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Pharmacologic Treatment of Chronic Systolic Heart Failure

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.

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Pharmacologic Treatment of Chronic Systolic Heart Failure

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  1. Pharmacologic Treatment of Chronic Systolic Heart Failure John N. Hamaty D.O. FACC, FACOI

  2. 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

  3. 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

  4. 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

  5. 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?

  6. 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

  7. Competitive Aldosterone Antagonists • Aldosterone stimulates renal sodium retention and myocardial hypertrophy • Spironolactone decreases mortality and morbidity in NYH class III and IV

  8. 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

  9. 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

  10. 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

  11. 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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