Recent guidelines in the Management of Heart failure.pptx

Medical management of heart failure

1. Recent guidelines in the Management of Heart failure Moderator : Dr. Prabhu, Professor, Dept of General Medicine Presentor: Dr.T.Aravindan, Post graduate

2. Definition : AHA defines Heart failure as a complex clinical syndrome that results from structural or functional impairment of ventricular filling or ejection of blood, which in turn leads to the cardinal clinical symptoms of dyspnea and fatigue and signs of HF, namely edema and rales. one-half of patients who develop HF have a normal or preserved EF (EF ≥50%). Prevalence in European countries: HF is approximately one in five for a 40-year-old.

3. Pathogenesis Index event —> impact on heart muscle – loss of cardiac myocytes —> inability of the myocardium to generate force The index event can be a sudden onset event, insidious onset, or a genetic event Initially asymptomatic - RAAS and the adrenergic nervous system activation or activation of countervailing vasodilatory molecules ANP, BNP, Bradykinin, Prostaglandin, NO Neprilysin

4. LV Remodeling Stimuli : Mechanical stretch of the myocyte, circulating neurohormones (e.g., norepinephrine, angiotensin II), inflammatory cytokines (e.g., tumor necrosis factor [TNF]), other peptides and growth factors Response: Myocyte hypertrophy; alterations in the contractile properties of the myocyte; - Progressive loss of myocytes through necrosis, apoptosis, and autophagic cell death; - β-adrenergic desensitization;

5. Reorganization of the extracellular matrix with dissolution of the organized structural collagen weave surrounding myocytes Left ventricular (LV) dilation Increased LV sphericity LV wall thinning Mitral valve incompetence Increasing LV dilation also results in tethering of the papillary muscles – mitral regurgitation lesion can form

6. Myocardial relaxation is an adenosine triphosphate (ATP)-dependent process that is regulated by uptake of cytoplasmic calcium into the SR by SERCA2A If ATP decreased, as in Ischemia, slowed myocardial relaxation, shortened Left ventricular filling. Elevated LV filling pressures increases in pulmonary capillary pressures Dyspnea results

7. Biomarkers BNP NT - pro BNP ST 2 GALECTIN 3

8. Stages of Heart failure Stage A: At Risk for HF : Without symptoms, structural heart disease, or cardiac biomarkers of stretch or injury Stage B: Pre-HF : No symptoms or signs of HF and evidence of 1 of the following : Structural heart diseases Evidence for increased filling pressures Persistently ncreased BNP or TROP I (in the absence of competing diagnoses)

9. Stage C: Symptomatic HF : Structural heart disease with current or previous symptoms of HF. Stage D: Advanced HF : Marked HF symptoms that interfere with daily life and with recurrent hospitalizations despite attempts to optimize GDMT.

10. Classification of HF by LVEF HF with reduced EF : LVEF ≤40% HF with improved EF : Previous LVEF ≤40% and a follow-up measurement of LVEF >40% HF with mildly reduced EF: LVEF 41%–49% Evidence of spontaneous or provokable increased LV filling pressures (e.g., elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement) HF with preserved EF : LVEF ≥50%

11. Investigations Initial Laboratory work up and a 12 lead Electrocardiographic Testing Use of Biomarkers : BNP or NT-proBNP to establish prognosis, risk stratification, and inform the trajectory of the patient Causes of increased Natriuretic peptide Cardiac : HF, including RV HF syndromes, ACS, Heart muscle disease, including LVH, Pericardial disease, AF, Myocarditis , Cardiac surgery Cardioversion, Toxic-metabolic myocardial insults

12. Noncardiac causes : Advancing age, Anemia, Renal failure, Pulmonary : Obstructive sleep apnea, severe pneumonia, pulmonary embolism, pulmonary arterial hypertension Critical illness: Bacterial sepsis Severe burns

13. Stage wise management approach At Risk for HF (Stage A) : Primary Prevention healthy lifestyle, controlled Blood pressure and blood sugars If diabetic and with high cardiovascular risk, SGLT2i should be used to prevent hospitalizations of HF Genetic counseling

14. Stage B (Patients With Pre-HF) LVEF ≤40%, ACEi should be used Recent or remote history of MI or ACS, statins should be used If both the above condition, beta blockers - to reduce mortality If At least 40 days post-MI with LVEF ≤30% and NYHA class I symptoms while receiving GDMT and have expected survival for >1 year, ICD recommended Contraindications : thiazolidinediones and nondihydropyridinecalcium channel blockers

15. Stage “C”- Heart failure If fluid retention - Diuretics are recommended to relieve congestion, improve symptoms, and prevent worsening HF. If not respond to moderate-or high-dose loop diuretics, can add thiazide (e.g., metolazone) HFrEF and NYHA class II to III symptoms, the use of ARNis recommended to reduce morbidity and mortality. If intolerant to ACEi and ARNi not available, ARBs can be preferred

16. Contd., Stage C HFrEF, with current or previous symptom, 1 out of 3 beta blockers : bisoprolol, carvedilol, sustained-release metoprolol succinate (economic) NYHA class II-IV symptoms, Mineralocorticoid Receptor Antagonists (MRAs) Provided - eGFRis >30 mL/min/1.73 m2and serum potassium is <5.0mEq/L Sodium-Glucose Cotransporter 2 Inhibitors : reduce hospitalization for HF and cardiovascular mortality, irrespective of the presence of type 2 diabetes.

17. HFrEFwho cannot be given first-line agents, such as ARNi, ACEi, or ARB, because of drug intolerance or renal insufficiency, combination of hydralazine and isosorbide dinitrate Other Drugs : HF class II to IV symptoms, omega-3 polyunsaturated fatty acid (PUFA) supplementation Drugs that can worsen or not recommend in HF: HFrEF, class IC antiarrhythmic medications DPP-4 inhibitors saxagliptin and alogliptin increase the risk of HF Thiazolidinediones, calcium channel blockers, Vit E, NSAIDS

18. Chronic HFrEF (LVEF ≤35%) who are receiving GDMT, including a beta blocker at maximum tolerated dose, and who are in sinus rhythm, Ivabradine can be used Symptomatic HFrEFdespite GDMT, Digoxin can be used If recent worsening of HF : an oral soluble guanylate cyclase stimulator (vericiguat) HF With Preserved Ejection Fraction : ACE inh, B blockers nitrates or phosphodiesterase-5 inhibitor

19. ESC Definition of Advanced HF (Stage D) Severe and persistent symptoms of HF (NYHA class III [advanced] or IV) Severe cardiac dysfunction defined by ≥1 of these: - LVEF ≤30% •Isolated RV failure •Nonoperable severe valve abnormalities •Nonoperable severe congenital heart disease •EF ≥40%, - elevated natriuretic peptide levels and evidence of significant diastolic dysfunction

20. Hospitalizations or unplanned visits in the past 12 mofor episodes of: •Congestion requiring high-dose intravenous diuretics or diuretic combinations •Low output requiring inotropes or vasoactive medications •Malignancies Severe impairment of exercise capacity with inability to exercise or low 6-minute walk test distance

21. Novel trials and targets CHARM trial - ARBs - effective in reducing hospitalisations , morbidities and mortalities I-PRESERVE DIG trial - no role for digoxin in the treatment of HFpEF Phosphodiesterase-5 inhibitor sildenafil improved filling pressures and right ventricular function (20 mg TDS for 3 months) NEAT-HFpEF study - Isosorbide mononitrate did not improve exercise capacity ALDO-DHF trial - only Echo findings of diastolic failure improved, no exercise capacity improvement

22. Contd. ARB with an endopeptidase inhibitor, LCZ696, —-> Increases the generation of myocardial cyclic guanosine 3′,5′-monophosphate Thus enhances myocardial relaxation, and reduces ventricular hypertrophy Reduces circulating natriuretic peptides and reduce left atrial size to a significantly greater extent — PARAGON-HF (pivotal trial under process)

23. Novel therapies that are failing in the Trials Serelaxin , a recombinant form of relaxin 2 hormone – improved dyspnea but gradually worsened heart failure Ularitide - a novel vasodilator - no long term beneficial outcome Omecamitiv mecarbil - Omecamtiv mecarbil (OM) is a myosin specific activator that increases myocardial contractility independent of calcium fluxes. OM increases the number of myosin heads that are able to connect and pull-on actin filaments during systole GALACTIC-HF trial- significant reduction of 8%

24. Thank you