1. secondary HF therapies
1.1. HCN channel blocker
1.1.1. ivabradine
1.1.1.1. add on or sub for BB
1.1.1.2. AE: bradycardia, HTN, afib, luminous phenomena (visual brightness)
1.1.1.3. CI: ONLY used in pts with LVFH + normal sinus rhythm and HR
1.2. SGLT-2 inhibitor
1.2.1. dapagliflozin; empagliflozin
1.2.1.1. added therapy; excess glucose excretion enabled thru SGLT2 inhibition; reduced BG levels
1.2.1.2. CI: ONLY used in pts with HF +DM
2. acute decompensated HF
2.1. nesiritide
2.1.1. binds to vascular SM->
2.1.1.1. increased cGMP cascade of intracellular events ->
2.1.1.1.1. SM relaxation/dilation
2.1.2. AE: hypotension, HA, tachycardia
2.2. milrinone, inamrinone
2.2.1. IV; vasodilator//positive inotrope
2.2.2. AE: ventricular arrhythmias, thrombocytopenia; hypersensitivity
2.2.3. CI: furosemide in IV line w/ these 2 drugs
2.2.4. goal: short term use then transition to usual HF meds
2.2.5. inamrinone is longer acting
3. investigational drugs
3.1. vasopeptidase inhibitors
3.1.1. block ACR and endopeptidase -> better dilation
3.2. Cytokine antagonists
3.2.1. TNF blockers
3.3. endothelin antagonists
3.3.1. block endothelin receptors or endothelin formation -> less vasoconstriction
4. non pharm txts
4.1. restrict sodium intake, restrict fluid intake, caloric supplementation (cardiac cachexia: muscle wasting and unintentional weight loss), CPAP for HF and obstructive sleep apnea, cardiac rehab (reduces morbidity and mortality), pneumococcal and flu vaccine
5. AVOID in HF PTS
5.1. antiarrhythmic agents
5.1.1. can exert cardio depresseant and proarrhythmic effects
5.1.2. exception: amiodarone
5.2. calcium channel blockers
5.2.1. can lead to worsening HF
5.2.2. associated w/increase risk of cardiovascular events
5.3. NSAIDS
5.3.1. can cause NA retention, peripheral vasoconstriction
5.3.2. enhance toxicity of diuretics and ace inhibitors (increase BP, increase HR)