CHF and angiotensin II receptor antagonists

[progers]

Guys,

I have recently seen a cardiologist who is a heart failure specialist and he thinks I have congestive heart failure. I have always had diastolic problems, as do most people with HCM but I have new symtoms, such as nocturnal dyspenea etc. My new heart failure doc (who is not an HCM specialist) has put me on Candesartan, which is an 'angiotensin II receptor antagonist'. Does anyone know anything about this drug for people with HCM? I do know that it should not be used in people with obstruction because it can worsen symptoms, but following my myectomy, I no longer have obstruction.

Cheers,

Paul

[AnnetteP]

Wow, nearly a year after this question was posted, a new study has come out supporting the use of candesartan in non-obstructive patients. This study found that "candesartan reduced the symptoms of HCM, including decreasing the thickening of the left ventricle." Here's the "but": "This effect was found to be dependent on the underlying gene mutations in each patient."

Interesting study. Here is the link if you care to read an article on it:
http://www.genengnews.com/news/bnitem.aspx?name=47676970

[EmilysDad]

Very interesting. It seems to favor the B-myosin long chain sarcomeric mutation, which is pretty common. The full article is only available by subscription but here's the Abstract:

The Effects of Candesartan on Left Ventricular Hypertrophy and Function in Nonobstructive Hypertrophic Cardiomyopathy. A Pilot, Randomized Study
Martin Penicka*@, Pavel Gregor*, Roman Kerekes{dagger}, Dan Marek{ddagger}, Karol Curila*, Jiri Krupicka{sect}, and

From the Cardiocenter,* Third Faculty of Medicine, Charles University and University Hospital Kralovske Vinohrady, Prague; the Department of Internal Medicine,{dagger} Associated Medical Institution, Krnov; the First Department of Medicine–Cardiology,{ddagger} University Hospital Olomouc; and Department of Cardiosurgery,{sect} Na Homolce Hospital, Prague, Czech Republic

@ To whom correspondence should be addressed. E-mail: penicka@fnkv.cz.


Abstract

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.