cardiovascular disease. Therefore, the diagnosis of left ventricular hypertrophy is clinically important. In current clinical practice, echocardiography is the method of choice for diagnosing left ventricular hypertrophy. This review describes current, clinically applied techniques of measuring left ventricular mass using M-mode and two-dimensional echocardiography. Using M-mode techniques, left ventricular hypertrophy is usually present when myocardial mass estimates exceed 150 g/m2 in males and 120 g/m2 in females. Using two-dimensional echocardiography, upper limits of normal have been described to be slightly lower (102 g/m2 in males and 88 g/m2 in females). In serial clinical two-dimensional echocardiographic studies, image acquisition and quantitation predominantly determine total variability in left ventricular mass estimates. Using any single technician and any single reader, left ventricular mass estimates in normal subjects may vary by 35 g (standard deviation) between serial studies. Strategies to reduce the magnitude of this variability include increasing the number of technicians and readers acquiring and analyzing a single study.
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PMID:Diagnosis of left ventricular hypertrophy by echocardiography. 138 99

Felodipine is a vascular-selective, dihydropyridine calcium antagonist previously investigated as a conventional tablet formulation administered twice daily. More recently considerable experience has been gained with an extended release (ER) formulation which has the convenience of once daily administration. Felodipine ER has been well studied in patients with essential hypertension. As monotherapy in mild to moderate essential hypertension, felodipine ER is at least as effective in reducing blood pressure as other calcium antagonists, beta-blockers, diuretics and ACE inhibitors, with some results favouring felodipine ER at a statistically significant level at the dosages used. It is also effective combined with controlled release metoprolol or enalapril in patients with mild to moderate essential hypertension. In patients with more severe forms of essential hypertension uncontrolled by beta-blocker and/or diuretic therapy, felodipine ER was effective as an 'add-on' therapy in placebo-controlled trials, and, at the dosages used, more effective than either sustained release nifedipine or nitrendipine. Felodipine produces effective control of blood pressure without negative effects on cardiac performance. In addition to its antihypertensive action, results suggest that felodipine therapy is associated with significant regression of left ventricular hypertrophy. Furthermore, it appears suitable for use in patients with concomitant diabetes, renal dysfunction or asthma, and is also being investigated for use in patients with congestive heart failure or angina pectoris. Felodipine ER is an effective drug for the treatment of all grades of essential hypertension, and can be used both as monotherapy and in combination with other antihypertensive agents. Further clinical experience should fully establish the long term tolerability of felodipine ER and consequently its place in therapy relative to other accepted antihypertensive drugs. However, with the convenience of once daily administration, felodipine ER is a worthwhile innovation in the treatment of hypertension.
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PMID:Felodipine. A review of the pharmacology and therapeutic use of the extended release formulation in cardiovascular disorders. 138 18

Losartan, a recently developed nonpeptide angiotensin II (Ang II) receptor antagonist, was administered orally to 10-week-old spontaneously hypertensive rats (SHR) for 2 weeks. Cardiac weight and tissue Ang II, as well as plasma renin activity (PRA) and Ang II, were determined. Treatment with Losartan (10 mg/kg per day) lowered blood pressure markedly. Losartan reduced significantly the left ventricular weight by 11% compared with control rats. The left ventricular Ang II content was lowered by Losartan (18.6 +/- 0.9 pg/tissue; 21.9 +/- 0.9 pg/tissue, control, p less than 0.05), whereas PRA and plasma Ang II concentration were increased by the treatment. With the control and Losartan-treated animals, there was a significant positive correlation between the left ventricular weight and the tissue Ang II content (r = 0.563, p less than 0.05). These results provide evidence that cardiac tissue Ang II, rather than circulating Ang II, plays an important role in the pathophysiology of left ventricular hypertrophy of this animal model of human hypertension.
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PMID:Effects of losartan, a nonpeptide angiotensin II receptor antagonist, on cardiac hypertrophy and the tissue angiotensin II content in spontaneously hypertensive rats. 138 40

Five-week-old male spontaneously hypertensive rats (SHR) were either exposed to hypoxia or maintained in normoxia. Groups of rats were returned to normoxia after 8 or 12 weeks exposure to hypoxia while others remained in hypoxia or normoxia throughout the study. Subdivisions of the groups were sacrificed 2 or 6 weeks after return to normoxia at the same time as were rats continuously exposed to either normoxia or hypoxia. Hypoxia attenuated the development of systemic hypertension (P less than 0.05); however, this protection dissipated partially when rats were returned to normoxia. Norepinephrine concentration was significantly elevated and serotonin turnover (5-hydroxyindoleacetic acid/serotonin 5HIAA/5HT) was significantly decreased in caudal brainstem of hypoxic SHR and both were gradually normalized upon return to normoxia. Similarly, left ventricular hypertrophy was attenuated and adrenal catecholamine contents were increased with hypoxic exposure. Both gradually normalized upon return to normoxia. Mechanisms associated with the development of spontaneous hypertension reemerge when adult, previously hypoxic SHR are returned to a normoxic environment. These findings implicate long-term changes in central noradrenergic and serotonergic function as components of the cardiovascular adaptation to hypoxia which includes hypoxic moderation of spontaneous hypertension.
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PMID:Reemergence of spontaneous hypertension in hypoxia-protected rats returned to normoxia as adults. 138 55

The major target organs that become damaged as a consequence of long-standing arterial hypertension are the kidneys, heart, and brain. Left ventricular hypertrophy (LVH) cannot be considered only as an adaptive process to elevated blood pressure (BP), and the heart is also a major target organ in malignant arterial hypertension (MH). Magnetic resonance (MR) was used as a method for visualization of the heart in 68 patients with MH including 18 with essential hypertension, 16 with chronic glomerulonephritis, 13 with chronic pyelonephritis, 16 with renovascular hypertension, eight with adrenal tumors, and in 20 healthy volunteers (as a comparison group). Electrocardiogram-gated, double spin-echo magnetic resonance imaging was performed to image the right and left ventricles (RV and LV), interventricular septum, apex and LV posterior wall, left atrium, and aortic root. In all the patients, symmetric LV hypertrophy was registered and in the most severe cases LV wall thickness was more than 20 mm. There was no LV cavity enlargement or local contractility abnormalities. There was close correlation of LVH and diastolic BP. The degree of LVH and diastolic dimensions of the LV differed between etiologies of MH. These findings show that different pathophysiologic mechanisms of development of MH influence the processes of myocardial hypertrophy. The highly informative yield of MR tomography for evaluating structural and functional changes of the heart under MH must be underlined.
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PMID:Magnetic resonance imaging of cardiac hypertrophy in malignant arterial hypertension. 138 64

This study was undertaken to study the effects of hyperlipidemia and hypertension on the coronary circulation and on the myocardium of Watanabe heritable hyperlipidemic (WHHL) rabbits. Surgery to induce hypertension by the one-kidney, one-clip technique was performed on the WHHL rabbits at 3 months of age. At 3 and 6 months after surgery, the right and left coronary arteries and the left ventricle and posterior papillary muscle from normotensive and hypertensive animals were assessed. Atherosclerotic involvement was found at the coronary origin in 94% of the arteries evaluated. Lesions were usually confined to the proximal 1-2 mm of the coronary artery. The prevalence of coronary atherosclerosis in the WHHL rabbit was found to be higher than previously reported in rabbits of the same age. Hypertension-induced muscular and vascular changes such as left ventricular hypertrophy, medial thickening of the arteries, and hyaline arteriolosclerosis were found in most of the hypertensive animals. These changes were rarely seen in the normotensive rabbits. Characteristics of ischemia and cell injury such as eosinophilic fibers, fiber vacuolization, and contraction band necrosis were found more often in hypertensive than in normotensive WHHL rabbits. Confluent areas of severe necrosis indicative of myocardial infarction were not found; myocardial damage was diffuse and involved individual cells and small microscopic areas. This model may be valuable in further studies of coronary artery disease and myocardial injury that result from the combination of hypercholesterolemia and hypertension.
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PMID:Effects of hypertension and hyperlipidemia on the myocardium and coronary vasculature of the WHHL rabbit. 138 26

The early cardiac involvement is well known in arterial hypertension, particulary the diastolic and left ventricular hypertrophy. The right ventricle and pulmonary circulation may likewise be affected early in the course of disease. Scarce though it is, studies on the right repercussion of hypertension have shown an increase in pulmonary resistance and right-sided pressures in hypertensive patients. In spite of the limitations arising from the complex geometry of the right ventricule, echocardiography may be the most important non-invasive technique in the evaluation of the structural and functional repercussion of hypertension on the right ventricle. Our studies have revealed an increase in the diastolic thickness of the right ventricular free wall in hypertensive patients, as well as a good correlation between the diastolic thickness of the free walls of both ventricles. Most studies suggest a functional relationship between both ventricles. Structural alterations may occur in the right ventricle, along with hemodynamic alterations, thus suggesting structural and functional similarity of both ventricles, regarding cardiac response to arterial hypertension.
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PMID:[Functional and anatomic involvement of the right ventricle in arterial hypertension]. 138 58

Left ventricular hypertrophy (LVH) is a well defined cardiovascular risk factor and is frequently detected by echocardiography in hypertensive patients. Systolic cardiac function at rest is usually preserved in hypertension, however, diastolic function may be frequently altered. Evidence for these changes has been demonstrated by Echo-Doppler even without concomitant existence of LVH. Quantitative and qualitative changes in contractile proteins and interstitial tissue as well as reduction of coronary reserve may be related to the mentioned dysfunction. Recent studies have confirmed the precocity of diastolic dysfunction both in laboratory animals as well as man. Further significant differences have been shown between normotensives with and without a family history of systemic hypertension. The relative importance of diastolic disfunction is also related to its possible role in the genesis of cardiac failure and its probable role in the modulation of cardiopulmonary reflexes in addition to the hemodynamics of arterial hypertension. It is not yet known if the presence of diastolic dysfunction is a mechanism or a risk marker like LVH.
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PMID:[Precocity of diastolic dysfunction in hypertensive cardiopathy]. 138 59


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