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Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
Heart failure update 2012
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Heart failure update 2012

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Heart failure update 2012 by john hakim, MD

Heart failure update 2012 by john hakim, MD

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  • 1. Heart Failure Update 2012 John Hakim, MD, FACC Southern Maryland Hospital Food for thought
  • 2. Outlineof CHF Talk.  Definition  Pathophysiology  Medical Treatment  Mechanical Treatment  Device Treatment  Transplantation Option  Future Hopes and Dreams
  • 3. Definition of Heart Failure • HF is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.  In systolic heart failure the dominant feature is a reduction in cardiac output  In diastolic heart failure the dominant feature is impaired filling of the left ventricle.
  • 4. Heart Failure is a Major and Growing Public Health Problem in the U.S. Approximately 5 million patients in this country have HF Over 550,000 patients are diagnosed with HF for the first time each year Primary reason for 12 to 15 million office visits and 6.5 million hospital days each year In 2001, nearly 53,000 patients died of HF as a primary cause
  • 5. Heart failure is a major cause of Hospitalization
  • 6. Heart Failure is Primarily a Condition of the Elderly The incidence of HF approaches 10 per 1000 population after age 65 HF is the most common Medicare diagnosis-related group More dollars are spent for the diagnosis and treatment of HF than any other diagnosis by Medicare
  • 7. New York Heart Association Classification.  Class I Physical activity is not limited and does not cause significant fatigue, heart palpitations, trouble breathing, or chest pain.  Class II Physical activity is somewhat limited. You are comfortable at rest, but ordinary activity causes fatigue, heart palpitations, trouble breathing, or chest pain.  Class III Physical activity is markedly limited. You are comfortable at rest, but less-than- ordinary activities cause fatigue, heart palpitations, trouble breathing, or chest pain.  Class IV All physical activity causes discomfort. Symptoms also are present at rest. Minor physical activity always makes symptoms worse.
  • 8. Prognosis  Class IV has 30 to 70% annual mortality  Class III has 10 to 20% annual mortality  Class II has 5 to 10% annual mortality
  • 9. Character of Heart failure Signs and symptoms of intravascular and interstitial volume overload, including shortness of breath, rales, and edema Manifestations of inadequate tissue perfusion, such as impaired exercise tolerance, fatigue, and renal dysfunction.
  • 10. Right Sided Heart failure  Fluid retention without dyspnea or rales.  Often associated with weight gain, dilation of the right ventricle.  The focus of this talk is Chronic Left Sided Heart failure.
  • 11. Types of Left sided Heart failure  Systolic dysfunction- reduced LV ejection fraction.  Diastolic dysfunction- increased ventricular stiffness or impaired myocardial relaxation. Often with preserved LV ejection fraction.  Physiologic states where the heart cannot compensate for increased circulation or metabolic requirements. (Regurgitatant valvular disease, intra cardiac shunts, disorders of heart rate or rhythm.)
  • 12. Causes of CHF Structural abnormalities (congenital or acquired) that affect the peripheral and coronary arterial circulation, pericardium, myocardium, or cardiac valves, thus leading to the increased hemodynamic burden or myocardial or coronary insufficiency responsible for heart failure; Fundamental causes, comprising the biochemical and physiological mechanisms, through which either an increased hemodynamic burden or a reduction in oxygen delivery to the myocardium results in impairment of myocardial contraction; and
  • 13. Etiology of Heart failure  Any condition that causes myocardial necrosis or chronic pressure or volume overload can cause CHF.  Hypertension is a factor in 75% of patients.
  • 14. Classical Symptoms of Heart Failure  Fatigue or inability to exercise well; having less energy, feeling more tired than usual;  Dyspnea at rest or exertion.  Paroxysmal nocturnal dyspnea shortness of breath while sleeping or that wakes you at night  Orthopnea-Shortness of breath while lying down, gets worse when you lie flat  Cough – can be wet or dry, with crackles, and usually worse with lying down.  Weight gain • Swelling in the feet or ankles, usually worse at the end of the day or after standing for long periods; shoes may no longer fit. • Sometimes edma is painful but usually pressure indents the skin • Abdominal swelling with decreased appetite and decreased muscle strenght (Cardiac Chachectia) • Abdominal distention (Ascites) usually a sign of right heart failure.  Urination • frequent urination, usually at night. Increased urination (Due to high BNP)
  • 15. Signs of heart failure  Exertional dyspnea  Orthopnea  Gallup sounds  Lung Crepitations  Pulmonary edema  Edema
  • 16. Acute Heart Failure Symptoms  Caused by rapid fluid buildup in the lungs (congestion, pulmonary edema). Symptoms develop suddenly and may include:  Severe shortness of breath.  An irregular or rapid heartbeat.  Coughing up foamy, pink mucus.
  • 17. COMMON CAUSES OF SYSTOLIC FAILURE  Ischemic Heart disease and Prior MI account for 2/3 of systolic heart failure  Essential Hypertension is a major cause of ischemic and non ischemic systolic heart failure  Hypertension increases afterload and accelerates the progression of heart failure. HTN causes chronic pressure overload.  Other causes of Non ischemic heart failure are genetic diseases, Toxic/drug induced, Immune mediated, infiltrative process, Metabolic disorders
  • 18. All-cause Mortality vs LVEF (Median 29%) Survival Probability Time (days) LVEF<30% LVEF≥30%* *p=0.005 vs LVEF<30%
  • 19. Cause of Systolic Heart failure Acquired vs Genetic Causes • Acquired Causes • Hypertension • Diabetes • Dyslipidemia • Valvular heart disease • Coronary or peripheral vascular disease • Myopathy • Rheumatic fever • Mediastinal irradiation • Sleep Apnea • Exposure to cardiotoxic agents (Adrianomycin, Danaurubicin, Em brel) • Current and past alcohol consumption • Smoking • Collagen vascular disease • Exposure to sexually transmitted diseases • Thyroid disorder • Pheochromocytoma • Obesity  Genetic Causes  Predisposition to atherosclerotic disease or Valvular disease  (Hx of MIs, strokes, PAD)  Sudden cardiac death  Myopathy  Conduction system disease (need for pacemaker)  Tachyarrhythmia  Cardiomyopathy (unexplained HF)  Skeletal Myopathy
  • 20. Complications of Chronic Heart failure  An irregular heartbeat leading to death (VT)  A stroke leading to death  A heart attack leading to death  Deep vein thrombosis  Pulmonary embolism  Anemia  Cognitive impairment  Mitral valve regurgitation
  • 21. Common test ordered in CHF medical history and a physical exam. Lab tests Electrocardiogram Chest X-ray. Echocardiogram Brain natriuretic peptide (BNP)/ TSH/  Nuclear stress test/MUGA  Cardiac catheterization.
  • 22. Diastolic Heart Failure
  • 23. DIASTOLIC HEART FAILURE  Patients with symptoms and signs of Heart Failure with normal systolic function and diastolic dysfunction. • 30 to 50% of patients with Heart failure symptoms have normal LV systolic function. • Abnormal LV filling and elevated filling pressures. • Usually due to Impaired relaxation of the LV and increased stiffness of the cardiac muscle.  Most prevalent in patients over 75 years old.
  • 24. Copyright ©2000 BMJ Publishing Group Ltd. Jackson, G et al. BMJ 2000;320:167-170 Hypertrophic Cardiomyopathy
  • 25. Pathogenesis of Diastolic Heart Failure  Pathologic Myocardial hypertrophy • HTN, Hypertrophic Cardiomyopathy  Aging  Ischemic fibrosis  Restrictive Cardiomyopathy • Infiltrative disorders (Amyloid, Sarcoid) • Storage Diseases (Hemochromatosis)  Endomyocardial disorders  Valvular heart disease • (obstructive or regurgitation)
  • 26. DIASTOLIC HEART FAILURE usually due to Hemodynamic stress  Patients with diastolic heart failure do not tolerate hemodynamic stress well  Atrial fibrillation causes loss of atrial contraction and often leads to Diastolic CHF  Tachycardia shortens diastole and leads to CHF  Elevation in BP worsens myocardial relaxation  Ischemia worsens diastolic function raising LA and PA pressures. (This is why ischemia causes SOB)  Aortic Stenosis causes worsening diastolic function.
  • 27. Diastolic CHF All treatments are empiric(No trial data)  2005 ACC/AHA guidelines supports 4 treatments of diastolic CHF • Control of systolic and diastolic HTN • Control of atrial rate in patients with A fib • Control of pulmonary congestion and edema with diuretics • Coronary revascularization of patients with CAD, where ischemia causes worse diastolic function.
  • 28. Diastolic Heart Failure often presents with Acute Pulmonary Edema  Treatment • Loop diuretics (furosemide)  Both immediate action to dilate pulmonary arteries and longer action to diurese • Afterload Reduction  Nitrates  Morphine  Ace inhibitors (Captopril, enalapril, etc)
  • 29. Systolic Heart Failure The ballooning of the Heart
  • 30. Heart Failure Pathophysiology (the whole body participates)
  • 31. Neurohormonal activation Decreased cardiac output activates many neuro-hormonal compensatory systems that in the short term act to preserve circulatory hemostasis and maintain arterial pressure. When in excess these systems play a role in worsening of CHF
  • 32. Medical Treatment of Systolic Heart Failure What Improves Survival  ACE inhibitors  Beta Blockers  Spironolactone (Aldactone) /Eplenrone (Inspira)  -Hydralazine and Nitrates (V-Heft)  Angiotensin Receptor Blockers (ARB)  Device Therapy (AICD)
  • 33. DIURETICS Sodium and Water retention are the hallmark of CHF and diuretics are mandatory treatment for patients with pulmonary or Peripheral edema. Patients with CHF should be encouraged to weigh themselves daily and seek advice if a weigh gain of more than 1.5kg in 24 hrs
  • 34. Why give ACE inhibitors? Directics activate the Renin Angiotensis system and should be given in combination with and ACE inhibitor. Correction of fluid overload with diuretics should be undertaken before starting an ACE inhibitor. Adding an ACE inhibitor to a patient on high dose diuretic may result in significant first dose hypotension.
  • 35. ACE-INHIBITORS ACE inhibitors relieve symptoms, reduce hospitalizations and improve survival in patients with systolic and diastolic heart failure and should be used regardless of the severity of CHF. Patients with the lowest EF derive the greatest benefits from ACE inhibitors. The evidence that ACE inhibitors improve survival and symptomatic wellbeing is incontrovertible.
  • 36. Beta Blocker- Why do they work In heart failure, the nervous system is over stimulated. Norepinephrine levels rise. Increased levels of circulating norepinephrine cause heart remodeling and arrhythmias. High levels of norepinephrine are directly toxic to heart cells and increase risk of death. Beta Blockers – block the toxic effect of nervous system over stimulation and norepinephrine.
  • 37. Normal The Normal Heart is a 1-Organ That Functions in a 1 -Environment 1 1 1 2 1 1 2 1 1 1 1 11
  • 38. Normal Heart failure Heart Failure Converts the Circulation From a 1- to a 1/ 2 / 1- Environment 1 1 1 2 1 1 2 1 1 1 1 11 2 1 1 1 2 1 1 1 2 2 1 21 2 1 1
  • 39. NE NE NE Cardiac cell toxicity Carvedilol 1 2 1 Metoprolol Cofactors
  • 40. [123I]mIBG Planar Imaging for Cardiac Assessment Normal innervation NHYA Class II NYHA Class IV Quantitation of cardiac uptake of [123I]mIBG expressed in terms of the ratio of counts/pixel between regions of interest (ROIs) drawn around the heart (H) and in the upper mediastinum (M), the H/M ratio. H/M ratio: 2.2 1.7
  • 41. Results of Direct Comparison Trials with Metoprolol and Carvedilol in CHF Patients LV Ejection Fraction (%) 0 +2 +4 +6 +8 +10 +12 Metoprolol (n=123) Carvedilol (n=125) Packer M et al. Am Heart J 2001;141(6):899-907 P = 0.009
  • 42. BETA-BLOCKERS  BETA-BLOCKERS inhibit the adverse effects of chronic activation of the sympathetic nervous system acting on the myocardium  Patients with minimal symptoms (NYHA 2) derive little symptomatic benefit from beta blockers.
  • 43. BETA-BLOCKERS Beta-BLOCKERS approved for the management of CHF are: Carvedilol, Metoprolol and bisoprolol.  All three drugs have been shown to prolong survival but they are not the same.
  • 44. Primary Argument Supporting the Belief That Only 1 -Blockade is Important Mortality results in earlier large-scale trials MERIT-HF (metoprolol) 34% in risk CIBIS-2 (bisoprolol) 34% in risk COPERNICUS (carvedilol) 35% in risk
  • 45. 0.60 0.80 1.00 -blocker better -blocker worse - only 32 Post-Infarction Trials (n=26,580) Usual antisympathetic blockade
  • 46. 0.60 0.80 1.00 -blocker better -blocker worse - only -blockers with ISA 32 Post-Infarction Trials (n=26,580) Less than usual antisympathetic blockade Usual antisympathetic blockade
  • 47. -1 + -2 and/or -1 0.60 0.80 1.00 -blocker better -blocker worse - only -blockers with ISA 32 Post-Infarction Trials (n=26,580) More than usual antisympathetic blockade Less than usual antisympathetic blockade Usual antisympathetic blockade
  • 48. -1 + -2 and/or -1 0.60 0.80 1.00 -blocker better -blocker worse - only -blockers with ISA = 13% 32 Post-Infarction Trials (n=26,580)
  • 49. -1 + -2 and/or -1 0.60 0.80 1.00 -blocker better -blocker worse 0.50 0.75 1.00 -blocker better -blocker worse - only -blockers with ISA = 13% 32 Post-Infarction Trials (n=26,580) 27 Heart Failure Trials (n=15,851) 1.25
  • 50. -1 + -2 and/or -1 0.60 0.80 1.00 -blocker better -blocker worse 0.50 0.75 1.00 -blocker better -blocker worse - only -blockers with ISA = 13% = 13% 32 Post-Infarction Trials (n=26,580) 27 Heart Failure Trials (n=15,851) 1.25
  • 51. Metoprolol (selective blockade) Carvedilol (comprehensive blockade) Baseline 1020 deaths COMET Study Design 3029 pts class II-III CHF LVEF < 35%
  • 52. Metoprolol tartrate Carvedilol 3.125 mg BID Baseline 6.25 mg BID 12.5 mg BID 1020 deaths COMET Study Design 5 mg BID 12.5 mg BID 25 mg BID 3029 pts class II-III CHF LVEF < 35% 25 mg BID 50 mg BID
  • 53. Packer M et al. Am Heart J. 2001;141:884–888. + 12 + 6 0 – 6 – 12 – 18 – 24 P=.009 P=.072 LV Ejection Fraction (%) LV End-Diastolic Volume (mL/m2) + 12 + 10 + 8 + 6 + 4 + 2 0 Metoprolol (n=123) Carvedilol (n=125) Mean duration 8.75 mos Comparison of Carvedilol With Metoprolol on LV Function
  • 54. COMET (Carvedilol or Metoprolol European Trial)  Compares comprehensive 1-, 2-, 1-blockade with carvedilol to 1-selective blockade with metoprolol tartrate  Prespecified end points: all-cause mortality, combined risk of all-cause mortality and hospitalization  More than 3000 patients with class II–IV heart failure due to ischemic or nonischemic Cardiomyopathy • With over 1020 events, COMET is the largest trial ever conducted in heart failure  Intended follow-up was at least 3.5 years • 10,000 patient-years makes COMET the longest trial ever conducted in heart failure Poole-Wilson PA et al. Eur J Heart Fail. 2002;4:321–329.
  • 55. Randomized (No run-in phase) 3029 patients with stable heart failure, New York Heart Association Class II–IV, receiving standard treatment including ACE inhibitors Time to 1020 deaths Estimated to be 4 to 6 years Screening Titration to maximum tolerated or target dose (Start: carvedilol 3.125 mg bid, metoprolol tartrate 5 mg bid) Assessments every 4 months during maintenance phase (n 1500) Metoprolol 50 mg bid (n 1500) Carvedilol 25 mg bid Poole-Wilson PA et al. Eur J Heart Fail. 2002;4:321–329. Poole-Wilson PA et al. Lancet. 2003;362:7–13. COMET Study Design
  • 56. Time (years) PercentageMortality(%) 0 10 20 30 40 0 1 2 3 4 5 Relative risk 95% CI P value Carvedilol vs Metoprolol 0.83 0.74–0.93 .0017 Metoprolol Carvedilol Effect of Carvedilol vs Metoprolol on Mortality Poole-Wilson PA et al. Lancet. 2003;362:7–13. 17% Risk reduction
  • 57. COMET: Median Survival Carvedilol 8.0 years Metoprolol 6.6 years Carvedilol prolonged median survival by 1.4 years beyond that achieved with metoprolol Assuming constant hazard Poole-Wilson PA et al. Lancet. 2003;362:7–13.
  • 58. EPHESUS TRIAL: Inspra
  • 59. Spironolactone and Epelnerone ALDOSTERONE RECEPTORS WITHIN THE HEART MEDIATE FIBROSIS, HYPERTROPHY AND ARRHYTHMOGENESIS  REDUCTION IN ALL CAUSE MORTALITY AND SYMPTOMATIC RELIEF IN PATIENTS WITH ADVANCED CHF AT DOSES 25MGM/DAY
  • 60. Spironolactone and Epelnerone  HYPERKALAEMIA,PARTICULARLY WHEN USED WITH ACE-INHIBITORS/ATRAs  IN PATIENTS WITH IMPAIRED RENAL FUNCTION.MONITORING OF POTASSIUM LEVELS ESSENTIAL  USED IN COMBINATION WITH ACEINHIBITOR,LOOP DIURETIC +/- DIGOXIN
  • 61. Digoxin  BLOCKAGE OF THE SODIUMPOTASSIUM ATPase PUMP RESULTS IN INCREASED INOTROPIC RESPONSIVENESS  THE DATA SUGGESTS THAT DIGOXIN HAS NO INFLUENCE ON SURVIVAL BUT REDUCES HOSPITALISATION AND IMPROVED THE QUALITY OF LIFE OF MANY PATIENTS
  • 62. Heart Failure-Medical Treatment  Digoxin improves Symptoms and prevents hospitalizations in men but not women.  Niseritide (Natracor) induces diuresis and improves symptoms but does not improve longevity  Amiodarone helps prevent arrythmic events
  • 63. Heart Failure Device Treatment  Bi-Ventricular pacemaker helps improve cardiac output and improves symptoms sometimes.  Automatic Implantable Defibrillator improves survival in patients with EF less than 35%. (Better than drug therapy alone)
  • 64. COMPANION: Secondary End Point of All-cause Mortality Bristow MR et al. Paper presented at American College of Cardiology. March 31, 2003; Chicago, Ill. 12-month OPT Event Rate (1-y) = 19.0% P=.12, CRT vs OPT P=.002, CRT-D vs OPT 12-month event rate reductions: CRT = by 23.9% CRT-D = by 43.4% Any Death %PatientsEvent-Free Days from Randomization 0 120 240 360 480 600 720 840 960 1080 60 50 70 80 90 100 CRT = cardiac resynchronization therapy. CRT-D = cardiac resynchronization therapy plus implantable cardioverter defibrillator. OPT = optimal drug therapy. CRT-D OPT CRT
  • 65. REMATCH-LVADs in Extremely Severe Heart Failure 100 80 60 40 20 0 0000 6 12 18 24 30 No. at Risk LV assist device Medical therapy 68 18 22 11 5 1 61 27 11 4 3 0 Months Survival(%) Medical therapy LV assist device Rose EA. N Engl J Med. 2001;345:1435–1443.
  • 66. People Don’t want and LVAD, they want a Heart
  • 67. Heart Transplant Waiting List January 9th 2012 73 people Washington DC metropolitan area waiting for heart transplant 3155 people In USA waiting for heart Transplant 2011, 1,760 patients on the heart wait list received heart transplants. That figure represents a decrease from the 2,333 hearts transplanted in 2010 and the 2,211 in 2009.
  • 68. Heart Transplantation  There were 2,125 heart transplants performed in the United States in 2005 and 2,016 in 2004.  Each year thousands more adults would benefit from a heart transplant if more donated hearts were available.  In the United States, 72.4 percent of heart transplant patients are male; 70.0 percent are white; 19.1 percent are ages 35-49 and 45.0 percent are ages 50-64.  As of Aug. 11, 2006,the one-year survival rate was 86.1 percent for males and 83.9 percent for females; the three-year survival rate was about 78.3 percent for males and 74.9 percent for females. The five-year survival rate was 71.2 percent for males and 66.9 percent for females.
  • 69. Markers of Heart Failure  Identify Markers and we can better treat the disease  Albumin  BNP  Chest to HEART MIBG ratio- a marker for denervation of the heart and loss of sympathic tone- assessment of myocardial sympathetic innervation, as determined by the heart to mediastinum (H/M) ratio on planar 123I-mIBG imaging as either normal (>1.6) or abnormal (<1.6), for identifying HF subjects at higher risk of experiencing an adverse cardiac event.
  • 70. UACR= urinary albumin to creatinine ratio. Macroalbuminuria=UACR >25 mg/mmol. Microalbuminuria=UACR 2.5–25.0 mg/mmol (men) or 3.5–25.0 mg/mmol (women). *compared with normoalbuminuria (UACR<2.5 mg/mmol), n=1349 End point Microalbuminuria, n=704* Macroalbuminuria, n=257* Per 100- mg/mmol UACR increment CV death or HF hospitalization 1.43 (1.21–1.69) 1.75 (1.39–2.20) 1.07 (1.00–1.14) All-cause mortality 1.62 (1.32–1.99) 1.76 (1.32–2·35) 1.08 (1.00–1.17) HF hospitalization 1.31 (1.07–1.59) 1.67 (1.28–2·17) 1.07 0.99–1.15) Albumin excretion is prognostic marker in heart failure (Analysis from CHARM Study) Adjusted hazard ratios (95% CI) for clinical outcomes by degree of albuminuria (defined by UACR with cut points and as continuous variable) in CHARM Jackson CE et al. Lancet 2009; 374:543–550.
  • 71. All-cause Mortality vs BNP (Median 140) Survival Probability Time (days) <Media n* Less than 140 BNP >Median Greater Than 140 BNP *p<0.00001
  • 72. H/M=0.96 Died at 8 mo HF Progression H/M=1.38 Died at 8 mo, SCD (No ICD) H/M=1.67 No event 1 2 Three Patients with NYHA Class II HF and LVEF between 20 and 25%. Patient 1 has highly elevated BNP (>1000). BNP in patients 2 and 3 is normal (<100). Based upon the results of ADMIRE-HF, 2-year cardiac mortality risk for patient 1 is 10 times that of patient 3. (IF your Chest to HEART MIBG ratio is greater than 1.6 you don’t die)
  • 73. All-cause Mortality vs BNP (Median 140) & H/M Time (days) BNP>140 & H/M ≥1.60 BNP>140 & H/M<1.60* BNP<140 & H/M<1.60 BNP<140 & H/M ≥1.60 Survival Probability *p=0.024 vs BNP>140 & H/M ≥1.60
  • 74. Current and Future Therapies  Drugs  CHF disease management programs  Resynchronizatin therapy + ICD  Renal Denervation  ultrafiltration does not work if diuretic resistant  LVADs • Total artificial heart  Cardiac transplant • (batista,cardiomyoplast y & ―acorn‖ does not work) Early-stage Treatment Late-stage Treatment Resynchronization therapy is an effective early-stage therapy
  • 75. Curing Heart failure by curing hypertension- Denervating the Kidney
  • 76. Stem Cells trial Shows Promise for Ischemic heart failure.  -11/6/2012 AHA Encouraging two-year follow-up from the Stem Cell Infusion in Patients with Ischemic Cardiomyopathy (SCIPIO) trial  -c-KIT-positive Ccardiac stem Cells in patients with left ventricular dysfunction (LVEF <40%) following an MI. In the trial, the cells were harvested from the patient's right atrial appendage, isolated and expanded, and then infused to repair an infarction during coronary bypass surgery.  -Echocardiography showed the average LVEF in the 18 patients treated with the CSC infusion increased from 29.0% before infusion to 36.0% (p <0.001) four months after the procedure. During that period, LVEF improved only from 29.2% to 29.4% in 13 control patients.
  • 77. Balloon Pump to augment Coronary Perfusion
  • 78. eecp
  • 79. EECP  Reduced frequency or complete elimination of angina symptoms.  Better ability to exercise free from chest pain and breathlessness.  Decrease in need for anti-angina nitrate medication  Clinical tests show:  Decreased exercise-induced signs of angina on ECG (prolonged time to ST depression on exercise stress testing)  Increased blood supply to heart muscle , demonstrated by myocardial perfusion scan techniques before and after EECP (Technetium scan, Cardiovascular MRI, stress ECHO)  Improvement of EF in some Patients.
  • 80. Future Horizons and Pipe Dreams  Heart Transplantation- A viable option for a select few patients.  Left Ventricular Assist devices and the Artificial heart, are available options and used mainly as a bridge to transplant and not destination therapy.  Stem cell transplantation and myocaridal cell imlantation have not yet proven viable.
  • 81. Worldwide REGISTRY DATABASE: Number of Transplants Reported ORGAN Transplants Reported from 7/1/2006 through 6/30/2007 Total Transplants Reported through 6/30/2007 Heart 3,114 80,106 Heart-Lung 63 3,341 Lung 2,099 25,950 ISHLT 2008 J Heart Lung Transplant 2008;27: 937-983
  • 82. The HeartMateII is a continuous flow cardiac assist device. Heart surgeon "Bud" Frazier and his team are working with two such devices to develop a continuous flow artificial heart. (Courtesy: Texas Heart® Institute) Artificial Heart
  • 83. Evidence-Based Treatment Across the Continuum of Systolic LVD and HF Control Volume Improve Clinical Outcomes Diuretics Renal Replacement Therapy* Digoxin -BlockerACEI or ARB Aldosterone Antagonist or ARB Treat Residual Symptoms CRT an ICD* HDZN/ISDN* *In selected patients
  • 84. Drugs to avoid in heart failure  NSAID – I buprophen( Advil, Motrin), Naproxen ( Alieve, Naprosyn). Cox-2 inhibitors (Celebrex)  The NSAID can cause kidney to retain salt and water, and Interfere with ACE/ARB class  Use Acetemenphen Or Narcotics instead for pain and aches.
  • 85. Drugs to Avoid in CHF  Anti-Arrhythmics in Class 1 ( Sodium Blockers and Class 3 ( Potassium Channel blockers)  The only heart rhythm drugs safe in Systolic dysfuction are Amiodarone and Dofeditilide (Tikosyn)
  • 86. Drugs to Avoid in CHF  Avoid Non Dihydropyridine Calcium Channel blockers.  Non- dihydropridine Calcium Channel blockers (Verapamil & Diltiazem) decrease the strength of myocardial contractility and decrease heart rate.  Verapamil and Diltiazem can worsen Heart failure and do not improve survival.
  • 87. 1,5 Dihydropiridines are neutral in Heart failure as Anti-hypertensives  Amlodipine and Felodipine have not been shown to decrease survival in heart failure.
  • 88. Kaplan–Meier Plots of the Time to the First Primary Event (Death or Cardiovascular Morbidity) among 571 Patients with Chronic Heart Failure Receiving Amlodipine and 582 Receiving Placebo. Packer M et al. N Engl J Med 1996;335:1107-1114.
  • 89. Drugs to Avoid In CHF  Antacids that contain sodium (salt): To relieve heartburn or indigestion.  Why: Just like eating salty foods, sodium from medications can cause your body to retain fluid, making swelling and shortness of breath worse and raising blood pressure.  Alternatives: Some companies produce low-sodium antacids. Look at the ingredients list and warning statements to see if sodium is listed (companies are required to put it on the label if there are 5 mg or more of sodium per dose). If you are not sure, ask your doctor or pharmacist.  Other Drugs to Avoid  Decongestants containing pseudoephedrine (such as Sudafed), which can raise blood pressure and force the heart to work harder  Alcohol and illicit drugs; they are a common cause of hospitalization for heart failure  Some nutritional supplements and growth hormone therapies (talk to your doctor about any you are considering taking)
  • 90. Other drugs to Avoid in Heart failure  Pain relievers called NSAIDs  Ibuprofen, such as Advil and Motrin  Naproxen, such as Aleve  Aspirin, such as Bayer • If your doctor has told you to take a low-dose aspirin every day for your heart problems, it's probably okay to take it. Low-dose aspirin can help prevent blood clots and may prevent a stroke or a heart attack. • Higher doses of aspirin may make your heart failure worse. Do not take aspirin for pain, such as from headaches or arthritis. Use acetaminophen, such as Tylenol, instead.  Pain relievers  Celecoxib  Etodolac  Indomethacin  Ibuprofen  Ketoprofen  Nabumetone  Naproxen  Piroxicam  Sulindac
  • 91. Drugs to Avoid in heart failure  Cold, cough, flu, or sinus medicines  Be sure to check the label. Do not take medicines that contain pseudoephedrine, ephedrine, phenylephrine, or oxymetazoline, such as: • Sudafed. • Nose sprays (decongestants), such as Afrin and Dristan. • Herbal remedies, such as ma huang and Herbalife.  Make sure your cough and cold medicines don't contain aspirin or ibuprofen.  Antiarrhythmics  These are drugs used to treat a fast or uneven heart rhythm. You may need to avoid the following: • Disopyramide • Dofetilide • Flecainide • Procainamide • Propafenone • Quinidine • Sotalol
  • 92. Drugs not to take with Heart failure  Antacids or laxatives that contain sodium  Check the label for sodium or saline. Examples include: • Antacids, such as Alka-Seltzer. • Laxatives, such as Fleet Phospho-Soda.  Calcium channel blockers  People with a certain kind of heart failure may need to avoid the following medicines: • Diltiazem • Verapamil  If you need to take a calcium channel blocker for another health problem, such as high blood pressure, your doctor will watch your health carefully.  Certain diabetes medicines  Most diabetes drugs are safe to take, but you may need to avoid the following: • Metformin • Rosiglitazone and pioglitazone1 ( Avandaia and ACTOS)
  • 93. Biggest Myth: Vitamins prevent CVD risk or heart failure risk.  The largest, randomized, double-blind trial to date has confirmed what smaller studies have suggested and what many physicians have long believed: a daily multivitamin does not reduce the risk of CVD  Physcians Health Study II results presented at AHA Nov 2012  PHS II launched in 1997, with a total of 14 641 US male physicians, age 50 or older at the outset, randomized to different vitamin arms or placebo. The other three arms of the study— looking at beta-carotene, vitamin E, or vitamin C  Over a median follow-up of 11.2 years, 1732 CV events occurred, but the rate of events was no higher among men taking placebo than those taking a daily multivitamin
  • 94. Ultrafiltration- doesn’t work  11/4/2012 AHA meeting- Ultrafiltration was associated with worsening renal function and more severe adverse events compared with optimum drug therapy in patients with acute decompensated heart failure in the CARRESS-HF trial  CARRESS-HF trial involved 188 patients with acute decompensated heart failure with worsening renal failure who were randomized to stepped pharmacological care or ultrafiltration. The primary end point was change in serum creatinine and change in weight (reflecting fluid offload) at 96 hours  -similar weight loss occurred in both groups (average about 12 pounds), but while there was little change in creatinine levels in the drug-treated group, there was a significant increase in creatinine in the ultrafiltration group. There was no difference between the two groups in death or hospitalization for heart failure, but there were more severe adverse events in the ultrafiltration group (72% vs 57%), mainly due to kidney failure, Bleeding and and IV-catheter-related complications.
  • 95. What doesn’t Help Aliskarin for dual ARB-Renin Blocade  November 3, 2012 in the New England Journal of Medicine.  Aliskiren Trial in Type 2 Diabetes Using Cardio-Renal Endpoints (ALTITUDE) trial, testing Aliskiren (Tekturna, Novartis Pharmaceuticals) as an adjunct to renin-angiotensin-aldosterone system (RAAS) blockade.  The drug not only failed to provide benefit to patients with type 2 diabetes at high risk of CV and renal events but may actually have been harmful .  In ALTITUDE, 8561 patients were randomly assigned to aliskiren (n=4274) or placebo (n=4287) on a background of an ACE inhibitor or ARB for approximately four years.  The primary end point was a composite of CV death, resuscitation from sudden death, nonfatal MI or stroke, unplanned hospitalization for heart failure, ESRD or renal death, or a doubling of serum creatinine for at least one month.  There was no statistical difference in the primary end point between the treatment groups, but the aliskiren group experienced more adverse events, especially hyperkalemia and hypertension.
  • 96. Neseritide- Doesn’t make a difference  ACC- 2010 - Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure(ASCEND-HF), there was "no evidence for a major benefit" from nesiritide vs placebo on top of standard care.
  • 97. Primary results and renal-function safety end point in ASCEND-HF, IV nesiritide in ADHF ASCEND-HF- End points Placebo (%), n=3511 Nesiritide (%), n=3496 p 30-d death/HF hospitalization* 10.1 9.4 0.31 •30-d death 4.0 3.6 •30-d HF rehospitalization 6.1 6.0 Dyspnea at 6 h* 42.1 44.5 0.030 •Moderately better 28.7 29.5 •Markedly better 13.4 15.0 Dyspnea at 24 h* 66.1 68.2 0.007 •Moderately better 38.6 37.8 •Markedly better 27.5 30.4 >25% decrease eGFR 29.5 31.4 0.11 a. *Co–primary end points eGFR=estimated glomerular filtration rate Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure 11/4/2010 American Heart Association
  • 98. The End Questions
  • 99. HFSA 2010 Practice Guideline (3.2) HF Risk Factor Treatment Goals Risk Factor Goal Hypertension Generally < 130/80 Diabetes See ADA guidelines1 Hyperlipidemia See NCEP guidelines2 Inactivity 20-30 min. aerobic 3-5 x wk. Obesity Weight reduction < 30 BMI Alcohol Men ≤ 2 drinks/day, women ≤ 1 Smoking Cessation Dietary Sodium Maximum 2-3 g/day 1Diabetes Care 2006; 29: S4-S42 2JAMA 2001; 285:2486-97 Adapted from:
  • 100. Common precursors of chronic heart failure  •Coronary artery disease (for example, consequent  upon acute myocardial infarction)  •Chronic hypertension  •Cardiomyopathy (for example, dilated,  hypertrophic, alcoholic, and idiopathic)  •Valve dysfunction (for example, diseases of the  aortic and mitral valve)  •Cardiac arrhythmias/conduction disturbance (for  example, heart block and atrial fibrillation)  •Pericardial disease (for example, constrictive  pericarditis)  •Infection (for example, rheumatic fever, Chagas  disease, viral myocarditis, and HIV
  • 101. History of Beta Blockade for CHF  1993, The Metoprolol in Dilated Cardiomyopathy Trial studied 383 patients with class 2-3 CHF for 18 months. The target dose of immediate-release metoprolol was 100 to 150mg per day. The metoprolol group showed reduced all- cause mortality compared to the placebo group, but the difference was small.  The major benefit was in need for heart transplant. Two metoprolol patients needed a heart transplant but 19 in the placebo group did. Metoprolol improved EF, quality of life, and exercise capacity compared to placebo
  • 102. USING BETA BLOCKERS IN PATIENTS WITH COMORBIDITIES  􀂄 AFTER MI-USE IN ALL PATIENTS WITHOUT A  CONTRAINDICATION  􀂄 COPD IS NOT A CONTRAINDICATION  UNLESS THERE IS SEVERE REACTIVE  AIRWAYS DISEASE  􀂄 PERIPHERAL VASCULAR DISEASE-USE  LOWER DOSES OF METOPROLOL OR  BISOPROLOL  􀂄 DIABETIC PATIENTS DERIVE SIGNIFICANT  BENEFIT-CARVEDILOL MAY BE PREFERRED
  • 103. Digoxin  􀂄 BLOOD LEVEL MONITORING REQUIRED  􀂄 LEVELS FOR HEART FAILURE ARE USUALLY  0.5-0.8NG/Ml FOR HEART FAILURE AND UP  TO 2NG/ML FOR ATRIAL FIBRILLATION  􀂄 DOSE DEPENDS ON DEGREE OF RENAL  FUNCTION.  􀂄 LOADING DOSES REQUIRED FOR MORE  RAPID RESPONSE  􀂄 MONITOR FOR NAUSEA AND VOMITING  WHICH ARE OFTEN EARLY SIGNS OF  TOXICITY
  • 104. Treatment of Diastolic CHF  APART FROM A FEW EXCEPTIONS DATA FROM LONG TERM INVESTIGATIONS OF ANY AGENT COMPARED TO PLACEBO IN PATIENTS WITH DIASTOLIC FAILURE ARE LACKING
  • 105. Diastolic CHF  REDUCTION IN LFT VENTRICULAR FILLING PRESSURES WITH THE USE OF DIURETICS AND/OR NITRATES  SLOWING OF THE HEART RATE WITH BETABLOCKERS AND /OR RATE LIMITING CALCIUM CHANNEL BLOCKERS SUCH AS VERAPAMIL (WHICH IS GENERALLY CONTRAINDICATED IN SYSTOLIC FAILURE)
  • 106. Diastolic CHF  RECENT STUDY WITH CANDERSARTAN IN PATIENTS WITH LVEF>40% DEMONSTRATED A SIGNIFICANT REDUCTION IN HOSPITALISATIONS FOR HEART FAILURE. THERE WAS NO SIGNIFIACNT DIFFERENCE IN THE RISK OF STROKES OR MYOCARDIAL INFARCTION
  • 107. Predictors of Mortality Based on Analysis of ADHERE Database  Classification and Regression Tree (CART) analysis of ADHERE data shows:  Three variables are the strongest predictors of mortality in hospitalized ADHF patients: BUN > 43 mg/dL Systolic blood pressure < 115 mmHg Serum creatinine > 2.75 mg/dL Fonarow GC et al. JAMA 2005;293:572-80

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