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

Left ventricular hypertrophy (LVH) is an independent risk indicator of cardiovascular disease. Obtaining reversal of hypertension-induced cardiac hypertrophy seems to be a desirable objective of antihypertensive treatment. A total of 2,357 patients were included in a meta-analysis on the effect of antihypertensive pharmacological therapy on LVH. Overall left ventricular mass (LVM) was reduced by 11.9% (95% confidence interval (CI) 10.1-13.7) in parallel with a reduction of mean arterial pressure of 14.9% (CI 14.0 to 15.8). When evaluating the effect of first-line therapies on calculated LVM using the same formula for all studies, the absolute reductions in g were 44.7 (ACE-inhibitors), 22.8 (beta-blockers), 26.9 (calcium antagonists) and 21.4 (diuretics) when adjusted for differences between studies (ANCOVA). It can be concluded that effective antihypertensive therapy reduces LVM. ACE-inhibitors, beta-blockers and calcium antagonists reduce LVM by reducing wall hypertrophy, the effect of ACE-inhibitors being the most pronounced. Diuretics reduce LVM mainly through an effect on left ventricular inner diameter. How these effects affect prognosis is still an open question.
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PMID:Regression of left ventricular hypertrophy--a meta-analysis. 134 56

For more than 20 years hypertrophy regression has been in the focus of hypertension research. Many studies in animals have shown impressive reduction of left ventricular hypertrophy after medical treatment of hypertension. The most important result seems to be that hypertrophy can be almost completely reversed in young animals, whereas in older animals regression of left ventricular hypertrophy appears to be less complete. Hypertrophy regression in man seems much more difficult to prove. The direct correlation between left ventricular muscle mass and ECG changes has been disappointing in many studies. Echocardiography is able to show a comparatively good impression of left ventricular muscle mass and therefore can also demonstrate regression of left ventricular hypertrophy within its methodological limits. There is no doubt that today magnetic resonance imaging has by far the best imaging quality of all the clinical methods and is able to demonstrate both hypertrophy and its regression with incomparable accuracy. In the present clinical study hypertrophy regression has been demonstrated after 6 months of treatment with Carvedilol.
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PMID:Left ventricular hypertrophy regression during antihypertensive treatment. 135 Apr 90

Diltiazem administered in drinking water (0.7 mg mL-1) to Goldblatt two kidney-one clip rats over 16 weeks did not prevent the development of hypertension and left ventricular hypertrophy (LVH). When the collagen content of the left ventricles was assayed (as hydroxyproline), it was found that the fibrosis, characteristic of LVH, was inhibited by diltiazem treatment, despite the fact that hypertension and LVH had developed. This study provides some indirect evidence for the notion that the collagen and myocyte compartments of the myocardium are under separate influences during LVH development in renovascular hypertension.
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PMID:Inhibition by diltiazem of left ventricle collagen proliferation during renovascular hypertension development in rats. 135 42

Beta-adrenergic blocking agents constitute first-line therapy for hypertension in many countries of the world. Comparative trials have been extensive in duration and have included large numbers of patients. Still, the desired cardioprotective effect of beta blockers has yet to be established. Their antiatherosclerotic effect has been noted in several animal experiments. Confirming evidence is needed before the clinical relevance of this effect can be evaluated, but these studies point to a potential therapeutic effect that may be immensely important in the future. Beta blockers can reverse left ventricular hypertrophy secondary to hypertension, but it remains to be shown that regression of left ventricular hypertrophy will reduce the associated risks.
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PMID:Adrenergic agents: clinical trials and experiences. 135 14

Hypertension increases the risk of reinfarction and sudden death in post-myocardial infarction (MI) patients. The same s true of coexisting left ventricular hypertrophy. Fortunately, these two risk factors may be modified by pharmacotherapy. In this article, Dr Boden describes the complementary use of beta blockers and selected calcium channel blockers for secondary prevention after acute MI, particularly in the subset of patients who also have hypertension.
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PMID:The post-myocardial infarction patient with hypertension. Long-term outcome. 135

Echocardiographically determined left ventricular mass (LVM) is currently considered to be the most powerful risk indicator for cardiovascular disease, yielding prognostic information beyond that provided by the evaluation of traditional cardiovascular risk factors, high blood pressure included. It has been considered logical to try to obtain regression of cardiac hypertrophy, even though the risk-reducing implications of such a measure remain to be fully established. Experimental and clinical studies have shown that some classes of antihypertensive compounds are less effective than others in causing reversal of left ventricular hypertrophy (LVH) in spite of being similarly efficacious in lowering blood pressure. In order to extract the maximum amount of information from clinical studies, a meta-analysis was performed. This analysis included 109 treatment studies, each conformed to strict present rules. Only studies with pharmacological antihypertensive therapy and echocardiographically determined LVM were included. An analysis of the effect of the four first-hand antihypertensive treatment principles, adjusted for differences between studies with ANCOVA, showed that the ACE inhibitors, beta-blockers and calcium antagonists all reduce LVM by reversing wall hypertrophy and that the effect is most pronounced with ACE inhibitors. Diuretics reduce LVM mainly by a reduction in left ventricular diameter. If the difference in ability to reverse LVH, between ACE inhibitors and beta-blockers/diuretics would correspond to a difference in prognosis, then the outcome of antihypertensive therapy might be expected to improve. This hypothesis is currently under investigation.
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PMID:Regression of left ventricular hypertrophy--are there differences between antihypertensive agents? 136 88

At the end of a short-term (3-month) study of antihypertensive treatment of mild-to-moderate hypertension, 141 of the 200 study patients continued into a 2-year follow-up of isradipine as monotherapy or in combination with other antihypertensive agents. Although all 141 patients completed the first year, only 102 completed the study. Twenty-four patients dropped out: 2 with flushing; 1 each with arrhythmia, edema, angina, and headache; 12 who were noncompliant; 2 with disease unrelated to the study drug; and 4 for reasons unknown. Before the follow-up, 70% of the 141 patients were taking isradipine; after 2 years, 63% were still taking isradipine as monotherapy. During the follow-up study, the blood pressure remained stable (142.9/86.8 mm Hg after 3 months, and 142.9/86.2 mm Hg after 2 years), whereas the normalization rate was only slightly changed (73 vs. 75.2%). The incidence of reported adverse events decreased with time. At the end of the short-term study, 44.7% of patients had reported one or more adverse events; after 2 years of treatment, only 14.4% reported adverse events. Two patients had ECG signs of left ventricular hypertrophy: one showed no relevant changes while the other presented clear signs of regression. No clinically relevant laboratory abnormalities were noted during the study. In conclusion, isradipine is effective, well tolerated and safe in the long-term treatment of mild-to-moderate hypertension.
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PMID:Long-term (2-year) isradipine data in the treatment of mild-to-moderate hypertension. 137 34

A reduced maximal coronary vasodilatator capacity is reported in patients with hypertensive heart disease, suggesting structural abnormalities of intramyocardial arterioles. Right septal endomyocardial catheter biopsies (EMCB) of 30 patients with arterial hypertension and of 10 heart donors were investigated morphometrically. In hypertension, the mean external diameter (21.9 +/- 3.0 vs. 17.4 +/- 2.9 microns, p less than or equal to 0.01) of arterioles and the mean arterial wall area (284 +/- 80 vs. 167 +/- 69 microns2, p less than or equal to 0.05) were increased as compared with heart donors. Perivascular fibrosis was markedly increased (260 +/- 183 vs. 41 +/- 30 microns2, p less than or equal to 0.05) as well as volume density of fibrosis (3.0 +/- 1.7 vs. 0.9 +/- 0.8 Vv%, p less than or equal to 0.01) in hypertensive heart disease. There was no significant correlation between echocardiographically determined left ventricular mass index (115 +/- 25 g/m2 for men and 104 +/- 12 g/m2 for women) and mean arteriolar wall area (r = +0.17) or volume density of fibrosis (r = +0.2) in hypertensive heart disease. Our investigations show that in patients with arterial hypertension there is a thickening of intramyocardial arteriolar walls and an increase in fibrosis. Intramyocardial vascular alterations seem to manifest in hypertension independent from left ventricular hypertrophy.
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PMID:Morphometric investigation of intramyocardial arterioles in right septal endomyocardial biopsy of patients with arterial hypertension and left ventricular hypertrophy. 138 Jun 13

In both men and women left ventricular hypertrophy (LVH) is the major risk factor associated with the appearance of diastolic and/or systolic myocardial failure. It is not the growth of cardiac myocytes, however, that is responsible for an abnormal structural remodeling of the hypertrophied myocardium in pathologic LVH, but instead, nonmyocyte cells whose behavior and growth are altered by chronic elevations in circulating hormones. Hormone-mediated cardiac fibroblast proliferation and/or enhanced collagen synthesis, for example, account for myocardial fibrosis. The signals mediating nonmyocyte cell involvement in LVH may also involve locally generated hormones having paracrine properties. Herein we review experimental findings pertaining to the reparative and reactive fibrosis of the myocardium seen in various forms of acquired and genetic arterial hypertension, where circulating or tissue renin-angiotensin-aldosterone systems are respectively activated. These hormonal systems determine whether myocardial structure will be altered in arterial hypertension and, accordingly, if myocardial failure ensues. The mechanisms by which these hormones lead to myocardial fibrosis remain to be elucidated and correspondingly will determine if fibrosis can be effectively prevented. At the same time, experimental strategies that regress excess collagen in LVH have been identified, but need to be developed further to determine if myocardial failure, caused by fibrosis, is indeed reversible in humans.
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PMID:Myocardial fibrosis and the renin-angiotensin-aldosterone system. 138 Jun 19

Arterial compliance in humans is generally measured by modeling analysis of pulse tracing or of pulse wave propagation in the arterial tree. It is decreased in hypertension in part because elevation of blood pressure stiffens the arteries by stretching the rigid collagen fibres of their walls. Using a modeling evaluation of the compliance-pressure relationship in large arteries, it is possible to correct compliance from the mechanical effect (passive effect) due to pressure elevation. This makes it possible to show that, at the same pressure as in normal controls, hypertensive patients maintain decreased arterial compliance. This finding suggests that functional and/or structural changes other than pressure-mediated stretching of arteries (active effect) contribute toward reducing arterial compliance. Thus, the response of compliance to antihypertensive drugs must be studied by differentiating between passive and active effects. The diameter and compliance-pressure relationship in arteries allow differentiation of a passive arterial effect due to the pressure-lowering action of the drug, and an active pharmacological effect calculated at the same pressure before and after drug administration. Four drugs--ketanserin, urapidil, nitrendipine, and nicardipine (acute administration)--are given as examples. No active or passive compliance changes are observed with urapidil and ketanserin. In contrast, an active increase in compliance is observed in isobaric conditions with calcium antagonists, together with large-artery dilation due to a potent smooth muscle-relaxing effect. This active increase in compliance is potentiated by a passive increase due to the pressure-lowering effect that reduces the mechanical stretch exerted by blood pressure on arterial bioelastomers. Finally, an optimum increase in arterial compliance is achieved by drugs that vasodilate large arteries by smooth muscle relaxation and concomitantly decrease blood pressure. This may be of importance because low compliance has adverse effects on the cardiovascular system by contributing to the pathogenesis of systolic hypertension and left ventricular hypertrophy. Loss of arterial compliance may also be an early marker of atherosclerosis.
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PMID:Role of arterial compliance in the physiopharmacological approach to human hypertension. 138 85


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