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MODULE 3 CHAPTER 1C HYPERTENSION AND HEART FAILURE Introduction- Good and Bad news Good news : Decrease in mortality Advances in therapy Evidence based practice Bad news : Increase in incidence Advances in therapy Increase in elderly population Hypertension and Heart Failure • Hypertension is the commonest cause of heart failure (HF) • Hypertension predisposes to asymptomatic LV dysfunction,HF with preserved ejection fraction (HFPEF) as well as HF with reduced ejection fraction (HFREF) • One of the most preventable complications from hypertension management is Heart Failure (HF) CV Complications of Untreated Hypertension (N=500) 50 50 45 40 35 Event 30 rate 25 (%) 20 18 15 16 12 8 10 5 2 0 Renal Failure Stroke MI, myocardial infarction; CHF, chronic heart failure. Perera GA J. Chron Dis. 1955;1:33-42. Enceph MI Angina CHF Cumulative Incidence of Heart Failure by Baseline Hypertension Status 25 Stage 2+ Men aged 60-69 y Stage 1 20 Normotensive 15 20 Cumulative 15 Incidence (%) 10 Women aged 60-69 y Stage 2+ Stage 1 10 5 Normotensive 5 0 2 40 25 4 6 8 0 10 12 14 16 2 40 Men aged 70-79 y Stage 2+ 30 Cumulative Incidence 20 (%) Stage 1 Normotensive 10 12 14 Normotensive 2 Time (y) Levy D et al. JAMA. 1996;275:1557-1562. Women aged 70-79 y Stage 1 0 8 10 12 14 16 20 0 6 8 Stage 2+ 10 4 6 30 10 2 4 4 6 8 10 12 14 Population-Attributable Risks for Development of CHF Women Men AP DM 5% 6% LVH 4% VHD 7% AP 5% HTN 39% DM 12% LVH 5% VH D 8% MI 34% MI 12% Population-attributable risk defined as: (100 x prevalence x [hazard ratio – 1])/(prevalence x [hazard ratio – 1] + 1) CHF, chronic heart failure; AP, angina pectoris; DM, diabetes mellitus; LVH, left ventricular hypertrophy; VHD, valvular heart disease; HTN, hypertension; MI, myocardial infarction. Levy D et al. JAMA. 1996;275:1557-1562. HTN 59% Left Ventricular Hypertrophy Independent Predictor of: – Myocardial infarction – Stroke – Heart Failure – Total Mortality – Sudden Death CV Death Stratified by Time-Varying Presence of Echo-LVH 7 LVH Absent LVH Present 6 Endpoint Rate (%) 5 HR=0.34, 95% CI 0.17-0.71 P-0.004 4 3 2 1 0 0 6 12 18 24 30 Month Hazard ratios represent risk reduction associated with absence versus presence of LVH 36 42 48 54 60 Hypertension: A Major Risk Factor for CHF Obesity Diabetes LVH Diastolic Dysfunction Hypertension CHF Smoking Dyslipidemia MI Left Ventricular Remodeling Systolic Dysfunction Subclinical Left Ventricular Dysfunction Time, decades Vasan RS, Levy D. Arch Intern Med. 1996;156:1789-1796. Death Overt Heart Failure Time, months Prevalence of Systolic and Diastolic Dysfunction by Age 60 45-54 50 55-64 65-74 % of Population 40 >75 ALL 30 20 10 0 Mild Moderate Diastolic Dysfunction Redfield MM et al. JAMA. 2003;289:194-202. Severe EF<50% EF<40% Systolic Dysfunction Heart Failure with Preserved Ejection Fraction (HF-PEF) Current Concerts and Treatment Introduction • Traditionally HF was thought to be due to systolic function abnormality shown by EF • It is now known that about half of cases of HF have preserved ejection fraction • Heart failure with a preserved ejection fraction (HFPEF) is proving to be intriguing with only a few established facts but many myths. • Over the past 20 years, significant advances in drug and device therapy have improved survival in patients with HFREF, yet evidence-based treatment for reducing cardiovascular mortality an morbidity in HFPEF is lacking. Heart Failure with Preserved Ejection Fraction (HF-PEF) • HFPEF is defined by heart failure symptoms with a normal or near-normal EF (>0.50 or 0.45). • This cut of point does not exclude occult mild systolic dysfunction. (not normal ejection fraction) • The term “preserved ejection fraction” is preferred because ejection fraction is what is commonly measured for systolic function. • HF-PEF is often equated with diastolic heart failure but it is not so simple Diagnostic Criteria • Symptoms and signs compatible with heart failure • Left ventricular ejection fraction >50% • LV EDV < 97ml/m2 • Exclusion of severe valvular disease and pericardial disease Hunt SA et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult. Circulation 112: e154–e235 Ejection Fraction in Subjects with CHF in the Cardiovascular Health Study 4,842 community-dwelling elderly (>66 yr.) subjects; CHF prevalence 8.8% 80% had normal EF(>45%) Men Women 10% Normal (55%) 31% 42% 27% Kitzman, et. al.Am. J. Cardiol. 87:413-419 (2001) Mildly Reduced (45% - 54%) Moderately (30-44%) or severely reduced (< 30%) 23% 67% 3 Mechanisms 1.An increase in intrinsic myocardial stiffness and impaired relaxation in diastole result in higher left atrial pressures to fill adequately 2.Increased systolic ventricular and arterial stiffening— that is, deranged ventriculoarterial coupling, may contribute to the pathophysiology of HFPEF 3.Enhanced sensitivity to volume overload from increased LV remodelling and dilatation with volumedependent elevation of filling pressures ↑ Vascular Stiffness ↓Vasodilitation Systemic Pulmonary ↑ RV Load Exercise Rest ↑ LV Stiffness ↓Relaxation LVH, Fibrosis, AGE, Titin, Myocyte Δs ↑ Exertional BP Load → Diastolic Dysf ↓ Systolic Reserve Atrial Dysfunction Atrial Failure (AF) Renal Dysfunction Anemia Infection Obesity Ejection fraction • The misunderstanding of the pathophysiology began when we defined systolic function solely on the basis of ejection fraction • EF DOES NOT REPRESENT WHOLE SYSTOLIC FUNCTION • Ejection fraction does not take into account systolic function in the longitudinal axis. A number of studies have now shown that LV longitudinal function is reduced not only in diastole but also in systole even though LV ejection fraction is within normal limits The exact understanding of mechanisms that contribute to development of HFPEF is still evolving • However, the main physiological difference between SHF and HFPEF is the increase in ventricular volume and change in shape due to ventricular remodeling. • Remodeling leads to increased ventricular volumes and reduced ejection fraction. The rate of occurrence of remodeling is a major differentiating factor. • For example; A myocardial infarction (or viral myocarditis) appears to be a potent stimulant for the remodeling process resulting in rapid progression to SHF compared to Hypertensive heart disease where remodeling is a slower process. In HHD compensatory increased radial contraction tends to normalize the ejection fraction however at later stages further remodeling will occur and the patient will slip from HFPEF to SHF hence DCM in “burnt out” hypertension. Echocardiography Bursi F, et al. JAMA 2006;296:2209-2216. HF-PEF Current treatment targets and options • LV volume & edema: Diuretics, salt restriction, nitrates • Rx HTN: Diuretics, CCB, BB, ACEI, ARB • Reverse LVH: ACEI,ARBS • Prevent ischemia: BB, CA, nitrates • Reduce HR, prevent AF: BB, rate lowering CA, ARB • Bradycardia: Atrial Pacing • Enhance relaxation: No current treatment • Prevent vascular events: ACEI, ARB, BB ANEMIA,KIDNEY DISEASE,PHT,FLUID OVERLOAD Control of Hypertension Regression of LVH is an important therapeutic goal, since it has been shown to play a significant role in the pathophysiology of HFPEF Effect of therapy with each of five antihypertensive drug classes on reduction in left ventricular mass in patients with hypertension. These data represent a meta-analysis of 80 trials of over 4100 patients. The decrease in left ventricular mass index, adjusted for the duration of therapy and diastolic pressure, was significantly higher with angiotensin II receptor blockers (13 percent), calcium channel blockers (11 percent), and angiotensin converting enzyme inhibitors (10 percent) compared to beta blockers (6 percent). Data from Klingbeil, AU, Schneider, M, Martus, P, et al, Am J Med 2003; 115:41. HFREF NYHA • Cl. I – 1 year – 5% ; 4 year mortality – 19% • Cl.II / III - 1 year – 15% ; 4 year mortality – 40% • CL.IV – 6 months – 44%; 12 months 64% (without ACEI) FRAMINGHAM CRITERIA : HEART FAILURE MAJOR CRITERIA MINOR CRITERIA • P.N.D. OR ORTHOPNOEA • ANKLE EDEMA • NECK VEIN DISTENTION • NIGHT COUGH • RALES • • EXERTIONAL DYSPNOEA CARDIOMEGALY • ACUTE PULMONARY EDEMA • HEPATOMEGALY • S3 GALLOP • PLEURAL EFFUSION • VENOUS PRESSURE > 16 Cm H2O • TACHYCARDIA ( > 120 / Min ) • HEPATO JUGULAR REFLEX SIMULTANEOUS PRESENCE OF 2 MAJORS OR I MAJOR AND 3 MINORS (Porth, 2009). Picture retrieved from http://www.starsandseas.com/SAS%20Physiolog y/Cardiovascular/Cardiovascular.htm Goals of therapy To relieve symptoms To give good quality of life To halt the progress of disease To reduce mortality Patient is happy Doctor is happy The ultimate goal is to make both doctor and patient happy Types of therapy 1 I – Mortality reducing drugs Angiotensin converting enzyme inhibitor Beta blockers Aldosterone antagonists Angiotensin receptor blockers Nitrates + Hydralazine II - Morbidity reducing drugs Diuretics (Loop and Thiazide) Digoxin III - Metabolically Active Drugs Trimetazidine L-Carnitine Co enzyme Q IV – Newer, emerging drugs Ivabradine Omega 3 fatty acids Types of therapy 2- Supportive Drugs • Anemia – Iron,Erhythropoitin • Oral anticoagulants • Electrolytes- Na, K correcting drugs • Drugs for Co-Morbids Types of therapy 3- harmful drugs • Routine inotropes • Anti arrhythmics (except B Blockers and Amiodarone) • Calcium blockers ( non DHP) • High dose Digoxin MANAGEMENT: GENERAL MEASURES • • • • • • • • • Correctable causes Daily weighing – Report if >2kgs in 1-3 days Self management of diuretics Compliance with medication Regular exercise Stop smoking, Alcohol Salt , fluid management- careful in summer,powercuts Vaccination Warning about other drugs (NSAIDS,VIT E, ALTERNATIVE MEDICINES) • Treating precipitating factors of HF Precipitating causes of Heart Failure • • • • • • • • • Anemia,arrhythmia, alcohol Beri beri Cardiac toxins Drugs – NSAIDS,Glitazones,Steroids Exercise – severe, emotion, embolism Fever Goitre Hypertension, hypoxia Infections , iatrogenic, iv fluids SUMMARY Disease Modifying mortality reducing drugs Symptom relieving quality of life providing drugs Metabolically acting drugs Newer drugs increase survival Decrease symptoms ? Symptoms Yet to be proven +_ symptoms - survival ? survival ACEI B.Blockers Diuretics Aldosterone antagonists Digoxin Trimetazidine Ivabradine L-Carnitine Omega 3 fatty acids Co enzyme Q ARB Nitrates + Hydralazine More often symptomatic patients MUST In all patients Individualize Industry feels good Who will feel good? 1-4 A-D Patient feels good Doctor feels good 2-4 C,D Sometimes in selected patients Treatment of Hypertension and CVD Outcomes Placebo Controlled Trials 0 Heart failure Fatal/nonfatal Fatal/nonfatal strokes CVD deaths CHD events -10 -20 Risk reduction (%) -16 -21 -30 -40 -38 -50 -60 -52 17 randomized, placebo-controlled trials (48,000 subjects)—14 diuretic and 3 beta blocker based trials. All differences are statistically significant. CVD, cardiovascular disease; CHD, coronary heart disease. Herbert PR et al. Arch Intern Med. 1993;153:578-581. Moser M, Herbert PR. J Am Coll Cardiol. 1996;27:1214-1218. THE VERY ESSENCE OF CARDIOVASCULAR PRACTICE IS THE EARLY DETECTION OF HEART FAILURE SIR THOMAS LEWIS 1933 THE VERY ESSENCE OF CARDIOVASCULAR PRACTICE IS THE PREVENTION OF HEART FAILURE PRACTICE IMPLICATION 2013 CONCLUSION • THE GREATEST BENEFIT OF TREATING HYPERTENSION IS THE PREVENTION OF HEART FAILURE AND STROKE END OF MODULE 3 CHAPTER 1C