Heart failure

Epidemiology

Sputum analysis in patients with pulmonary edema may show heart failure cells (hemosiderin-containing cells).
- Pulmonary venous congestion may result in intra-alveolar bleeding. Macrophages that subsequently phagocytose the erythrocytes are called “heart failure cells.” These cells may also be detected in the sputum of patients with pulmonary infarction, vasculitis, or aspiration of blood.
- Their color is most likely due to hemosiderin from ingested erythrocytes.

Pasted image 20230723213037.png

ECG-CHF triad
1. Low QRS voltages in the limb leads (caused by peripheral edema in CHF patients)
2. Left ventricular hypertrophy (prominent precordial QRS voltages)
3. Very slow R wave progression in chest leads (rS in V4)

Agent	Mortality Benefit
Angiotensin receptor-neprilysin inhibitor (e.g., sacubitril-valsartan) OR ACE inhibitor (e.g., lisinopril) OR Angiotensin II receptor blocker (e.g., losartan)	Yes
Beta blocker (e.g., metoprolol, carvedilol)	Yes
Mineralocorticoid receptor antagonist (e.g., spironolactone, eplerenone)	Yes
Sodium-glucose cotransporter-2 inhibitor (e.g., dapagliflozin, empagliflozin)	Yes
Diuretic (e.g., furosemide, metolazone)	No, only improves symptoms & reduces hospitalization.
Digoxin	No, only reduces hospitalization.

Explanation

Spironolactone also block the deleterious effect of aldosterone on the heart, causing regression of myocardial fibrosis and improvement in ventricular remodeling.

Angiotensin receptor-neprilysin inhibitors (ARNIs)
- Drug names: sacubitril/valsartan
  - To block the vasoconstrictive effect of angiotensin II accumulation, sacubitril needs to be combined with an ARB.
    - Neprilysin is a zinc-dependent metalloprotease that cleaves peptides at the amino side of hydrophobic residues and inactivates several peptide hormones including glucagon, enkephalins, substance P, neurotensin, oxytocin, and bradykinin.
- Indication: Stage C or D HFrEF (preferred initial agent for RAAS inhibition)