Literature DB >> 2937889

The influence of sympathetic nervous activity on regression of cardiac hypertrophy.

B E Strauer, F Bayer, H M Brecht, W Motz.   

Abstract

Pharmacotherapeutical means of reversing cardiac hypertrophy (prazosin, clonidine and nifedipine) were analysed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of cardiac hypertrophy, i.e. a therapeutic intervention on a critical precursor of hypertensive congestive heart failure, can be obtained by various antihypertensive agents. Prazosin, calcium channel blockers, clonidine and angiotensin converting enzyme inhibitors as well as a combined treatment regimen using alpha-receptor blockers together with diuretics and vasodilators can all induce regression of hypertrophy associated with an improvement in left ventricular function. Moreover, an improved coronary reserve may reduce the ischaemic risk of the hypertrophied myocardium. However, not all antihypertensive drugs seem equally effective in bringing about coronary regression of left ventricular hypertrophy (LVH). No regression or little regression has been found with diuretic monotherapy despite a satisfactory reduction in blood pressure. On the other hand, a trend towards a regression has been observed in patients in whom treatment with clonidine significantly reduced catecholamines.

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Year:  1985        PMID: 2937889

Source DB:  PubMed          Journal:  J Hypertens Suppl        ISSN: 0952-1178


  8 in total

Review 1.  Therapeutic effect on left ventricular hypertrophy by different antihypertensive drugs.

Authors:  W Motz; B E Strauer
Journal:  Clin Investig       Date:  1992

2.  Hemodynamic and neurohumoral effects of moxonidine in patients with essential hypertension.

Authors:  V Mitrovic; W Patyna; J Hüting; M Schlepper
Journal:  Cardiovasc Drugs Ther       Date:  1991-12       Impact factor: 3.727

Review 3.  Drug treatment of hypertension.

Authors:  B N Prichard
Journal:  Drugs       Date:  1988       Impact factor: 9.546

4.  Relation of cardiovascular risk factors to right ventricular structure and function as determined by magnetic resonance imaging (results from the multi-ethnic study of atherosclerosis).

Authors:  Harjit Chahal; Craig Johnson; Harikrishna Tandri; Aditya Jain; W Gregory Hundley; R Graham Barr; Steven M Kawut; Joao A C Lima; David A Bluemke
Journal:  Am J Cardiol       Date:  2010-05-13       Impact factor: 2.778

5.  Regression of left ventricular hypertrophy and systolic function in hypertensive patients during long-term treatment with ketanserin.

Authors:  V Coto; M Cocozza; U Oliviero; A Lucariello; T Picano; B Castaldo; V Iovino; L Cacciatore
Journal:  Cardiovasc Drugs Ther       Date:  1990-01       Impact factor: 3.727

6.  Regulation of c-Fos and c-Jun gene expression by phospholipase C activity in adult cardiomyocytes.

Authors:  Tushi Singal; Naranjan S Dhalla; Paramjit S Tappia
Journal:  Mol Cell Biochem       Date:  2009-02-19       Impact factor: 3.396

7.  Propranolol and thyroxine-induced hypertrophic rabbit hearts: effect on heart size and regional O2 supply/consumption variables.

Authors:  G J Grover; J M Houghton; H R Weiss
Journal:  Basic Res Cardiol       Date:  1988 May-Jun       Impact factor: 17.165

Review 8.  Upregulation of Phospholipase C Gene Expression Due to Norepinephrine-Induced Hypertrophic Response.

Authors:  Paramjit S Tappia; Naranjan S Dhalla
Journal:  Cells       Date:  2022-08-11       Impact factor: 7.666

  8 in total

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