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Do beta-blockers prolong survival in heart failure only by inhibiting the beta1-receptor? A perspective on the results of the COMET trial.

ESH: Eplerenone Provides Cardioprotective Benefits in Patients with Heart Failure Complicated By Myocardial Infarction

Characterizing the Young Patient With Aortic Dissection: Results From the International Registry of Aortic Dissection (IRAD)

J Card Fail. 2003 Dec;9(6):429-43.
Packer M.

Division of Circulatory Physiology, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.

Experimental and clinical studies indicate that carvedilol exerts multiple antiadrenergic effects in addition to beta(1)-receptor blockade, but the prognostic importance of these actions has long been debated. This controversy has now been substantially advanced by the results of the recently completed Carvedilol Or Metoprolol European Trial (COMET), which showed that carvedilol (25 mg twice daily) reduced mortality by 17% when compared with metoprolol (50 mg twice daily), P=.0017--a result that was consistent with the differences seen across earlier controlled trials with beta-blockers in survivors of an acute myocardial infarction and in patients with chronic heart failure. Questions have been raised about the interpretation of these findings in view of the fact that the trial did not use the dose or formulation of metoprolol that was shown to prolong life in a placebo-controlled trial (ie, Metoprolol CR/XL [Controlled Release] Randomized Intervention Trial in Heart Failure). Pharmacokinetic and pharmacodynamic analyses, however, indicate that the dosing regimen of metoprolol selected for use in the COMET trial produces a magnitude and time course of beta(1)-blockade during a 24-hour period that is similar to the dose of carvedilol targeted for use in the trial. These analyses suggest that the observed difference in the mortality effects of metoprolol and carvedilol is not related to a difference in the magnitude or time course of their beta(1)-blocking effects but instead reflect antiadrenergic effects of carvedilol in addition to beta(1)-blockade.


By Jill Stein

PARIS, FRANCE -- June 17, 2004 -- The angiotensin II receptor blocker telmisartan produces significantly greater left ventricular hypertrophy (LVH) regression than does the beta blocker carvedilol in hypertensive patients, according to study findings.

Presenting data on June 14th at the 14th meeting of the European Meeting on Hypertension, Domenico Galzerano, MD, from San Gennaro Hospital in Naples, Italy, said that the findings suggest that telmisartan provides an important mechanism beyond lowering blood pressure in producing LVH regression in hypertensive patients. "The greater LVH regression achieved with telmisartan may translate into improvements in the risk reduction for cardiovascular events," he added.

Researchers recruited 82 patients with mild to moderate hypertension and LVH to participate in the double-blind study. The patients were randomised to treatment with either telmisartan 80 mg or carvedilol 25 mg once daily for 44 weeks. No other antihypertensive treatment was allowed for the duration of the study.

Both drugs were well tolerated. Ten patients withdrew from the study because their diastolic blood pressure remained greater than 90 mm Hg, and 2 patients withdrew because of dizziness.

Significant reductions in 24-hour mean systolic and diastolic blood pressure were achieved with both telmisartan (P <.001) and carvedilol (P <.001) after treatment for 44 weeks.

The systolic blood pressure reduction achieved with telmisartan was 30.9 ± 9.0 mm Hg versus 28.7 ± 9.1 mm Hg with carvedilol. The difference between the 2 groups was not statistically significant.

The diastolic blood pressure decrease with telmisartan was 19.0 ±9.0 mm Hg, and the reduction achieved with carvedilol was 17.1 ±5.0 mm Hg. The difference between the 2 groups was not significant.

The results of 3-dimensional echocardiography showed that both drugs significantly reduced LV mass index after 44 weeks of treatment, P <.0001.

In telmisartan-treated patients, LV mass index was reduced by 21.9 ±5.9 g/m2, which represents a 15.7% reduction.

In carvedilol-treated patients, LV mass index was reduced by 12.8 ±3.5 g/m2, representing a 9.0 % regression. Telmisartan was significantly superior to carvedilol, P <.0001.

In addition, the use of magnetic resonance imaging to assess LVH regression yielded similar results: a 15.0% regression with telmisartan versus a 9.8% regression for carvedilol, P <.0001.

Overall, the results demonstrate that while telmisartan and carvedilol provide comparable antihypertensive efficacy, telmisartan is associated with significantly greater LVH regression, Dr. Galzerano said.

Left ventricular hypertrophy is a strong predictor of cardiovascular risk, especially in hypertensive patients, and LVH regression is a key objective when managing hypertension.

 

OBJECTIVES The goal of this study was to better characterize the young patient with aortic dissection(AoD).

BACKGROUND Aortic dissection is unusual in young patients, and frequently associated with unusual presentations.

METHODS Data were collected on 951 patients diagnosed with AoD between January 1996 and November 2001. Two categories of patients,  40 years and  40 years, were compared using chi-square cross tabulations for categorical and Student t test for continuous data.

 RESULTS Sixty-eight patients (7%) with AoD were  40 years of age. Compared with patients  40 years, younger patients were less likely to have a prior history of hypertension (p 0.05); however, younger patients were more likely to have Marfan syndrome, bicuspid aortic valve, and prior aortic surgery (all, p 0.05). Clinical presentations in the two age groups were similar; however, younger patients were less likely to be hypertensive (25% vs. 45%, p 0.003). The proximal aortas of young AoD patients were larger (all, p 0.05) compared with older patients. These differences in aortic size between age groups were not entirely related to Marfan syndrome. Mortality among young patients was similar to patients  40 years of age (22% vs. 24%, p NS), irrespective of the site of dissection.

CONCLUSIONS Compared with older patients with AoD, young patients have unique risk factors for dissection: Marfan syndrome, bicuspid aortic valves, and larger aortic dimensions. Surprisingly, the mortality risk for young AoD patients is not lower than older AoD patients.

 (J Am Coll Cardiol 2004;43:665–9)