Regression of Left Ventricular Hypertrophy in the Short-Term Treatment of Hypertension With Isradipine

Saragoça, M A; Portela, Jorge E.; Abreu, Patrícia; Plavnik, FL; Vanneta, Adália; Ajzen, H; Ramos, Oswaldo L.

doi:10.1093/ajh/4.2.188s

Cited by 16 publications

(2 citation statements)

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“…The short-term effects of isradipine on reversing LVH were studied in 20 patients with mild to moderate hypertension. 170 Mean LVMI decreased significantly after both 45 and 90 days of therapy (p<O.OOl). No significant differences in changes in LVMI were noted between patients receiving isradipine monotherapy and those requiring the addition of a diuretic to keep diastolic blood pressure below 90 mm Hg (62% of patients).…”

Section: Calcium Channel Blockersmentioning

confidence: 89%

Hypertension and Left Ventricular Hypertrophy: Is Drug Therapy Beneficial?

Eselin

Carter

1994

Pharmacotherapy

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Left ventricular hypertrophy (LVH) is a consequence of long-standing hypertension and is considered to be an independent risk factor for cardiovascular morbidity and mortality. Several antihypertensive agents are capable of inducing regression of LVH, but it is not known which class of drugs is most effective. The impact of drug-induced reversal of hypertrophy on ventricular function remains a controversial issue. Furthermore, the long-term clinical benefits of LVH regression have yet to be documented. Controversies also exist regarding the clinical outcomes associated with drug-induced LVH regression.

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Section: Calcium Channel Blockersmentioning

confidence: 89%

Hypertension and Left Ventricular Hypertrophy: Is Drug Therapy Beneficial?

Eselin

Carter

1994

Pharmacotherapy

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“…Clinical and experimental data indicate that treatment of hypertension with antihypertensive drugs induces regression of myocardial hypertrophy [3][4][5][6][7][8][9]11 ]. However, significance of this phenomenon for cardiac function remains unclear [10].…”

Section: Abstract: Hypertension; Treatment; Myocardial Hypertrophy; mentioning

confidence: 99%

Myocardial hypertropy in rabbits with renovascular hypertension under pharmacological blockade of angiotensin II synthesis and its interaction with specific receptors

et al. 1999

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The dynamics of blood pressure, the weight of the heart and its subdivisions, and morphology of myocardium were studied in the rabbits with experimental renovascular hypertension. Treatment with inhibitors of angiotensin II synthesis (lotensin) or its interaction with specific receptors (valsartan) decreased blood pressure and the weight of the left ventricle, but did not affect the interrelations between structural elements in the heart, which remained the same as in hypertension-induced myocardial hypertrophy. In addition, these drugs impaired some parameters of cardiac activity attesting to myocardial overload, increase in collagen content in the myocardium, and decrease in the ratio of the numbers of capillaries and mitochondria to the weight of myofibrils. Key Words: hypertension; treatment; myocardial hypertrophy; regressionClinical and experimental data indicate that treatment of hypertension with antihypertensive drugs induces regression of myocardial hypertrophy [3][4][5][6][7][8][9]11 ]. However, significance of this phenomenon for cardiac function remains unclear [10]. Our aim was to study the effect of regression of myocardial hypertrophy on the structure and function of "hypertensive heart". MATERIALS AND METHODSExperiments were performed on 40 male Chinchilla rabbits weighing 2.5-3.5 kg. The animals were divided into four groups of 10 rabbits: controls (sham-operated) and rabbits with renovascular hypertension modeled according to P. Page untreated and treated with lotensin, an inhibitor of plasma angiotensin-converting enzyme blocking synthesis of angiotensin II (Ciba, 50Department of Pathological Physiology, University of Peoples' Friendship, Moscow; Ins[itute of Pathology, Heidelberg University mg per os daily for 6 weeks) or valsartan, a blocker of angiotensin receptors (10 mg per os daily, Ciba).In acute experiments carried out 6 weeks after surgery, blood pressure was measured with an eleclromanometer in the proximal part of the carotid arlery. In addition, the peak systolic pressure was measured in both ventricles under normal conditions and under isovolumic contractions caused by a 5-see occlusion of the ascending aorta (lor left ventricle) and pulmonary artery (tor right ventricle). Wet and dry weights of the left and right ventricles and right atrium were determined. The data were used to calculate the duration of systolic phases and the real and maximum intensity of ventricular function (IVFr and IVFm, respectively) as the ratio of real (or maximum) isovolumic peak systolic pressure in the corresponding ventricle to its weight [1]. The samples were embedded in Araldite. The semithin and ultrathin sections prepared with a Reichert-Jung Ultracut ultramicrotome were examined under light and Zeiss-10 electron

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