What’s New in Heart Failure

Recognize and treat before symptomatic HF HFpEF vs HFrEF OMT/GDMT Treatment of HFrEF Advanced therapies defibrillators, CRT, transplant End of life issues

HF is a clinical syndrome characterized by typical symptoms that may be accompanied by signs caused by a structural or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress.

Terminology: (historical and based on measurement of LVEF) HFrEF < 40% HFpEF > 50% HFmrEF 40-49% Differentiation of patients based on LVEF is important due to differing underlying etiologies, demographics, comorbidities and response to therapies

Diagnosis of HFpEF is more challenging than the diagnosis of HFrEF LV is not dilated, instead typically LVH and LAE and signs of increased filling pressures are present Impaired LV filling (diastolic dysfunction) best determined by complicated echo criteria Not all HFpEF is due to diastolic dysfunction PAH Valvular HD Non cardiac pathology may mimic or exacerbate HF (anemia, CKD, liver disease, obesity, OSA/OHS, COPD)

Epidemiology 1-2% of Adult population ≥ 10% of those >70 years old 1/6 of patients > 65 years with DOE will have unrecognized HF(mainly HFpEF) Patients with HFpEF are older, more often women, HTN, AF

Diagnosis of HFpEF Signs and Symptoms overlap with HFrEF LVEF ≥ 50% Increased BNP Relevant structural heart disease LVH, LAE Diastolic Dysfunction Echo Parameters mitral inflow velocities mitral annular motion LA volume TR velocities

Naturetic Peptides BNP < 100 NT-pro BNP < 300 Negative predictive valves are high Positive predictive valves are lower Common triggers of increased BNP besides HF: AF, CKD, PE, Pulmonary HTN, COPD, Sepsis, CVA, Anemia, cirrhosis, cancer chemo Rx, HTN Obesity may lead to a low BNP

Diuretic Therapy: Clinical Considerations Use in all patients with vascular congestion and continue in most patients with prior vascular congestion Torsemide has better absorption and longer duration Hypotension and Azotemia- slow down the diuresis Don’t stop as long as patient remains asymptomatic with mild to moderate decrease in BP (~90 mmHg) or increase in creat (>2)

Diuretic Therapy continued With advanced HF medication absorption decreases Add metolazone for “sequential nephron blockade”, IV option Remember magnesium supplementation Fluid retention unresponsive to increasing diuretic therapy with declining BP and azotemia = ominous sign

ACEI Clinical Considerations In clinical practice majority of HF patients receive suboptimal doses Preferred over ARB’s because of greater experience and weight of evidence as to effectiveness Contraindications: angioedema, anuric RF, pregnancy Caution: hypotension (syst BP <80-90) creatinine > 3mg ldl, serum K+ >5.5, bilateral RAS No difference between available ACEI’s as to effects on symptoms or survival NSAI can block favorable effects

Beta blockers- Clinical Considerations Carvedilol, metoprolol succinate, bisoprolol, nebivolol ACEI and Bbl are complementary and can be started together in the stable HF patient Do not delay the addition of Bbl in the stable patient because of failure to reach higher target ACEI dose. Start at low dose and gradually up titrate Metoprolol succinate causes less abrupt hypotension and bradycardia than carvedilol

Mineralocarticoid Receptor Antagonist (MRA) Spironolactone, Eplerenone Benefit: Maintenance of higher serum K+ Blockade of harmful aldosterone effects Clinical Considerations: Avoid other K+ sparing diuretics (amiloride, triamterene) Do not use if GFR ≤ 30ml/min GFR 30-50ml/min, initial does 12.5mg/day If K+ ≥ 5.5, stop Avoid NSAI, K+ containing salt substitute

Angiotensin Receptor Neprilysin Inhibitor (ARNI) Sacubitril/Valvsartan = Entresto Neprilysin inactivates various vasodilating and naturetic hormones Sacubitril increases vasoactive and naturetic hormones, decreasing after load and increasing diuresis Valsartan ARB Paradigm- HF Reduced CV mortality and hospitalization in HF patients as well as reduced all cause mortality compared to a proven dose of ACEI (enalapril)

Sacubitril / Valsartan Clinical Considerations Replace ACEI as first line Rx or use in those who remain symptomatic despite OMT? Contraindicated concomitant ACEI/ARB (stop for 36hrs prior) Pregnancy, angioedema, aliskrien in diabetic Caution- elderly, volume depletion (decrease diuretic does), CKD, NSAI, lithium

Ivabradine (Corlanor) HR reduction is a potential therapeutic target in HFrEF Ivabradine slows HR by inhibition of If channel in SAN SHIFT- Ivabradine reduced composite of CV death or hospital admission for worsening HF, benefits were associated with reduced HR.

Ivabradine (Corlanor) Clinical Considerations: Of possible use in HFrEF in SR with HR ≥70 bpm on maximum tolerated Bbl Not a substitute for Bbl Not to be used in AF Side effects: bradycardia, conduction abnormalities, HTN, AF, visual effects

Hydralazine- Isosorbide Dinitrate (H-ISDN) No clear evidence of benefit in all patients with HFrEF Black patients (African decent) H-ISDN reduced mortality and HF hospitalization Consider in symptomatic HFrEF patients who are ACEI/ARB intolerant

Digoxin Effect on mortality and hospitalization- unclear Patients with AF and HFrEF digoxin may be useful to slow VR when other therapies not available Digoxin provides symptom relief (but not mortality benefit), thus digoxin should not be used in asymptomatic patients in SR Symptomatic patients on OMT, addition of digoxin is reasonable

Medications to avoid in HFrEF Glitazones NSAI Diltiazem/verapamil Addition of an ARB to an ACEI

Prevention of SCD-ICD Indications

Cardiac Resynchronization Therapy

Treatment of HFpEF Diuretics for vascular congestion Control of HTN (MRA may be of benefit) Control of HTN Maintenance/restoration of SR Rate Control /AC if in AF Exercise training is the only intervention shown to improve exercise capacity and QOL Treat contributing factors and comorbidities HTN, lung disease, OSA, CAD, AF, CKD, obesity, DM