Congestive Heart Failure
Due to Systolic Dysfunction

• Pharmacologic Therapy
• Beta-blockers-in heart failure
• ACE-inhibitors- use maximal dosages in heart failure
• Angiotensin blockers- instead of and as well as ace-inhibitor therapy with beta-blockers
• Spirinolactone in heart failure
• Nitrate and hydralazine combination for African-Americans

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• Prophylactic ICD therapy

Angiotensin blockers in heart failure

Val-HeFT

Val-HeFT was a large study of patients with stable heart failure with an ejection fraction under forty percent. In addition to conventional modern pharmacological therapy, participants received valsartan or placebo. The study found:

• a reduction in combined morbidity and mortality of 13.2 percent.
• a reduction in hospitalisation by 27.5%.
• no significant reduction in mortality alone.
• reduction (post-hoc analysis) in the combined end-point of morbidity and mortality in those not treated with an ace-inhibitor.

A neurohormonal study showed continued increase in BNP levels in the group that did not receive valsartan. In the group treated with valsartan, BNP levels decreased. Decreased levels were seen in all pharmacological subgroups, including those that received valsartan in addition to ace-inhibitor and beta-blocker therapy.

An echo substudy showed that the improvement in ejection fraction was greater in those treated with valsartan.

CHARM studies

The CHARM group of studies used candasartan in patients with heart failure. One of the studies involved participants with preserved systolic function, others those with impaired systolic function. Some of the findings of these studies include:

• those with impaired systolic function had an approximate 15% reduction in all cause mortality when
  • candasartan was used instead of an ace-inhibitor, and
  • candasartan was used as well as an ace-inhibitor.
• those with impaired systolic function had an approximate 20% reduction in the combined end-point of cardiovascular death or hospital admission for heart failure when
  • candasartan was used instead of an ace-inhibitor, and
  • candasartan was used as well as an ace-inhibitor.
• those with preserved systolic function did not have any significant reduction in all cause mortality and there was a trend towards reduction in the combined end-point of cardiovascular death and hospitalisation for heart failure.
• in contrast to Val-HeFT subgroup analysis showed benefit in those that had angiotensin blocker therapy added to the combination of ace-inhibitor and beta-blocker therapy.

Angiotensin blockers should be used in those that are intolerant of ace-inhibitors. It is important to emphasise that the strength of data for use of ace-inhibitors to reduce mortality is much stronger than for use of angiotensin blockers- thus a high threshold should be set to define intolerance to ace-inhibitor therapy.

Ideally, consideration should be given to the addition of angiotensin blockers in those already on ace-inhibitors, beta-blockers and aldosterone blockers. However, current restrictions on use of angiotensin blockers will not make this feasible, unless the patient is able to afford to purchase the angiotensin blocker.

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