Efficacy, Tolerability, and Impact on Quality of Life of Long-Term Treatment with Manidipine or Amlodipine in Patients with Essential Hypertension

Zanchetti, Alberto; Omboni, Stefano; Commare, Paolo La; Cesaris, R. De; Palatini, Paolo

doi:10.1097/00005344-200110000-00017

Cited by 53 publications

(19 citation statements)

References 18 publications

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“…Recent data have shown that not all dihydropyridine calcium antagonists are created equal with regard to vasodilatory edema. The third generation agents, such as lercanidipine and manidipine, have been shown to cause less edema than amlodipine [4,5]. Thus, despite lowering blood pressure to the same extent, the incidence of edema in patients on manidipine was only 8% compared with 21% in those on amlodipine (P < 0.0001) [4].…”

Section: Comparative Findingsmentioning

confidence: 99%

“…The third generation agents, such as lercanidipine and manidipine, have been shown to cause less edema than amlodipine [4,5]. Thus, despite lowering blood pressure to the same extent, the incidence of edema in patients on manidipine was only 8% compared with 21% in those on amlodipine (P < 0.0001) [4]. Similarly, in a crossover study in patients who had side effects with other dihydropyridine calcium antagonists, the incidence of vasodilatory edema was significantly reduced when the patients were switched to lercanidipine at similar blood pressure levels [5].…”

Section: Comparative Findingsmentioning

confidence: 99%

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Vasodilatory edema: A common side effect of antihypertensive therapy

2002

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Vasodilatory edema, a common adverse effect of antihypertensive therapy with vasodilators, is related to several mechanisms, including arteriolar dilatation (causing an increase in intracapillary pressure), stimulation of the renin-angiotensin-aldosterone system, and fluid volume retention. Vasodilatory edema is dose-dependent and most common with direct arteriolar dilators such as minoxidil or hydralazine, and in decreasing order of frequency with the dihydropyridine calcium antagonists, a-blockers, antiadrenergic drugs, and nondihydropyridine calcium antagonists. Not all dihydropyridine calcium antagonists are created equal with regard to vasodilatory edema. At an equal antihypertensive efficacy, lercanidipine and lacidipine are associated with less vasodilatory edema than amlodipine and nifedipine. The addition of an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) to a dihydropyridine calcium antagonist significantly reduces vasodilatory edema. In contrast, the addition of a diuretic has little effect on vasodilatory edema. Thus, low-dose combination therapy (of a dihydropyridine calcium antagonist with either an ACE inhibitor or an ARB) may be preferred over high-dose monotherapy.

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Section: Comparative Findingsmentioning

confidence: 99%

Section: Comparative Findingsmentioning

confidence: 99%

Vasodilatory edema: A common side effect of antihypertensive therapy

2002

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“…However, when reported by patients as 'leg swelling', one of these thirdgeneration CCBs has been associated with an oedema incidence of 22%. 26 Thus, although differences among CCBs in oedema incidence rates have been reported in a number of studies, 10,[27][28][29][30] it is evident that dose-dependent peripheral oedema remains a common side effect in patients receiving both established and newer CCBs. 10,31 Factors that may influence oedema Several factors can predispose the patient to an increased risk of oedema.…”

Section: Mechanism Of Ccb-induced Oedemamentioning

confidence: 99%

Mitigation of calcium channel blocker-related oedema in hypertension by antagonists of the renin–angiotensin system

Sierra

2009

J Hum Hypertens

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This review is aimed at examining calcium channel blocker (CCB)-related oedema and how this can be attenuated through the use of agents that inhibit the renin-angiotensin system. CCBs are effective antihypertensive agents, but their propensity for causing oedema may reduce compliance. A review of the literature has indicated that the absolute incidence of this side effect is difficult to determine because reported rates vary widely, a factor that may stem from differences in the surveillance technique (active vs passive). In a recent trial incorporating active surveillance, 25% of patients who received amlodipine 10 mg per day experienced oedema. CCB-induced oedema is caused by increased capillary hydrostatic pressure that results from preferential dilation of pre-capillary vessels. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) cause postcapillary dilation and normalize hydrostatic pressure, and are thus ideally suited for prevention/reversal of CCB-induced oedema. The efficacy of this strategy was proven using both subjective and objective techniques. ARB/CCB and ACEI/CCB combination therapy is also more effective than CCB monotherapy in controlling blood pressure. These combinations represent an important advance in the management of hypertension.

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“…3,4 With any form of edema, most physicians simply add a diuretic to the antihypertensive regimen. Unfortunately, diuretics have little effect on VDE.…”

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confidence: 99%

Vasodilatory edema: a common side effect of antihypertensive therapy

Messerli

2001

American Journal of Hypertension

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Ever since hydralazine, edema has been a welldocumented adverse effect of vasodilators. Pathogenesis of vasodilatory edema (VDE) is related to at least three mechanisms which include the following:1. Arteriolar vasodilation increases intracapillary pressure, thereby exuding fluid into the interstitium. 2. Many vasodilators stimulate the renin-angiotensin aldosterone system. 3. The kidney senses any fall in arterial pressure as decreased fullness of the circulation, erroneously interprets it as due to volume depletion, and in an attempt to restore arterial filling paradoxically retains sodium. 1Vasodilatory edema is dose dependent and most pronounced with arteriolar dilators (minoxidil, hydralazine), followed by the dihydropyridine calcium antagonists (DHP-CCBs), the alpha blockers, the anti-adrenergic drugs and the non-DHP-CCBs. Dihydropyridine calcium antagonists cause VDE predominantly by mechanisms 1 and 3 and less by stimulating the renin angiotensin system. However, because CCBs have a natriuretic effect, generalized salt retention is less than with the arteriolar dilators or the anti-adrenergic drugs. Vasodilatory edema is more common in women than in men, perhaps because women have a higher tendency to edema than men, or simply because they look at their ankles more carefully. Among the available DHP-CCBs, little difference in VDE has been documented, although no solid head-to-head comparisons allow us firm conclusions. With amlodipine and felodipine, VDE occurs in about 5% of patients with the 5 mg dose, in 25% with the 10 mg, and in more than 75% with 20 mg.2 The third generation CCBs, lecarnidipine and manidipine, cause considerably less VDE than amlodipine. 3,4 With any form of edema, most physicians simply add a diuretic to the antihypertensive regimen. Unfortunately, diuretics have little effect on VDE. Diuretics merely diminish fluid retention but do not affect the vasodilatory mechanism of the edema, which with CCBs is far more predominant. Indeed, as shown by Weir et al, 5 a decrease in VDE did occur with the addition of a diuretic. However, a greater reduction of VDE was achieved with the addition of an angiotensin-converting enzyme (ACE) inhibitor to the CCB. As a corollary to this elegant observation, we showed in a larger patient population 5 a similar reduction of VDE associated with CCB therapy by the addition of an ACE inhibitor. Adding an ACE inhibitor not only allows the VDE to melt away but also further lowers arterial pressure. In the study of Weir et al 5 and our study, 6 the combination of amlodipine 5/benazepril 20 had greater antihypertensive efficacy than monotherapy with amlodipine 10 mg. However, a study duration of 4 weeks is insufficient for amlodipine to exert its full effect, which takes up to 2 to 3 months to attain.After a few weeks of monotherapy, the physician may be faced with the dilemma of whether to uptitrate the CCB or resort to combination therapy. Given that the incidence of VDE with higher doses CCB therapy is substantial, adding an ACE inhibitor may be the prefe...

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Efficacy, Tolerability, and Impact on Quality of Life of Long-Term Treatment with Manidipine or Amlodipine in Patients with Essential Hypertension

Cited by 53 publications

References 18 publications

Vasodilatory edema: A common side effect of antihypertensive therapy

Vasodilatory edema: A common side effect of antihypertensive therapy

Mitigation of calcium channel blocker-related oedema in hypertension by antagonists of the renin–angiotensin system

Vasodilatory edema: a common side effect of antihypertensive therapy

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