Treatment of Heart Failure

Claire Hunter, MD

Treatment of Heart Failure

• Goals

• Improve quality of life

• Prolong life

• Ejection fraction most important prognostic factor

• Those with ejection fraction less than 20% have 50% 1-2 year survival

Treatment strategy

• Etiology of heart failure

• Precipitating agents of circumstances

• Evaluation of decompensation

• Nonpharmacologic and pharmacologic treatments

Etiology of Insult to myocardium

• Infarction/Ischemia--loss of myocyte function• Pressure overload• hypertensive heart disease• aortic stenosis• pulmonic stenosis• hypertrophic cardiomyopathy• Volume overload• aortic regurgitation • mitral regurgitation

Etiology continued

• Idiopathic dilated cardiomyopathy (may be viral)• Infiltrative in myocardium or interstitium• sarcoid• iron(hemochromatosis)• amyloid• radiation fibrosis• chemotherapeutic agents (anthracyclines)

Precipitating agents or circumstances

• Ischemia

• Dietary or medication noncompliance (sodium intake)

• Work overload--emotional stress or isometric activity

• Arrhythmias--atrial or ventricular

Evaluation of decompensation

• Dietary review• “Pill count”• Review social circumstances and enlist aid of

social worker if needed• Echocardiography--reassess left ventricular

function, valvular abnormalities• Arrhythmias• Ischemia evaluation (imaging stress or

angiography

Nonpharmacologic treatments

• Dietary reinforcements--2000 mg Na daily

• Rest (not necessarily bed rest)

• Decrease stress

• Assess any added medications that are deleterious

• nonsteroidal antiinflammatory agents

Pharmacologic treatments

• Positive inotropic agents

• digitalis

• catecholamines

• phosphodiesterase inhibitors

Digitalis

• Has not been proven to prolong survival

• Decreases hospitalizations

• Slight increase in arrhythmias

• Improves symptoms of congestion

Catecholamines

• Dobutamine (synthetic)

• Dopamine

• Increase heart rate and myocardial oxygen demand

• Tolerance to effects develops after 72 hours

• Have not been proven long term to improve survival

Phosphodiesterase Inhibitors

• Milrnone, amrinone

• In some trials increase mortality ( oral form and with chronic treatment)

• Short term intravenous treatment decreases pulmonary hypertension and left ventricular filling pressures; but may increase ventricular arrhythmias

Mechanism of heart failure

• Loss of myocardial function triggers

• SYMPATHETIC NERVOUS SYSTEM to compensate

• Cardiac output - heart rate x stroke volume

• Increases constricting and volume expanding hormones

Mechanism continued

• Failing heart down regulates B1 receptors

• Increased filling pressure in ventricle triggers plasma renin angiotensin system

(vasoconstriction and increased afterload)

Afterload reduction

• ACE inhibitors (angiotensin converting enzyme)

• ARB (angiotensin receptor blockers)

• Direct arterial dilators

Angiotensin converting enzyme inhibitors

• Proven to reduce development of overt heart failure in with asymptomatic left ventricular dysfunction

• Proven to prolong survival

• Reduce microalbuminuria in diabetics

Angiotensin Receptor Blockers

• Mortality results have been mixed in studies

• Beneficial symptomatically

• Whether equal to ACE inhibitors remains to be seen

Direct arterial dilators

• Hydralazine best oral example

• Nitroprusside best parenteral example

• Hydralazine used in combination with nitrates proven to prolong survival

• Not as good as ACE inhibitors at reducing mortality

Beta blockers

• Sympathetic activation• Leads to increased circulating catecholamines• By way of the B1 receptor they • Activate the Gs protein which• Activates adenylate cyclase which• Activates cAMP(increases)• Activate protein kinase• Leads to increased intracellular calcium• Leads to improved contractility

Beta receptor down regulation

• Occurs with sympathetic overstimulation

• Receptor uncoupling

• Leads to increased Gi (tonic inhibition)

• Calcium overload (toxic to myocardium)

Beta blockers

• Negative inotropic agents initially

• Restore B1 density and thus lead to

• Ultimate biologic improvement of ejection fraction

• Negate arrhythmogenic effects of catecholamines

Beta blockers

• Improve survival• Selective

• Sustained release metoprolol

• Bisoprolol

• Nonselective • Carvedilol (added value of antioxidant and

alpha effects)

Diuretics

• Treat volume overload

• Relieve symptoms of congestion

• Do not affect survival

• Do not alter remodelling

Diuretics continued

• Thiazides

• Loop diuretics

• Metolozone

Spironolactone

• Improves survival for Class III or IV heart failure

• Most likely due to effects on interstitium, not diuretic effects

• Potassium retention

• Beware of use in those whose creatinine is more than 2.5

Actions of BNP• Hemodynamic

balanced vasodilationcoronary arteries

• Neurohormonaldecreases aldosteronedecreases endothelin

• Renalincreases diuresisincreases natriuresis

BNP as a Therapeutic

Disease Management

• Telemonitoring

• Weekly educational mailings

• Medical claims declined by $1100 per patient in treatment group

• Claims increased $9600 in non-treatment group

Goals of Treatment

• Improve cardiac function and survival with• ACE inhibitors• Beta blockers• Diuretics if needed for symptoms• Spironolactone for Class III or IV

Accomplish these goals

• Decreasing sympathetic drive and its toxic effects on the myocardium

• Decreasing the constricting hormones that increase afterload and increase the work for the heart

• Positively impact remodelling so the heart can be more efficient