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Heart Failure With Preserved Ejection Fraction Prof.M.Khalilullah New Delhi, India Former Prof. & Head of Cardiology, Director, G.B.Pant Hospital, New.

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Presentation on theme: "Heart Failure With Preserved Ejection Fraction Prof.M.Khalilullah New Delhi, India Former Prof. & Head of Cardiology, Director, G.B.Pant Hospital, New."— Presentation transcript:

1 Heart Failure With Preserved Ejection Fraction Prof.M.Khalilullah New Delhi, India Former Prof. & Head of Cardiology, Director, G.B.Pant Hospital, New Delhi Director, The Heart Centre, New Delhi

2 Ist Pulmonary Balloon Valvuloplasty 23 rd March, 1985 Percutaneous Catheter Commissurotomy in Rheumatic Mitral Stenosis. N Engl J Med 1985; 313:1515-1518 27 th March 1985 28 th March 1985 July 1985

3 1987 1 st Balloon Renal Angioplasty 1986 Before After Double-balloon valvuloplasty of tricuspid stenosis.Am Heart J. 1987 Nov;114(5):1232–1233 Balloon dilatation of valv. AS, 1986

4 PDA Closure 1988 ASD Closure 1991 VSD Closure,1995 PTCA 1987

5 What is the difference between HFpEF, diastolic dysfunction, and diastolic HF? Heart failure with preserved ejection fraction (HFpEF)  Preferred term (ACC/AHA)  Most often have abnormalities in diastolic function (non-diastolic abnormalities in CV function also) Diastolic heart failure / Diastolic dysfunction  Other common terms for HFpEF but less specific

6 HFpEF is not “benign” Similar functional decline, hospital readmission rates, economic costs as HFrEF

7 What are the risk factors for HFpEF?  For HF in general  Age  Hypertension  Obesity  Dyslipidemia  Insulin resistance  For HFpEF  Older, more hypertensive, and higher prevalence of AF (than in HFrEF)  CAD prevalence comparatively lower  More common in women (by 2:1)

8 Are any interventions effective for primary prevention of HFpEF?  Control hypertension  Main factor in development and progression  Lower systolic & diastolic according to guidelines  Treat hyperlipidemia and hyperglycemia  Reduces risk for HFpEF and HFrEF  Encourage smoking cessation, exercise, healthy diet  Weight reduction can prevent diabetes, AF, obstructive sleep apnea, hypertension

9 Diagnosis  Signs and symptoms  Impaired exercise tolerance, orthopnea, dyspnea, and signs suggestive of HF  History may include hypertension and atrial fibrillation  Diagnosed based on H&P exam, x-rays, BNP levels, & ECHO  Criteria for diagnosing HFpEF  Signs / sxs of HF  Preserved systolic LV function (EF ≥45%–50%)  Evidence of: diastolic LV dysfunction, elevated LV filling pressures or surrogate markers of diastolic LV dysfunction

10 Which diagnostic tests should the clinician order for patients with suspected HF?  Electrocardiography  Radiography  Echocardiography  Laboratory tests  Plasma BNP or NT-proBNP  CBC: ? anemia, serum electrolytes, creatinine, glucose, liver function, urinalysis  Renal function and electrolytes

11 What additional tests should clinicians consider for patients with suspected HFpEF?  Cardiac catheterization (for new-onset HF)  Left heart: measure LVEDP + coronary angiography  Right heart: if needed to evaluate valvular heart disease suggested by echo, or if pulmonary hypertension not explained by left heart disease  When abnormal myocardial function present (? Infiltrative processes, constriction, others), consider:  Myocardial or fat pad tissue CT or MRI

12 What is the role of BNP in diagnosis and management?  Levels usually lower in HFpEF than HFrEF  When elevated: strong independent predictors of clinical events in HFpEF  No consensus on use to guide medical therapy  NT-proBNP  Superior for evaluating suspected acute HFpEF  Sensitive & specific for Dx acute HF in emergency dept: >450 pg/mL ( 900 pg/mL (≥50y)  BNP  Falsely negative in up to 20% with HFpEF  Doesn’t correlate with symptoms

13 How should HFpEF be treated?  Reduce preload  Use diuretics and vasodilators  BUT NOTE: Assess Volume Status carefully as aggressive reduction may cause hypotension if hypertensive & normovolemic  Consider control of hypertension with vasodilators alone  Treat acute HFpEF  First-line therapy: Vasodilators  I.V. nitrates + furosemide (improve cardiac output and reduce the symptoms)  Nitroglycerin to relieve acute pulmonary edema  Avoid aggressive diuresis (may cause hypotension)  Heart rate control, with particular attention in rapid AF

14  Provide long-term treatment of hypertension  Improves diastolic tissue velocity in hypertension w/o HF  If no comorbid conditions: thiazide diuretics  If coronary atherosclerosis or AF: beta-blocker  Reduce / reverse adverse remodeling: ARBs  Manage Atrial Fibrillation  In HFpEF + AF: restore normal HR and NSR to improve symptoms (maybe not outcomes)  Rate control first: AV nodal blocking agents + β-blockers  Rhythm control: when rate control not achieved or when symptoms persist despite rate control  Immediate electrical cardioversion: new-onset AF and myocardial ischemia, symptomatic hypotension, or pulmonary congestion or rapid ventricular response uncontrolled by appropriate pharmacologic measures  Anticoagulation: to reduce thromboembolism risk

15 When should inotropic agents be considered?  Not indicated  Increase inotropy and heart rate  Have no lusitropic/diastolic relaxation effects  Studies on digoxin showed no significantly positive result

16 How does drug therapy for HFpEF differ from that of HFrEF?  Many of the same drugs are used but evidence differs  HFrEF: Improved mortality and morbidity with ACE inhibitors, ARBs, β- blockers, and aldosterone antagonists  HFpEF: No similar improvements found from the therapies  HFpEF focus: symptom relief, BP and heart rate control

17 Are any novel drug therapies being investigated for HFpEF?  Spirinolactone  Proven therapy for HFrEF  Under investigation for HFpEF (TOPCAT study)  Sildenafil (phosophodiesterase-5 inhibition)  In small study: Reduced pulmonary arterial pressure, improved right ventricular systolic function, reduced right atrial pressure, improved QOL  Efficacy being studied in larger RELAX trial

18 What are potential triggers of decompensation?  Dietary indiscretion  Use of NSAIDs  Medication nonadherence  Dysrhythmias (particularly AF)  Ischemia or infarction  Hypertension  Worsening renal function  Valvular cardiac disease  Alcohol abuse  Infection

19 What is the role of diet and monitoring weight?  Advise patients to weigh themselves daily  Unexpected weight gain may warrant prompt action  If weight gain, increased edema, other HF symptoms occur, patient should promptly call health care provider  Sodium restriction recommended in symptomatic HF  To prevent fluid retention  Fluid restriction (≤1.5-2 L/day)  For severe symptoms of HF, especially hyponatremia

20 What should clinicians advise patients with HFpEF about exercise?  Advise regular, moderate daily activity  Aerobic exercise especially beneficial  Improve CV performance  Lowers blood pressure  Prevents or reverses deconditioning  Increases energy levels  Reduces symptoms of HF

21 What is the prognosis of HFpEF?  Annual death rate ≈5%  ≈50% die of noncardiovascular diseases  Risk factors for mortality in HFpEF  Increasing age, male gender  Higher natriuretic peptide levels, higher NYHA class  Coronary artery or peripheral vascular disease  Diabetes mellitus, chronic renal insufficiency  Lower EF, restrictive filling pattern on Doppler ECHO  Low and very high BMI (in HFpEF)

22 How should patients with HFpEF be followed?  Educate patients on signs of fluid retention  Provide guidelines for using a flexible diuretic regimen  Provide telephone access to health care providers  Emphasize low-salt diet + medical regimen compliance  Frequency of follow-up visits depends stability of patient  See w/in 7d of hospital discharge for decompensated HF  See well-compensated patient every 4 to 6 months

23 When should patients with HFpEF be hospitalized?  Respiratory failure secondary to pulmonary edema  Moderate to severe volume overload  Atrial fibrillation with rapid ventricular response  Severe hypotension or hypertension  Need for close monitoring during therapy (e.g., of renal function, electrolytes)

24 When should clinicians consider consulting a cardiologist?  Diagnosis of HFpEF uncertain  Cause of HFpEF unclear  Patient symptomatic despite treatment  Frequent hospitalizations for decompensation  Comorbid cardiac conditions complicate management (CAD or dysrhythmia)

25 Ivabradine  Ivabradine is a highly selective blocker of inward “funny” channels, which are central regulators of spontaneous depolarization in pacemaker cells.  Thus ivabradine selectively decreases heart rate without having negative inotropic or lusitropic effects, as can occur with beta-blockers.  Furthermore, animal and human studies have shown that ivabradine can decrease heart rate while simultaneously improving stroke volume and cardiac output.

26 Ivabradine –If channel inhibition  Heart rate reduction by If-inhibition improves vascular stiffness and left ventricular systolic and diastolic function in a mouse model of heart failure with preserved ejection fraction.  Genetic mouse model of HFpEF (db/db)  Invasive hemodynamics with Ivabradine  Ivabradine improved diastolic function (Reil et al, Eur Heart J, 2012:1-11)

27  An elegant study, which used a novel HFpEF animal model, the db/db (leptin-receptor deficient) mouse, found that heart rate lowering with ivabradine had several beneficial effects, including reduced effective arterial elastance (Ea), increased aortic distensibility and decreased LV end-systolic elastance (Ees).  In addition, ivabradine accelerated myocardial relaxation by increased phosphorylation of phospholamban, reversing the SERCA2a inhibition that was present in the db/db mouse.

28 Ivabradine phase II study in HFpEF Primary objective Ivabradine vs placebo on diastolic function, exercise capacity and neuroendocrine activation over an 8-month treatment period in patients with chronic HF-PEF. Primary endpoint Co-primary endpoint based on echocardiography (E/e'), neuroendocrine activation (NT-proBNP) and six-minute walk test evaluated at 8 months. Secondary objectives - To evaluate the effects of ivabradine compared to placebo on cardiac function and structural parameters, quality of life (KCCQ), NYHA classification and other biomarkers. - To evaluate the safety and tolerance profile of ivabradine compared to placebo. (Start: May 2013 !)

29 Ivabradine - conclusion In conclusion, Kosmala, Marwick and colleagues should be congratulated for carrying out a carefully conduced and detailed exercise hemodynamic study in HFpEF patients, By taking ivabradine, a blocker of the inward “funny” current and matching it with the right type of HFpEF patient, coupled with appropriate endpoints (peak VO2 and exercise E/e), the authors were successful matchmakers and may have found a novel therapy for an otherwise difficult-to-manage patient population.

30 SUMMARY HFpEF constitute about 50% of all Pts of HF. More common in females, with elderly age, HTN, DM,COPD, AF. Comorbidities contribute to progress of disease. Accurate diagnosis & proper Rx may prolong life, reduce hospital re admissions and improve QOL. Newer drugs like ivabradine, sidnofil, neprilysin inhibitions, MR antagonist are under trial. New devices & interventions to be developed. - Renal denervation, interatrial shunting, vagus / baroreceptor stimulation


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