Ventricular and vascular remodeling — effects inhibitors ACE and a II receptor antagonists in hypertensive patients

Petrovic, J.; Petrovic, D.; Petrovic, M.; Petrasinovic, Zorica; Kanjuh, Vladimir; Ostojic, Miodrag

doi:10.1016/s0021-9150(00)81042-4

Cited by 2 publications

(3 citation statements)

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“…44 After six months of treatment, echocardiographically determined LVMI was reduced by 11.9% in patients receiving ramipril (n=25), 10.9% in patients receiving telmisartan (n=25), and 15.0% in patients receiving both ramipril and telmisartan (n=25). Thus, telmisartan 40 mg is as effective as ramipril 2.5 mg in producing LVH regression, with a combination of both drugs being even more effective.…”

Section: Telmisartan and Left Ventricular Hypertrophy -Clinical Evidencementioning

confidence: 95%

“…41 After 12 months of telmisartan treatment, mean SBP was reduced from 143.5+10 mmHg to 126+8 mmHg (p<0.001), and DBP from The effects of treatment with telmisartan 40 mg, ramipril 2.5 mg or a combination of the two drugs on LVMI have been compared in 75 middle-aged (40-59 years) patients with hypertension. 44 After six months of treatment, echocardiographically determined LVMI was reduced by 11.9% in patients receiving ramipril (n=25), 10.9% in patients receiving telmisartan (n=25), and 15.0% in patients receiving both ramipril and telmisartan (n=25). Thus, telmisartan 40 mg is as effective as ramipril 2.5 mg in producing LVH regression, with a combination of both drugs being even more effective.…”

Section: Telmisartan and Left Ventricular Hypertrophy -Clinical Evidencementioning

confidence: 95%

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Telmisartan Effectiveness on Left ventricular MAss Reduction (TELMAR) as assessed by magnetic resonance imaging in patients with mild-to-moderate hypertension — a prospective, randomised, double-blind comparison of telmisartan with metoprolol over a period of six months — rationale and study design

Friedrich

Dahlöf

Sechtem

et al. 2003

J Renin Angiotensin Aldosterone Syst

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The Telmisartan Effectiveness on Left ventricular MAss Reduction (TELMAR) trial will assess the effect of the angiotensin II (Ang II) receptor blocker, telmisartan, on left ventricular hypertrophy (LVH) compared with the b-blocker, metoprolol, at similar antihypertensive doses. The rationale is that antihypertensives reduce LVH, a cardiac adaptation to pressure overload, principally by pressure-related effects. Ang II plays a key role in pressure-independent mechanisms causing LVH, and angiotensin-converting enzyme (ACE) inhibitors induce more pronounced LVH regression than some other antihypertensives. Blocking Ang II Type 1 receptors may be more effective than ACE inhibition in reducing LVH. TELMAR is a prospective, randomised, double-blind, double-dummy, parallel-group trial. A total of 140 patients (age 18 80 years) with uncontrolled essential hypertension (mean daytime systolic blood pressure [SBP] >140 mmHg or diastolic blood pressure [DBP] >90 mmHg and/or night-time SBP >120 mmHg or DBP >70 mmHg, measured by ambulatory blood pressure monitoring [ABPM]) and left ventricular mass index related to height (LVMI) >0.8 g/cm for females, >1.1 g/cm for males (defined by magnetic resonance imaging [MRI]) will be randomised to once-daily telmisartan or metoprolol. The telmisartan dose will be 40 mg for the first two weeks, 80 mg for 5.5 months and 40 mg for the last two weeks. Metoprolol will be given at a dose of 47.5 mg for two weeks, 95 mg for 5.5 months and 47.5 mg for two weeks. Concomitant add-on medication with hydrochlorothiazide and amlodipine will be allowed. The primary endpoint is the percentage change in LVMI at treatment end versus baseline, using MRI. Secondary variables include blood pressure changes and response rates assessed by ABPM and manual cuff sphygmomanometry, and end-systolic wall stress, systolic left ventricular function (LVF) and diastolic LVF determined by MRI. A separate study was performed prior to the main trial to define the normal range of MRI data in an age-matched population.

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Section: Telmisartan and Left Ventricular Hypertrophy -Clinical Evidencementioning

confidence: 95%

Section: Telmisartan and Left Ventricular Hypertrophy -Clinical Evidencementioning

confidence: 95%

Telmisartan Effectiveness on Left ventricular MAss Reduction (TELMAR) as assessed by magnetic resonance imaging in patients with mild-to-moderate hypertension — a prospective, randomised, double-blind comparison of telmisartan with metoprolol over a period of six months — rationale and study design

Friedrich

Dahlöf

Sechtem

et al. 2003

J Renin Angiotensin Aldosterone Syst

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“…35 Initial, small-scale clinical studies reported only in abstract form provide evidence that telmisartan reduces LVH. [36][37][38] Ivanova and colleagues 39 , for example, detected a significant 10.9% reduction (P=0.02) in LVMI as determined by echocardiography in 24 patients with a baseline LVMI of 151.6 g/m 2 after the receipt of telmisartan 40-80 mg monotherapy for 24 weeks. The percentage reduction in 24-h mean systolic blood pressure was 10.9% and that in 24-h mean diastolic blood pressure was 10.6%.…”

Section: Effect Of Telmisartan On Left Ventricular Massmentioning

confidence: 99%

End-organ damage: does it really matter how we prevent it?

Dahlöf

2003

European Heart Journal Supplements

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Studying left ventricular hypertrophy (LVH) allows the most comprehensive evaluation of end-organ damage prevention. Clinical trials show that reninangiotensin-aldosterone system blockade confers protective effects that are not simply due to antihypertensive activity. Angiotensin II receptor blockers (ARBs), which offer specific and complete inhibition of the action of angiotensin II at the level of the angiotensin II type 1 (AT 1 ) receptor, have proved more effective than other antihypertensive classes in reversing LVH and interstitial collagen accumulation. The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, for example, showed that a losartan-based therapy resulted in better LVH regression than an atenolol-based one, despite similar blood pressure control with both treatment regimens. Other clinical studies demonstrated that ARBinduced reduction in fibrosis is linked to functional improvement. It is still not known whether more effective angiotensin II blockade will provide more complete LVH reversal, improve cardiac function, prevent damage to other target organs and enhance prognosis. To find the answer, The ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET) Trial Programme will compare 24-h active AT 1 blockade with telmisartan versus established angiotensinconverting enzyme (ACE) inhibition using ramipril versus AT 1 blockade plus ACE inhibition.

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Ventricular and vascular remodeling — effects inhibitors ACE and a II receptor antagonists in hypertensive patients

Cited by 2 publications

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End-organ damage: does it really matter how we prevent it?

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