Recent management in Heart Failure

Recent Updated Pathogenesis and Management of Heart Failure:The role of Angiotensin Receptor Blockers?

Dr. dr. ANWAR SANTOSO, SpJP(K), FIHA, FAsCC, FICA.Dept. of Cardiology Faculty of Medicine ~ University of IndonesiaNational Cardiovascular Centre Harapan Kita Hospital - INDONESIA

Diabetes is the No. 1 risk factor for HF in women with coronary diseaseBibbins-Domingo K Jr et al. Circulation.2004;110:1424-30.Adjusted hazard ratioDiabetesAtrial fibrillationMyocardial infarction >1 eventCreatinine clearance 35Left bundle branch blockLV hypertrophySystolic BP 1403.12.92.52.32.11.91.91.61.500.511.522.533.5HERS studyVBWG21. Bibbins-Domingo K, Lin F, Vittinghoff E, Barrett-Connor E, Hulley SB, Grady D, Shlipak MG. Predictors of heart failure among women with coronary disease. Circulation. 2004;110:1424-1430.

Investigators in the Heart and Estrogen/progestin Replacement Study (HERS) evaluated risk factors for developing HF in 2391 postmenopausal women with coronary disease who did not have HF at baseline.1 Of the nine predictors of HF among postmenopausal women with coronary disease, diabetes was the strongest risk factor (adjusted hazard ratio [HR],3.1; 95% confidence interval [CI], 2.34.2).

The Donkey Analogy Ventricular dysfunction limits a patient's ability to perform the routine activities of daily livingLets compare our heart to this donkey, and our body to the wagon that this donkey has to pull every day.

A healthy heart is like an energetic donkey, which without fatigue, pulls the wagon full of weights. Conversely, a diseased heart will have difficulty meeting metabolic demands (or pulling the wagon).

MAP = (SV x HR) x TPRSympathetic Nervous System ContractilityTachycardiaVasoconstrictionCompensatory Mechanisms: Sympathetic Nervous SystemDecreased MAPThe sympathetic nervous system ( SNS ) is stimulated due to a decrease in mean arterial pressure. Sympathetic outflow is increased to the heart and the peripheral circulation which causes an increase in the patients heart rate and an increase in contractility. In addition, vasoconstriction occurs which increases the peripheral vascular resistance. Stroke volume is subsequently increased which in turn increases mean arterial pressure. Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52. CNS sympathetic outflowDisease progression Cardiac sympatheticactivity1-receptors2-receptors1-receptorsVasoconstrictionSodium retentionMyocardial toxicityIncreased arrhythmias Sympatheticactivity to kidneys+ peripheral vasculatureActivationof RAS1-b1-Sympathetic Activation in Heart FailureThe sympathetic nervous systems goal is to increase cardiac sympathetic activity. This response is mediated through three receptors: Beta 1, Beta 2, and Alpha 1. In normal situations the Beta 1 receptor increases cardiac sympathetic activity. In heart failure patients, the Beta 1 and Beta 2 receptors are activated. Alpha receptors and their role is yet to be fully delineated.Beta 1, Beta 2, and Alpha 1 receptors lead to myocardial toxicity in the ventricles. Myocardial toxicity leads to decreased ejection fraction, arrhythmias, and tachyarrhythmias caused by sympathetic activation.Increase in sympathetic activity also affects the kidneys and peripheral vasculature through the Beta 1 and Alpha 1 receptors. This mediates activation of the renin-angiotensin system ( discussed on the next slide ), which causes vasoconstriction, sodium retention, and thirst. All of these responses causes the disease to progress.Prolonged neurohormone release also has direct adverse effects on the heart tissue itself. Norepinephrine, for example, is known to be directly cardiotoxic. In fact, studies have established that in patients with heart failure, the probability of survival is markedly worse for those whose plasma norepinephrine levels are >400 pg/ml than for those whose levels are