Control of blood pressure and reduction of echocardiographically assessed left ventricular mass with one‐daily timolol.

Rowlands, D. B.; Glover,; Stallard, T. J.; Littler, W. A.

doi:10.1111/j.1365-2125.1982.tb04939.x

Cited by 40 publications

(6 citation statements)

References 23 publications

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“…Increased sympathetic activity potentiates LVH. Sympatholytics, such as alpha-methyldopa [21,24]; angiotensin converting enzyme inhibitors, such as captopril and enalapril [22,25]; calcium channel blockers [26]; and beta blockers [20,27] have been associated with a decrease in LV mass during therapy. Vasodilator therapy, such as with hydralazine [28], has been shown to have no effect on LV mass, and the response to diuretic therapy has been variable [18].…”

Section: Discussionmentioning

confidence: 99%

“…In some studies of LVH regression, patients were included despite pretreatment values of LV wall thickness in the normal range [27,29]. In most studies of LVH regression, patients with hypertension and LVH have been under recent or active treatment previously with various antihypertensive drugs; these drugs are usually "washed out" for several days or weeks, and then a trial is begun with the study drug.…”

Section: Discussionmentioning

confidence: 99%

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Regression of left ventricular hypertrophy in ?Previously untreated? hypertensive blacks after 6 months of blood pressure reduction with alpha- and beta-adrenergic blockade and thiazide therapy

Foster

Plehn

Bernard

et al. 1992

Cardiovasc Drug Ther

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In 10 hypertensive black patients who were "previously untreated" (defined as no antihypertensive therapy for a minimum of 12 months prior to enrollment) and who had LVH (defined by an increase in both wall thickness and echocardiographically determined LV mass), we studied the effects of treatment with either labetalol, an alpha- and beta-adrenergic blocker (three patients), or labetalol plus hydrochlorothiazide (seven patients). After 6 months of effective antihypertensive therapy, there was a 12% decrease in LV mass for the entire group. However, the extent of LVH regression was highly variable among individual patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Regression of left ventricular hypertrophy in ?Previously untreated? hypertensive blacks after 6 months of blood pressure reduction with alpha- and beta-adrenergic blockade and thiazide therapy

Foster

Plehn

Bernard

et al. 1992

Cardiovasc Drug Ther

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“…This has been well demonstrated with beta blockers [2,8,9,14,17], converting-enzyme inhibitors [6,7,18,19], and centrally acting drugs [20]. Results with diuretics are still controversial.…”

Section: Discussionmentioning

confidence: 99%

“…Most antihypertensive drugs have been reported to induce regression of left ventricular hypertrophy (LVH) in hypertensive patients, and there are as yet unconfirmed data to suggest that reversal of cardiac hypertrophy is beneficial [1][2][3][4][5][6][7][8][9][10][11].…”

Section: Abstract Left Ventricular Hypertrophy Regression Calcium mentioning

confidence: 99%

Left ventricular mass changes with nicardipine therapy in essential hypertension

Gosse

Lacroix

Roudaut

et al. 1989

Cardiovasc Drug Ther

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Eighteen hypertensive patients (13 males, 5 females; age 48 +/- 13; diastolic blood pressure greater than 95 mmHg), either previously untreated or who had been off treatment for more than 3 months, underwent M-mode echocardiography before (DO) and after (D90) 3 months of nicardipine therapy (60-90 mg/day). All echocardiograms were read blind, and left ventricular mass (LVM) was calculated (Devereaux's formula). Blood pressure was significantly reduced after 3 months from 167 +/- 15/102 +/- 8 mmHg on DO to 152 +/- 16/92 +/- mmHg on D90 (p less than 0.001). The reduction in LVM was not significant: 266 +/- 95 g on DO, 247 +/- 78 g on D90. There was a trend to a higher (although nonsignificant) LVM reduction in patients with left ventricular hypertrophy at entry (-11%, n = 11) than in patients without left ventricular hypertrophy (-2%), n = 7).

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“…Measurements were performed after DOCA treatment (8 mg/kg SC) twice weekly for 20 and 40 days. Chlorthalidone was given daily (8 mg PO) simultaneously with DOCA in group treated for 20 days; in 40-day group, chlorthalidone was given daily over the last 20 sured daily over 24 hours for both treatment periods. Plasma samples (collected at the end of the treatment period) and urine were collected and frozen for estimation of sodium and potassium concentrations, which were measured in a flame photometer (Corning-EEL-100/13681, Evans Electroselenium Ltd, Essex, England).…”

Section: Methodsmentioning

confidence: 99%

Effects of chlorthalidone on ventricular hypertrophy in deoxycorticosterone acetate-salt hypertensive rats.

Cabral¹,

Carvalhinho²,

Vasquez³

et al. 1994

Hypertension

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Diuretics have been the mainstay of long-term treatment of hypertension, but there is no evidence suggesting that diuretics may be effective in reducing cardiac hypertrophy associated with hypertension. Thus, the present study was carried out to elucidate if long-term treatment with chlorthalidone (8 mg per animal per day added to food) affects the development of and reverses the ventricular hypertrophy in deoxycorticosterone acetate (DOCA) (8 mg/kg SC twice a week)-salt hypertensive rats. Chlorthalidone was given to one group during all 20 days of DOCA administration (preventive regimen) and to another group 20 days after DOCA treatment was initiated until the 40th day (therapeutic regimen). Chlorthalidone was found to reduce or prevent the development of ventricular hypertrophy, as assessed by a reduction in ventricular mass and cardiac protein as well as arterial hypertension. Both chlorthalidone regimens prevented the increase or induced a significant decrease in the plasma concentration of sodium and in cardiac sympathetic tone, which were both increased in DOCA-salt-treated rats. These data provide evidence that long-term chlorthalidone treatment is effective in preventing or reducing ventricular hypertrophy along with arterial hypertension. However, whether this is due to a reduction in plasma sodium or other additional mechanisms, such as a reduction in cardiac sympathetic tone, remains to be determined. with arterial hypertension, in recent years many J. \ -investigators have demonstrated that this associated ventricular hypertrophy is a phenomenon of multifactorial origin whose development is not solely dependent on an increased pressure load but also on local growth factors and cardioadrenergic activity.

show abstract

Control of blood pressure and reduction of echocardiographically assessed left ventricular mass with one‐daily timolol.

Cited by 40 publications

References 23 publications

Regression of left ventricular hypertrophy in ?Previously untreated? hypertensive blacks after 6 months of blood pressure reduction with alpha- and beta-adrenergic blockade and thiazide therapy

Regression of left ventricular hypertrophy in ?Previously untreated? hypertensive blacks after 6 months of blood pressure reduction with alpha- and beta-adrenergic blockade and thiazide therapy

Left ventricular mass changes with nicardipine therapy in essential hypertension

Effects of chlorthalidone on ventricular hypertrophy in deoxycorticosterone acetate-salt hypertensive rats.

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