Heart Failure/Cardiomyopathies Flashcards
Order of most effective for decreasing mortality in heart failure of ACEi/ARBs, mineralocorticoid antagonists, beta blockers
Best mortality benefit in beta blockers, then mineralocorticoid receptor antagonists, then angiotensin acting drugs
HOCM - affected gene
- cardiac myosin binding protein C most common
- Beta myosin heacy chain second most common
Most common cause of death in young athletes
HOCM
Indications for ICD in HOCM
1) Left ventricular wall thickness >30 mm
2) Family history of premature sudden cardiac death
3) Previous cardiac arrest/ventricular tachycardia
4) Previous episodes of documented non-sustained VT (>3 beats, rate >120 bpm)
5) Unexplained syncope
Drugs to avoid in HF
NSAIDS, pioglitazone, ?metformin, TNF blockers, TCAs, corticosteroids, non-dihydropyridine CCBs
Most characteristic feature of HOCM on ECHO
- Ratio of septal to posterior wall thickness greater than 1.3: 1.0
NYHA Classification
I: No limitations normal physical activity
II: Slight limitation. Ordinary physical activity results in fatigue, palpitations, dyspnoea or angina
III: Marked limitation of physcial activity. Less than ordinary activity results in symptoms
IV: Unable to carry out any physical activity without discomfort
What murmur usually accompanies obstructive HOCM
Mitral regurgitation - holosystolic murmurbest heard at lower left sternal border as well as the apex
Medications useful in HOCM
- Beta blockers- ameliorate angina and syncope
- Amiodarone- reduce frequency of supraventricular arrythmias
- Non-dihydropyridine ca blocker- reduce the stiffness of the left ventricle, reduce the elevated diastolic pressures, increase exercise tolerance, and, in some instances, reduce the severity of outflow tract pressure gradients.
- Disopyramide- reduce LV contractility
Medications not useful in HOCM
Digitalis, diuretics, nitrates, dihydropyridine calcium blockers, vasodilators and betaadrenergic agonists are best avoided, particularly in patients with known LV outflow tract pressure gradients.
Alcohol ingestion may produce sufficient vasodilatation to exacerbate an outflow pressure gradient
Notes on loop diuretics
- E.g. furosemide, bumetanide, torsemide
- Work at Thick ascending limb loop of Henle, reduce reabsorption of NaCl, inhibit the Na/K/Cl co-transporter → increased delivery of Na to DCT (+ H+, K+, Cl-) → water follows by osmosis → diuresis
- Increase Na excretion by 20-25%, enhance free water clearance
- Maintain efficiency unless renal function severely impaired
- Acute heart failure → continuous infusion furosemide same outcome as 12 hour bolus IV
Associated electrolyte disturbances
- Hypo- Na, K, Cl, Ca, Mg,
- Metabolic alkalosis
- Hyperuricaemia (causes decreased uric acid secretion)
Notes on acetozolamide
- Carbonic anhydrase inhibitor
- Decreases proximal tubular sodium reabsorption
- Added to loop diuretics in heart failure, 500mg IV
- Increases sucess of decongestion in acute decompensation with previous chronic heart failure not treated with SGLT2 inhibitors
- No effect on mortality or heart failure rehospitalisation
Notes on thiazide diuretics (and thiazide like)
- E.g. bendroflumethiazide, indapamide, chlortalidone, metalazone
- Inhibit Na/Cl co-transporter in DCT of nephron → inhibits reabsorption of Na and water
- Synnergistic effect with loop diuretics
Electrolyte disturbances
- Hypo - Na, K
- Hyperglycaemia, hyperlipidaemia, hypercalcaemia, hyperuricaemia
Notes on Angiotensin Receptor-Neprilysin Inhibitors
- E.g. Valsartan/Sacubitril
- Neprilysin = degrades vasoactive peptides e.g. natriuretic peptides, bradykinin, adrenomedullin
- Valsartan/entresto reduces CV mortality/HF hospitalisation in patients with LVEF <35% compared to ACEI
Role of SGLT2 inhibitors in management of heart failure
- E.g. ampagliflozin, canagliflozin, dapagliflozin
- Inhibit sodium-glucose transport protein 2 in the kidney
- Inhibit glucose reabsorption kidney → reduces BSLs, also reduces sodium reabsorption in proximal tubule, improved sodium and water excretion
- Initially GFR falls by 5ml/min, albuminuria falls 30-40%
- Increased sodium delivery to macula densa → arterial vasoconstriction → normalises perfusion pressure, reduces rate in decline in GFR
- BP and cardiac preload and afterload also reduced
Benefits
- Reduces all cause death, CV mortality, hospitalisation for HF, and first adverse kidney outcome independent of age, sex, DM, ARNI treatment and baseline GFR
Notes on beta blocker therapy in CHF
- Beta blockers offer greatest mortality benefit in HFrEF
- Carvedilol
- Beta blocker + a1 blockade - vasodilation effect
- COMET Trial 2003 → patients with Class II-IV CHF, with EF <35% on diuretics and ACE randomised to carvedilol or metoprolol tartrate → reduction in mortality in carvedilol group
Drugs that reduce mortality in HFreF
Overall management of HFrEF
