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CONGESTIVE HEART FAILUREMarcy W. Long, MMS, PA-CBaylor Scott and White HealthRound 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 PATHOPHYSIOLOGYWhat is happening to my heart?
Activation NeurohormonalCascade
Sympathetic nervous system (SNS) Renin-angiotensin-aldosterone system (RAAS) Arginine-vasopressin (AVP) and endothelin (ET) axis
NEUROHORMONAL ACTIVATIONSympathetic 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/ 1.3yCarvedilol
MI 3-21d, EF < 40%, on ACEI
CAPRICORNLancet 2001
¯ 32%2647 pts/ 1.3yBisoprolol
NYHA III-IV and EF < 35%
CIBIS-IILancet 1999
¯ 48% in death/hosp/incr meds
1094 pts/ 6-12mCarvedilol
NYHA II-III and EF < 35%
US Carvedilol HF Study GroupCirculation 1996
¯ 17% in carvedilol3029 pts/ 4.8yCarved vsmetop
NYHA II-IV and EF < 35%
COMETLancet 2003
¯ 35%2289 pts/ 10.4mCarvedilol
NYHA IV and EF < 25%
COPERNICUSNEJM 2001
¯ 19%3991 pts/ 1yMetoprolol XL
NYHA II-III and EF < 40%
MERIT-HFJAMA 2000
Mortality# pts/ dur/ drugEntry CriteriaTrial
ACE INHIBITORS
¯ 28% vs isordil/hydral
804 pts/ 6m-5yEnalapril v I/H
EF <45% and NYHA II-III
V-HeFT IINEJM 1991
¯ 27%1986 pts/ 30mRamipril
MI w/in 2-9d and evidence of CHF
AIRELancet 1993
¯ 16%2569 pts/ 41mEnalapril
EF <35% and acute CHF (II-III)
SOLVD-rxNEJM 1991
¯ 24%1749 pts/ 24mTrandolapril
MI w/in 2-6d and EF <35%
TRACENEJM 1995
¯ 19% 2231pts/ 4yCaptopril
MI w/in 3-16d and EF <40%
SAVENEJM 1992
¯ 8% NS¯ 29% death/HF
4228 pts/ 37mEnalapril
EF <35% andNYHA I
SOLVD-prevNEJM 1992
¯ 31%253 pts/ 6mEnalapril
NYHA IVCONSENSUSNEJM 1987
MortalityNumber pts/ duration/ drug
Entry criteriaTrial
ANGIOTENSIN RECEPTOR BLOCKERS
• ARB + ACEI ¯ 16%• No incr death in ACEI/ARB/beta
2548 pts/ 2yCandesartan vs placebo
NYHA II-IVEF <40% On an ACEI
CHARM-addedLancet 2003
• NS: ACEI better5477 pts/ 2.7yValsartan v Captopril
Acute MI and CHFOPTIMAALLancet 2002
• V vs C: equivalent• V + C: the most adverse events
14703 pts/ 2yValsartan vs Captopril vs both
MI w/in 12h-10d + EF < 40% or CHF
VALIANTNEJM 2003
• ARB ¯ 20%-2028 pts/ 2yCandesartan vs plac
NYHA II-IV; EF <40% +ACEI intolerant
CHARM-alternLancet 2003
•Similar mortality•CHF hosp: ¯ 27%• death if ACEI/ARB/B
5010 pts/ 2yValsartan vs placebo
NYHA II-IV, EF < 40%90% on ACEI
Val-HeFTNEJM 2001
No superiority of one agent over another
3152 pts/ 1.5yLosartan v Captopril
>60y, EF < 40%,NYHA II-IV
ELITE-IILancet 2000
Mortality# Patients,Duration, Drug
Entry criteriaTrial
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<0.001) • Secondary Outcome(s): Death from CV causes (27% vs 37% p<0.001);
Hospitalization for cardiac causes (32% vs 40% p<0.001) • Pitt B, et al. NEJM 1999 Sep 2;341(10):709-17
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 vasodilators)
• Showed improved mortality benefits
• showed improved left ventricular function
• Trials published in NEJM 1986, 314:1547-52, NEJM 1991; 325:301-10, NEJM 2004;351:2049-2057
Angiotensin-Neprilysin Inhibition VS Enalapril in HF (PARADIGM-HF)
8442 patients
NYHA Class II-IV, EF < 40%, pro BNP ≥ 600
Randomized to LCZ696 VS Enalapril
1° Endpoint – CV Death, HF hospitalization
Secondary – Time to death, KCCQ, Time to new A fib, Renal function
NEJM 2014; 371: 993-1004.
PARADIGM-HF• Showed decrease in CV death• Showed decrease in over all Heart failure hospitalization• Showed decrease in overall mortality (death from any cause)
• But……..• Some side effects noted with both arms
• Hypotension ARNI > Enalapril• Elevated serum creatinine ARNI < Enalapril• Elevated potassium ARNI = Enalapril• Cough ARNI < Enalapril• Angioedema à with or without airway compromise ARNI > Enalapril
• NEJM 2014; 371: 993-1004.
IVABRADINE
• Works by selective inhibition of the If current channel at the SA node• Slows heart rate by blocking this channel. Has no negative inotropic effect
and no effect on ventricular repolarization• Major Trial was Shift Lancet. 2010 376(10):875-885
• Showed 5% absolute reduction in heart failure hospitalization as well as a 2% reduction in heart failure mortality
2017 ACC/AHA/HFSA FOCUSED UPDATE OF THE 2013 ACCF/AHAGUIDELINE FOR THE MANAGEMENT OF HEART FAILURE
HEART FAILURE PRESERVED EF TREATMENT
• In patients with increased risk, control blood pressure to <130/80• In these patients it is appropriate to use BB, ACEi, ARBS• Diuretics for salt and water retention• Control/treat comorbidities
• anemia• HTN• Atrial Fibrillation• Sleep apnea
HEART FAILURE WITH REDUCED EF TREATMENT STAGE A• Weight Loss, Healthy diet, Exercise
• Avoid Smoking, ETOH abuse, Illicit drug use
• Periodic evaluation for signs and symptoms of HF
• Evaluation of LV function in those with a strong family history of cardiomyopathy or received cardiotoxic drugs
• NEW HTN Recommendations• Optimal BP should be < 130/80 (Class I, LOE B-R)
• NEW BNP Recommendations• BNP-based screening followed by team-based care, including a cardiovascular specialist
optimizing GDMT, can be useful to prevent the development of left ventricular dysfunction (systolic or diastolic) or new-onset HF (Class II, LOE B-R)
HFREF STAGE B TREATMENT
• Aggressive risk factor modification• Medical therapy• ACEI (or ARB) & Beta Blockers• No role for digoxin or aldosterone antagonists
• ICD in selected patients• Coronary revascularization if evidence of ischemia and
viable myocardium• Valve replacement or repair in selected patients
HFREF STAGE C TREATMENT
MEDICATIONS• ACE-I/ARB’s or ARNI• Beta-Blockers• Aldosterone Antagonist• Possibly ISDN/Hydralazine• Possibly Ivabridine• Possibly Digoxin• Diuretics if needed
ADDITIONAL TXS• ICD VS CRT-D• Cardiac Rehab/Exercise Training• Consider Referral to Heart Failure
Specialist• New Systolic BP Target < 130 mmHg
(Class I, LOE C-EO)• Consider referral to advanced heart
failure specialist
HFREF STAGE C GUIDELINESRenin - Angiotensin System Inhibition• ACE-I (Class I, LOE A) or• ARBs (Class I, LOE A) or• ARNI (Class I, LOE B-R)
AND
HF Evidence-Based Beta Blockers• Metoprolol Succinate (Toprol XL)• Carvedilol• Bisoprolol
AND
Aldosterone Antagonism• Spironolactone• Epleronone
Recommended for patients with chronic HFrEF to reduce Morbidity and Mortality
HFREF STAGE C GUIDELINES
ACE-I is beneficial for patients with prior or current symptoms of chronic HFrEF to reduce morbidity and mortality (I, A)
ARB’s to reduce morbidity and mortality is recommended in patients with prior or current symptoms of chronic HFrEF who are intolerant to ACE-I because of cough or angioedema (I, A)
HFREF STAGE C GUIDELINESIn patients with chronic symptomatic HFrEF NYHA class II or III who
tolerate an ACE-I or ARB, replacement by an ARNI is Recommended to further reduce morbidity and mortality (I, B-R)
ARNI should NOT be administered concomitantly with ACE-I or within 36 hrs of the last dose of an ACE-I (III, B-R)
ANRI should NOT be administered to patients with a history of Angioedema (III, C-EO)
HFREF STAGE C GUIDELINES
IVABRADINE (IIa, B)
- To reduce HF Hospitalization in NYHA Class II – III, Stable Chronic HFrEF(LVEF < 35%), receiving guideline-directed evaluation and management including
- A Beta-Blocker at Maximum Tolerated Dose- Sinus Rhythm- A HR > 70 bpm at Rest
- Guideline Emphasizes to make sure patient is on Maximal B-blocker prior to initiating Ivabradine
HFREF STAGE D TREATMENTS
• Palliative Care
• Left Ventricular Assist Devices
• Orthotopic Heart Transplantation• Recipient heart replaced with donor heart
THANK YOU!