Left ventricular assist devices (VAD) /Heart transplant
Compassionate end of life care/hospice
Therapeutic Objectives
Protect/Preserve myocardium
Improve hemodynamics
Prevent ischemic events
Prevent sudden arrhythmic death
Pharmacologic treatment of HF
Diuretic (if evidence of fluid retention)
ACE inhibitor or ARB (assuming no CI)
β-blocker
ARNI (angiotensin-receptor-neprilysin inhibitor)
Digoxin
Aldosterone antagonist
Nitrates/Hydralazine
Sodium-glucose cotransporter type 2 (SGLT2)
Calcium Channel Blockers
Anticoagulation
Antiarrhythmics
RAAS
Renin-angiotensin-aldosterone system
SGLT2
Sodium-glucose cotransporter type 2
HFpEF
Heart failure with preserved ejection fraction
HFrEF
Heart failure with reduced ejection fraction
Treatment algorithm for patients with ACC/AHA Stage A and B heart failure
1. Assess etiology
2. Plan treatment strategy
Guideline-directed medical therapy (GDMT)
ARNI or ACE inhibitor or ARB
Evidence-based β-blocker
Aldosterone antagonist
Sodium-glucose cotransporter-2 (SGLT2) inhibitor
ARNI
Angiotensin receptor II receptor blocker/neprilysin inhibitor
ACE inhibitor
Angiotensin-converting enzyme inhibitor
ARB
Angiotensin II receptor blocker
β-blockers
Carvedilol, Metoprolol succinate, and Bisoprolol prolong survival, decrease hospitalizations, reduce the need for transplantation, and promote "reverse remodelling" of the left ventricle
β-blockers are recommended for all patients with HFrEF unless contraindicated
Therapy must be instituted at low doses, with slow upward titration to the target dose
Recent evidence suggests that ARNI sacubitril/valsartan is preferred over ACE inhibitors (or ARBs) for HFrEF unless other circumstances (eg, affordability) are present in individual patients
The ARNI, sacubitril/valsartan, is approved to treat patients with HFrEF and many with HFpEF
In patients with HFrEF, ARNI is preferred over either ACE inhibitors or ARBs to improve survival, slow disease progression, reduce hospitalizations, and improve quality of life
Patients receiving ACE inhibitors or ARBs can be switched to ARNI or ARNI can be used as initial treatment in patients with newly detected HFrEF without previous exposure to ACE inhibitors or ARBs
The doses for these agents should be targeted at those shown in clinical trials to improve survival
SGLT2 inhibitors dapagliflozin or empagliflozin reduce the risk of cardiovascular death, hospitalization, and worsening HF in patients with HFrEF
In addition, dapagliflozin and empagliflozin improve complex outcomes in patients with HFpEF
In both HFrEF and HFpEF, these benefits were demonstrated in patients with and without type 2 diabetes
SGLT2 inhibitors require assessment of renal function prior to initiation
Chronic loop diuretic therapy frequently is used in patients with HFrEF or HFpEF, but it is not mandatory
Diuretic therapy is required only in those patients with peripheral edema and/or pulmonary congestion
Many patients will need continued diuretic therapy to maintain euvolemia after fluid overload is resolved
Step 1 medications for HFrEF Stages C and D
ARNI or ACE inhibitor or ARB
Evidence-based β-blocker
Aldosterone antagonist
Sodium-glucose cotransporter-2 (SGLT2) inhibitor
Diuretics
Decrease Na and water retention to reduce preload, decrease signs/symptoms of fluid retention, improve exercise tolerance, quality of life, and cardiac function, reduce HF hospitalizations
Diuretics do not alter disease progression or prolong survival
Diuretics should not be used alone in patients with HF
All patients with evidence of fluid retention require diuretics
Many patients require chronic diuretic therapy to maintain euvolemia
Body weight changes are a sensitive marker of fluid retention/loss
Patients should report weight gain of > 0.25-0.5 kg/day over several days
Thiazide diuretics
Weak diuretics with more persistent antihypertensive activity than loop diuretics, infrequently used alone in HF, can use with loop diuretics to promote diuresis, preferred in some patients with mild fluid retention & elevated BP
Loop diuretics
Furosemide, bumetanide, toresmide, mainstay of HF therapy, efficacy reduced by competitors of the organic acid transport pathway, excess dietary Na+, co-administration with NSAIDs, efficacy maintained in impaired renal function