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  • CONGESTIVE HEART FAILURE Marcy W. Long, MMS, PA-C Baylor Scott and White Health Round Rock Cardiology

  • DISCLOSURES

    •No Relevant disclosures

  • OBJECTIVES

    •Discuss epidemiology of heart failure •Define the different types of heart failure • Explain the different heart failure classifications • Review heart failure pathophysiology •Discuss strategies for heart failure treatment with

    focus on HFrEF

    • Keep the Audience awake and interested in heart failure after lunch

  • DEFINITIONS • Heart failure, sometimes known as congestive heart failure,

    occurs when your heart muscle doesn't pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently. • The Mayo Clinic

  • DEFINITIONS • As blood flow out of the heart slows, blood returning to the heart

    through the veins backs up, causing congestion in the body's tissues. Often swelling (edema) results. Most often there's swelling in the legs and ankles, but it can happen in other parts of the body, too. • Sometimes fluid collects in the lungs and interferes with breathing,

    causing shortness of breath, especially when a person is lying down. This is called pulmonary edema and if left untreated can cause respiratory distress. • Heart failure also affects the kidneys' ability to dispose of sodium and

    water. This retained water also increases swelling in the body's tissues (edema).

    • The American Heart Association

  • TYPES OF HEART FAILURE

  • CHARACTERISTICS

  • WHEN THE LEFT HAS LOST…..

  • DEFINITIONS OF HEART FAILURE • Classification EF (%) Description • HFrEF • ≤ 40 Also referred to as systolic HF. Randomized clinical trials have mainly enrolled patients with

    HFrEF, and it is only in these patients that efficacious therapies have been demonstrated to date

    • a. HFpEF Borderline • 41 to 49 These patients fall into a borderline or intermediate group. Their characteristics,

    treatment patterns, and outcomes appear similar to those of patients with HFpEF

    • b. HFpEF Improved • > 40 It has been recognized that a subset of patients with HFpEF previously had HFrEF. These

    patients with improvement or recovery in EF may be clinically distinct from those with persistently preserved or reduced EF. Further research is needed to better characterize these patients

  • DEFINITIONS OF HEART FAILURE

    • HFpEF

    • ≥ 50 Also referred to as diastolic HF. Several different criteria have been used to further define HFpEF. The diagnosis of HFpEF is challenging because it is largely one of excluding other potential noncardiac causes of symptoms suggestive of HF. To date, efficacious therapies have not been identified

  • EPIDEMIOLOGY

    • 5.7 Million adults have heart failure in the United States • About half of people who develop heart failure die within 5 years of

    diagnosis • Heart disease is the leading cause of death for African American and white

    women in the United States • Heart failure is the only major cardiovascular disorder on the rise. An

    estimated 400,000 to 700,000 new cases of heart failure are diagnosed each year and the number of deaths in in the United States from this condition has more than doubled since 1979, averaging 250,000 annually

  • EPIDEMIOLOGY

    • Annually, >1 Million patients are hospitalized with the primary diagnosis of heart failure in the United States

    • Heart failure is the leading cause of hospitalization among adults >65 years of age in the United States

    • The total cost of heart failure care in the US exceeded $30 billion annually in 2012 • Health care costs, medications, lost of productivity

    • Estimated that total heart failure costs in the US will exceed $70 billion by 2030

    • CDC, AHA

  • HEART FAILURE PATHOPHYSIOLOGY What is happening to my heart?

  • Activation Neurohormonal Cascade

    Sympathetic nervous system (SNS) Renin-angiotensin-aldosterone system (RAAS) Arginine-vasopressin (AVP) and endothelin (ET) axis

  • NEUROHORMONAL ACTIVATION Sympathetic Nervous System

    • Epinephrine, Norepinephrine • Tachycardia, éContractility, éSystemic Vascular Resistance

    RAAS • Angiotensin II, Aldosterone (Salt

    retention, vasoconstriction, LV remodeling)

    Arginine Vasopressin • Water Retention

    Endothelial Hormones • Endothelin (potent vasoconstrictor) • Prostacyclin, Prostaglandin E, Nitrous

    Oxide (potent vasodilators)

    Natriuretic Peptides • ANP and BNP

  • SOME CONSEQUENCES OF PATHWAY ACTIVATION

    Tachycardia and Increased Contractility • Acutely: Improves cardiac output and blood pressure • Chronically: Increases myocardial oxygen consumption, myocardial ischemia, atrial

    & ventricular arrhythmias

    Salt and Water Retention • Acutely: Supports blood pressure (BP) & cardiac output (CO) • Chronically: Vascular congestion, peripheral & pulmonary edema, SOB, orthopnea

    Peripheral Vasoconstriction • Acutely: Supports blood pressure (BP) & cardiac output (CO) • Chronically: Decreases cardiac output & organ perfusion

  • CLASSIFICATION OF HEART FAILURE

    • NYHA Functional Classification

    • Class I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. • Class II Slight limitation of physical activity. Comfortable at rest, but

    ordinary physical activity results in symptoms of HF. • Class III Marked limitation of physical activity. Comfortable at rest, but

    less than ordinary activity causes symptoms of HF. • Class IV Unable to carry on any physical activity without symptoms of

    HF, or symptoms of HF at rest.

  • STAGES OF HEART FAILURE

    • Stage A: High risk for developing HF, but without structural heart disease • Stage B: Structural Heart Disease (low EF, LVH, prior MI, Valve

    disease), but never experienced CHF symptoms • Stage C: Structural Heart Disease w/ current or prior

    symptoms • Stage D: Refractory Heart Failure despite guideline directed

    medical therapy.

  • ACCF/AHA Stages of HF NYHA Functional Classification

    A At high risk for HF but without structural heart disease or symptoms of HF None

    B Structural heart disease but without signs or symptoms of HF I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF.

    C Structural heart disease with prior or current symptoms of HF I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF.

    II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF.

    III Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF.

    IV Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest. Yancy C et al. Circulation 2013;128:e240-e327

    D Refractory HF requiring specialized interventions

  • WHAT IS BEHIND THE TREATMENT • Beta Blockers

    • ACEi

    • ARB

    • Aldosterone antagonist

    • Hydralazine/Isosorbide dinitrate

    • ARNI

    • Ivabradine

  • BETA BLOCKERS

    ¯ 23%1959 pts/ 1.3y Carvedilol

    MI 3-21d, EF < 40%, on ACEI

    CAPRICORN Lancet 2001

    ¯ 32%2647 pts/ 1.3y Bisoprolol

    NYHA III-IV and EF < 35%

    CIBIS-II Lancet 1999

    ¯ 48% in death/hosp/incr meds

    1094 pts/ 6-12m Carvedilol

    NYHA II-III and EF < 35%

    US Carvedilol HF Study Group Circulation 1996

    ¯ 17% in carvedilol3029 pts/ 4.8y Carved vsmetop

    NYHA II-IV and EF < 35%

    COMET Lancet 2003

    ¯ 35%2289 pts/ 10.4m Carvedilol

    NYHA IV and EF < 25%

    COPERNICUS NEJM 2001

    ¯ 19%3991 pts/ 1y Metoprolol XL

    NYHA II-III and EF < 40%

    MERIT-HF JAMA 2000

    Mortality# pts/ dur/ drugEntry CriteriaTrial

  • ACE INHIBITORS

    ¯ 28% vs isordil/hydral

    804 pts/ 6m-5y Enalapril v I/H

    EF

  • ANGIOTENSIN RECEPTOR BLOCKERS

    • ARB + ACEI ¯ 16% • No incr death in ACEI/ARB/beta

    2548 pts/ 2y Candesartan vs placebo

    NYHA II-IV EF

  • ALDOSTERONE ANTAGONIST • The effect of Spironolactone on morbidity and mortality in patients with severe

    heart failure. Randomized ALdactone Evaluation Study (RALES)

    • Randomized, double blind, placebo controlled trial • To evaluate the effect of Spironolactone on survival of patients with history of

    NYHA Class IV symptoms due to reduced LV systolic function on optimal medical therapy including ACEi

    • Baseline Therapy: ACEi 95%, Beta-blockers 11%, Digoxin 74%, Loop diuretics 100% • Primary Outcome: All cause mortality (35% vs 46% p

  • HYDRALAZINE/ISOSORBIDE DINITRATE

    • V-HEFT I, V-HEFT II, A-HEFT (vasodilator studies vs. placebo, vasodilators vs. ACEi, African American Heart failure trial ACEi/ARBs,BB, diuretics with addition of vasod