Transcript 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
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.