1. What’s New in Heart Failure

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

3. 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.

5. 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

6. 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)

7. 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

11. 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

12. 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

16. 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)

17. 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

19. 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

20. 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

21. 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

22. 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)

23. 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

24. 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.

25. 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

26. 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

27. 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

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

29. Prevention of SCD-ICD Indications

30. Cardiac Resynchronization Therapy

31. 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