Document Detail


The effects of candesartan on left ventricular hypertrophy and function in nonobstructive hypertrophic cardiomyopathy: a pilot, randomized study.
MedLine Citation:
PMID:  19074594     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypertrophic cardiomyopathy is caused by mutations in the genes that encode sarcomeric proteins and is primarily characterized by unexplained left ventricular hypertrophy, impaired cardiac function, reduced exercise tolerance, and a relatively high incidence of sudden cardiac death, especially in the young. The extent of left ventricular hypertrophy is one of the major determinants of disease prognosis. Angiotensin II has trophic effects on the heart and plays an important role in the development of myocardial hypertrophy. Here in a double-blind, placebo-controlled, randomized study, we show that the long-term administration of the angiotensin II type 1 receptor antagonist candesartan in patients with hypertrophic cardiomyopathy was associated with the significant regression of left ventricular hypertrophy, improvement of left ventricular function, and exercise tolerance. The magnitude of the treatment effect was dependent on specific sarcomeric protein gene mutations that had the greatest responses on the carriers of ss-myosin heavy chain and cardiac myosin binding protein C gene mutations. These data indicate that modulating the role of angiotensin II in the development of hypertrophy is specific with respect to both the affected sarcomeric protein gene and the affected codon within that gene. Thus, angiotensin II type 1 receptor blockade has the potential to attenuate myocardial hypertrophy and may, therefore, provide a new treatment option to prevent sudden cardiac death in patients with hypertrophic cardiomyopathy.
Authors:
Martin Penicka; Pavel Gregor; Roman Kerekes; Dan Marek; Karol Curila; Jiri Krupicka;
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Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't     Date:  2008-12-12
Journal Detail:
Title:  The Journal of molecular diagnostics : JMD     Volume:  11     ISSN:  1525-1578     ISO Abbreviation:  J Mol Diagn     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2008-12-30     Completed Date:  2009-05-05     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  100893612     Medline TA:  J Mol Diagn     Country:  United States    
Other Details:
Languages:  eng     Pagination:  35-41     Citation Subset:  IM    
Affiliation:
Cardiocenter, Third Faculty of Medicine, Charles University and University Hospital Kralovske Vinohrady, Prague, Czech Republic. penicka@fnkv.cz
Data Bank Information
Bank Name/Acc. No.:
ClinicalTrials.gov/NCT00430833
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MeSH Terms
Descriptor/Qualifier:
Adult
Angiotensin II Type 1 Receptor Blockers / administration & dosage*
Benzimidazoles / administration & dosage*
Blood Pressure / drug effects
Cardiac Myosins / genetics
Cardiomyopathy, Hypertrophic / complications*,  drug therapy,  genetics,  physiopathology
Carrier Proteins / genetics
Double-Blind Method
Female
Humans
Hypertrophy, Left Ventricular / drug therapy*,  genetics,  physiopathology
Male
Middle Aged
Mutation
Myosin Heavy Chains / genetics
Pilot Projects
Tetrazoles / administration & dosage*
Time Factors
Treatment Outcome
Ventricular Function, Left / drug effects*
Chemical
Reg. No./Substance:
0/Angiotensin II Type 1 Receptor Blockers; 0/Benzimidazoles; 0/Carrier Proteins; 0/Myosin Heavy Chains; 0/Tetrazoles; 0/myosin-binding protein C; EC 3.6.1.-/Cardiac Myosins; S8Q36MD2XX/candesartan
Comments/Corrections
Comment In:
J Mol Diagn. 2009 Jan;11(1):12-6   [PMID:  19056845 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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