Pharmacologic Treatment of Chronic Systolic Heart Failure

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Pharmacologic

Treatment of Chronic

Systolic Heart Failure

John N. Hamaty D.O. FACC,

FACOI

Heart Failure

Final common pathway in most heart diseases

550,000 new cases each year

20.1/100,000 mortality rate

No change in mortality

Diastolic Heart Failure

Impaired ability to accept blood and relax during diastole

Both types increase with age, African

Americans

40-70% incidence more often female, obese, older HTN and less likely to have

CAD

Less symptomatic and lower morbidity and mortality

B-Adrenergic Receptor Blockers

Improve survival

Improve ejection fraction

Remodeling

Quality of life

Reduce SCD

Inhibiting adverse effects of the sympathetic nervous system

Diminish RAAS activation

Angiotensin-Converting Inhibitors

Decrease conversion of angiotensin I-II

Improve survival

Decrease rate of hospitalization

Improve symptoms

Inhibit neurohormonal activation

Reverse remodeling

Decrease incidence of SCD?

Angiotensin Receptor Blockers

Efficacy similar to ACE inhibitors

Alternative to ACEI in patients not tolerant of ACEI

VAL-HeFT- ACEI +B-BL+ARB increase morality

CHARM- improve mortality

Competitive Aldosterone

Antagonists

Aldosterone stimulates renal sodium retention and myocardial hypertrophy

Spironolactone decreases mortality and morbidity in NYH class III and IV

Selective Aldosterone Blockers

Eplerenone (EPHESUS Trial)-post acute myocardial infarction trial

When added to optimal medical therapy excluding spirnolactone

Reduced morbidity and mortality in patients with acute MI with left ventricular dysfunction and heart failure

Future: New Insights

Tissue doppler-decreased flow velocities predict LVH before it occurs

Ultrasonic tissue character-tissue edema, fibrosis and calcification. Can predict tissue damage before it occurs in HTN

Myocyte enhancer factor 2-developmental gene for CAD/nonischemic HF

Pharmacogenetics

Alpha-adducin gene-found it 2/3 HTN patients. Diuretics will not reduce risk

Adrenergic receptors- 2 variants in African

Americans. 10 fold risk of developing HTN and candidates for early tx with b-blockers

Conclusions

Antagonizing this neurohormonal cascade has been the focus of recent clinical trials.

Further directions in HF therapy are likely to focus on limiting or preventing activation of the neurohormonal cascade through earlier recognition and treatment of patients at risk for HF.

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