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Ramipril and telmisartan exhibit differential effects in cardiac pressure overload-induced hypertrophy without an additional benefit of the combination of both drugs.
J Cardiovasc Pharmacol Ther. 2013 Jan; 18(1):87-93.JC

Abstract

OBJECTIVES

We aimed to characterize different cellular effects of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin 1 (AT1) receptor blockers (ARBs) as mono- or combination therapy in cardiac pressure overload. Methods and

RESULTS

C57B1/6 mice received either the ACEI ramipril (2.5 mg/kg body weight), the ARB telmisartan (20 mg/kg body weight), or the combination. In all groups, pressure overload was induced by transverse aortic constriction (TAC). Cardiac hypertrophy (heart weight/tibia length) induced by TAC was reduced in all 3 treatment groups, with the most pronounced effect in the telmisartan group. The cardiomyocyte short-axis diameter and cardiac fibrosis were increased by TAC and similarly reduced by ACEI, ARB, and the combination therapy. The TAC-induced increase in the number of proliferating Ki67(pos) cardiomyocytes and noncardiomyocytes was reduced more potently by ACEI than by ARB. Four days of drug treatment induced a significant increase in Scal(pos)/VEGFR1(pos) endothelial progenitor cells (EPCs) in all animals in the treated SHAM groups. After 1 day of aortic constriction, only ramipril increased EPC numbers; after 5 weeks, telmisartan monotherapy did not change the EPC levels compared to vehicle or the combination therapy but raised it compared to ramipril. Neither TAC nor one of the therapies changed the number of cardiac capillaries per cardiomyocytes.

CONCLUSIONS

ACE inhibition and AT1 receptor blockade have beneficial effects in remodeling processes during cardiac pressure overload. There are small differences between the 2 therapeutical approaches, but the combination therapy has no additional benefit.

Authors+Show Affiliations

Klinik für Innere Medizin III, Kardiologie, Angiologie und Internistische Intensivmedizin, Universitätsklinikum des Saarlandes, Homburg/Saar, Germany. patrick-mueller@web.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22368266

Citation

Müller, Patrick, et al. "Ramipril and Telmisartan Exhibit Differential Effects in Cardiac Pressure Overload-induced Hypertrophy Without an Additional Benefit of the Combination of Both Drugs." Journal of Cardiovascular Pharmacology and Therapeutics, vol. 18, no. 1, 2013, pp. 87-93.
Müller P, Kazakov A, Semenov A, et al. Ramipril and telmisartan exhibit differential effects in cardiac pressure overload-induced hypertrophy without an additional benefit of the combination of both drugs. J Cardiovasc Pharmacol Ther. 2013;18(1):87-93.
Müller, P., Kazakov, A., Semenov, A., Jagoda, P., Friedrich, E. B., Böhm, M., & Laufs, U. (2013). Ramipril and telmisartan exhibit differential effects in cardiac pressure overload-induced hypertrophy without an additional benefit of the combination of both drugs. Journal of Cardiovascular Pharmacology and Therapeutics, 18(1), 87-93. https://doi.org/10.1177/1074248411434773
Müller P, et al. Ramipril and Telmisartan Exhibit Differential Effects in Cardiac Pressure Overload-induced Hypertrophy Without an Additional Benefit of the Combination of Both Drugs. J Cardiovasc Pharmacol Ther. 2013;18(1):87-93. PubMed PMID: 22368266.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ramipril and telmisartan exhibit differential effects in cardiac pressure overload-induced hypertrophy without an additional benefit of the combination of both drugs. AU - Müller,Patrick, AU - Kazakov,Andrey, AU - Semenov,Alexander, AU - Jagoda,Philippe, AU - Friedrich,Erik B, AU - Böhm,Michael, AU - Laufs,Ulrich, Y1 - 2012/02/24/ PY - 2012/2/28/entrez PY - 2012/3/1/pubmed PY - 2013/8/2/medline SP - 87 EP - 93 JF - Journal of cardiovascular pharmacology and therapeutics JO - J Cardiovasc Pharmacol Ther VL - 18 IS - 1 N2 - OBJECTIVES: We aimed to characterize different cellular effects of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin 1 (AT1) receptor blockers (ARBs) as mono- or combination therapy in cardiac pressure overload. Methods and RESULTS: C57B1/6 mice received either the ACEI ramipril (2.5 mg/kg body weight), the ARB telmisartan (20 mg/kg body weight), or the combination. In all groups, pressure overload was induced by transverse aortic constriction (TAC). Cardiac hypertrophy (heart weight/tibia length) induced by TAC was reduced in all 3 treatment groups, with the most pronounced effect in the telmisartan group. The cardiomyocyte short-axis diameter and cardiac fibrosis were increased by TAC and similarly reduced by ACEI, ARB, and the combination therapy. The TAC-induced increase in the number of proliferating Ki67(pos) cardiomyocytes and noncardiomyocytes was reduced more potently by ACEI than by ARB. Four days of drug treatment induced a significant increase in Scal(pos)/VEGFR1(pos) endothelial progenitor cells (EPCs) in all animals in the treated SHAM groups. After 1 day of aortic constriction, only ramipril increased EPC numbers; after 5 weeks, telmisartan monotherapy did not change the EPC levels compared to vehicle or the combination therapy but raised it compared to ramipril. Neither TAC nor one of the therapies changed the number of cardiac capillaries per cardiomyocytes. CONCLUSIONS: ACE inhibition and AT1 receptor blockade have beneficial effects in remodeling processes during cardiac pressure overload. There are small differences between the 2 therapeutical approaches, but the combination therapy has no additional benefit. SN - 1940-4034 UR - https://www.unboundmedicine.com/medline/citation/22368266/Ramipril_and_telmisartan_exhibit_differential_effects_in_cardiac_pressure_overload_induced_hypertrophy_without_an_additional_benefit_of_the_combination_of_both_drugs_ L2 - https://journals.sagepub.com/doi/10.1177/1074248411434773?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -