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GUIAS PARA EL MANEJO DEL FALLO CARDIACO

GUIAS PARA EL MANEJO DEL FALLO CARDIACO. RAFAEL E. CALDERON,MD. CARDIOLOGIA DE TRANSPLANTE Y FALLO CARDIACO OCTUBRE DEL 2002. Cost* of Heart Failure to Society. $22.5 billion. Hospital/Nursing home. 2.2. Home health/ Other medical durables. 15.5. 2.2. Indirect costs.

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GUIAS PARA EL MANEJO DEL FALLO CARDIACO

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  1. GUIAS PARA EL MANEJO DEL FALLO CARDIACO RAFAEL E. CALDERON,MD. CARDIOLOGIA DE TRANSPLANTE Y FALLO CARDIACO OCTUBRE DEL 2002

  2. Cost* of Heart Failure to Society $22.5 billion Hospital/Nursing home 2.2 Home health/Other medical durables 15.5 2.2 Indirect costs Healthcare providers 1.5 Drugs 1.1 *Direct and indirect costs in billions of $; estimated for year 2000 AHA. 2000 Heart and Stroke Statistical Update

  3. Predisposing Factors Toxins/drugs(EtOH) HTN Valvular disease Unknown Infections Environmental Genetic HTN Age Metabolic(Diabetes) Cardiomyopathy MI HF HFSA. Pharmacotherapy 2000;20:495

  4. Risk Factors, Ischemia, and Heart Failure in the Cardiovascular Continuum Arrhythmia MI Coronary thrombosis Loss of muscle Sudden death Myocardial ischemia Neurohormonal activation CAD Remodeling Atherosclerosis LVH Ventricular dilation • Risk factors • Hyperlipidemia • HTN • Diabetes • Insulin resistance HF Death Adapted with permission from Dzau V, Braunwald E. Am Heart J 1991;121:1244

  5. Pathophysiologic Effects of Angiotensin II PAI-1/ thrombosis Ang II Abnormal vasoconstriction Platelet aggregation Contractility Superoxide production Activate SNS Vascular smooth muscle growth Collagen Myocyte growth Aldosterone Vasopressin Remodeling Endothelin

  6. Guide for Heart Failure Therapy Goal: Prolong life and improve its quality • Slow progression of underlying disease(s) • Improve hemodynamics • Improve neurohormonal profile • Prevent sudden death • Decrease symptomatic arrhythmias • Relieve symptoms and improve exercise tolerance • Decrease ER visits, hospitalizations, and costs Objectives: HFSA. Pharmacotherapy 2000;20:495

  7. Why Symptom Relief is Not Enough • Heart failure is more than a symptomatic disease • Produces symptoms, limits functional capacity, and impairs quality of life • Heart failure is a progressive disease • Worsening symptoms and clinical deterioration, repeated hospitalization, and death • Death occurs frequently even in the presence of minimal symptoms or the absence of progressive symptoms • Symptoms do not always correspond with ejection fraction

  8. Evolution of Drug Therapies for CHF 18th Century 19th Century 1970s-1980s 1980s 1990s 1960s • Digitalis • Weak diuretics • Thiazides and furosemide • Vasodilators • IV inotropics • ACE inhibitors • Beta-blockers • Potential role for Angiotensin II antagonists • Aldosterone antagonists

  9. Systemic Effects of RAS Activation in CHF

  10. Schematic Representation of Mortality in Heart Failure Patients V-HeFT II(Class II–III)2n=804 trend toward  death 60 CONSENSUS I(Class IV)1n=25327%  mortalityP=0.003 40 SOLVD-Treatment (Class II–III)3n=256916%  mortalityP=0.0036 28%  mortality P=0.016 Mortality rate(%) 20 SOLVD-Prevention(Class I–II)4n=4228trend toward  death 0 6 48 54 60 12 18 24 30 36 42 0 Months 1CONSENSUS Trial Study Group. N Engl J Med 1987;316:1429; 2Cohn JN et al. N Engl J Med 1991;325:303; 3SOLVD Investigators. N Engl J Med 1991;325:293; 4SOLVD Investigators. N Engl J Med 1992;327:685

  11. ACE Inhibitors in CHF:Summary of Key Points • Consistent evidence that neurohormonal blockade alters natural history of CHF • ACE inhibitors improve survival across entire heart failure spectrum - mild, moderate, severe • Ace inhibitors delay progression of asymptomatic LV dysfunction to overt CHF

  12. The Case for ß-Blockade in Heart Failure Neurohormonal activation underlies disease progression and provides basis for treatment selection Weight of data for ß-blockade equals or exceeds that of ACE inhibitors ß-Blockade is added to ACE inhibitors for more complete neurohormonal blockade Carvedilol blocks ß1-, ß2-, and 1-receptors and is the only agent with ß-blocking properties approved and formulated for use in heart failure

  13. ß-Blockers in Heart Failure:Key Clinical Trials RISK REDUCTION / TOTAL MORTALITY TARGET DAILY DOSE TRIAL DRUG US Carvedilol (n = 1094) Carvedilol 50-100 mg 65% (P <0.001) MERIT-HF (N = 3718) Metropolol 200 mg 34% (P = 0.0062) CIBIS II (n = 2647) Bisoprolol 10 mg 33% (P <0.0001) Copernicus (n = 2289) Carvedilol 50 mg 35% (P = 0.0014)

  14. Risk reduction: 38% Placebo P=0.00003 TOPROL-XLRisk reduction: 38%P = .00003 MERIT-HF Cardiovascular Mortality 20 15 Percent of patients 10 5 0 0 3 6 9 12 15 18 21 Months of follow-up MERIT-HF Study Group. Lancet. 1999;353:2001-2007.

  15. Placebo TOPROL-XLRisk reduction: 41% P = .0002 MERIT-HFSudden Death 12 9 % of patients 6 3 3 6 9 12 15 18 21 Months of follow-up MERIT-HF Study Group. Lancet. 1999;353:2001-2007.

  16. DIG Study: Effect of Digoxin vs Placebo on Mortality in Patients With CHF and LVEF  45% Placebo P=0.80 Digoxin The Digitalis Investigation Group. N Engl J Med 1997;336:525-533.

  17. RADIANCE: Effect of Digoxin Withdrawal in Patients Optimally Treated With ACEIs • Risk of deterioration  6-fold •  Exercise tolerance •  Ejection fraction •  Quality of life Placebo (n=93) P<0.01 Digoxin (n=85) Packer M, et al. N Engl J Med 1993;329:1-7.

  18. RALES: Aldosterone Receptor Blockade Improves Outcomes in Severe Heart Failure Spironolactone Placebo RALES=RandomizedAldactone Evaluation Study Pitt B, et al N Engl J Med 1999;341:709-17

  19. Valsartan in Heart Failure Trial (Val-Heft) • Ace inhibitors are effective treatment for HF, post-MI, diabetic nephropathy, and atherosclerosis, but do not fully suppress RAAS • The RAAS exerts deleterious effects on the development and progression of HF • Addition of ARBs to usual therapy, including ACE inhibitors, is rational therapeutic approach • ARBs inhibit biologic effects of Ang II more completely than ACE inhibitors • ARBs potentially increase AT2 receptor stimulation resulting in increased bradykinin and NO production

  20. Heart Failure Hospitalizations 100 95 90 RR=27.5 % 85 P< 0.00001 Event-free Probability 80 75 70 Valsartan Placebo 65 0 0 3 6 9 12 15 18 21 24 27 Months Cohn JN. AHA 2000

  21. General Measures for the Management of Heart Failure Steering Committee and Membership of the Advisory Council to Improve Outcomes Nationwide in heart Failure Am J Cardiol. 1999;83 (Suppl 2A): 1A-39A

  22. Gottipaty et al: Proportional Mortality Increase • VEST study analysis • NYHA Class II-IV patients • 3,654 ECGs digitally scanned • Age, creatinine, LVEF, heart rate, and QRS duration found to be independent predictors of mortality at 1 year • Relative risk of widest QRS group 5x greater than narrowest

  23. QRS Variability in Congestive Heart Failure: Should QRS Criteria for Cardiac Resynchronization Therapy Be Expanded? (n = 31) Pts with QRS < 130 msec Pts with QRS  130 msec Aranda, et al HFSA Sept 2001

  24. Multicenter InSync Randomized Clinical Evaluation Results of a Randomized, Double-Blind, Controlled Trial to Assess Cardiac Resynchronization Therapy in Heart Failure Patients Presented by William T. Abraham, MD For the MIRACLE Investigators at the Late Breaking Clinical Trials II Session, American College of Cardiology Orlando, FL; March 20, 2001

  25. Unanswered Questions • Which subset of patients can benefit from biventricular pacing? • What are the long-term hemodynamic and structural consequences of CRT? • Is there potential to increase ischemic burden in patients with ischemic cardiomyopathy? • Will cardiac resynchronization therapy allow for increased use of beta-blocker therapy in patients with heart failure?

  26. Recommendations • Class I: There is evidence and/or general agreement that a given procedure/therapy is useful and effective. • Class II: There is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of performing the procedure/therapy • Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy. • Class IIb: Usefulness/efficacy is less well established by evidence/opinion. • Class III: There is evidence and/or general agreement that procedure/therapy is not useful/effective and in some cases may be harmful.

  27. Levels of Evidence • Level A: The data was derived from multiple randomized clinical trials • Level B: Data were derived from single randomized trial or nonrandomized studies • Level C: Consensus of opinion

  28. Clinical Assessment • Complete history (Class I Level of evidence C): comorbid conditions, cardiotoxic agents, STD’s, magnitude and duration of symptoms and family history • Physical exam (Class I Level of evidence C): Jugular venous pressure as ongoing assessment of volume status and S3 • Signs of hypoperfusion narrow pulse pressure, cool extremities, altered mentation, Cheynes-Stokes respiration, resting tachycardia.

  29. Clinical Assessment • Laboratory work up • CBC, U/A, SMA 20, TSH, CXR and 12 lead EKG (Class I Level of evidence C) • Serial monitoring of electrolytes and renal function (Class I Level of evidence C) • Screening for hemochromatosis, ANA levels, rheumatoid factor, urinary vanillylmandelic acid and metanephrines in selected patients (Class IIa Level of evidence C) • HIV status (Class IIb Level of evidence C) • Routine measurement of circulating levels of norepinephrine or endothelin (Class III Level of evidence C) • Routine Holter monitoring or signal averaged electrocardiography (Class III Level of evidence C)

  30. Clinical Assessment • Two-dimensional echocardiogram with Doppler flow. Single most useful diagnostic test. • Evaluation of LV function and other structural heart disease (Class I Level of evidence C) • Asymptomatic first degree relatives of idiopathic DCMP patients (Class IIa Level of evidence C) • Repeat measurement of EF in patients with change in clinical status (Class IIa Level of evidence C)

  31. Clinical Assessment • Functional capacity assessment during initial and follow up visits • Ability to perform routine and desired ADL’s (Class I Level of evidence C) • Maximal exercise testing with measurement of respiratory gas exchange and/or blood oxygen saturation to help determine whether HF is cause of exercise limitation when the contribution of HF is uncertain (Class IIa Level of evidence C) • Maximal exercise testing with measurement of respiratory gas exchange to identify high risk patients who are candidates for cardiac transplantation or other advanced treatments (Class IIa Level of evidence B) • Maximal exercise testing with measurement of respiratory gas exchange to facilitate prescription of exercise program (Class IIb Level of evidence C)

  32. Clinical Assessment • Noninvasive testing • Noninvasive imaging to detect ischemia and viability in patients with known CAD and no angina who are being considered for revascularization (Class IIa Level of evidence C) • Noninvasive imaging to define the likelihood of CAD in patients with LV dysfunction (Class IIb Level of evidence C)

  33. Clinical Assessment • Cardiac Catheterization with coronary arteriography • Patients with angina who are candidates for revascularization (Class I Level of evidence B) • Patients with chest pain who have not had evaluation of their coronary anatomy and who have no contraindications to coronary revascularization (Class IIb Level of evidence C) • Patients with known or suspected CAD but without angina who are candidates for revascularization (Class IIb Level of evidence C) • Repeat study or repeat noninvasive testing for ischemia in patients for whom CAD has been previously excluded as cause of LV dysfunction (Class III Level of evidence C)

  34. Clinical Assessment • Endomyocardial Biopsy overall usefulness is unclear • Patients suspected of having inflammatory or infiltrative disorder of the heart (Class IIb Level of evidence C) • Used to confirm disorders that may disqualify a patient for transplant (amyloidosis) or identify giant-cell myocarditis which due to rapid progression and poor response to therapy mandates immediate transplantation. • Routine evaluation of patients with HF (Class III Level of evidence C)

  35. Staging of HF • A new approach that emphasized both the evolution and progression of HF • It reliably and objectively identifies patients in the course of their disease • Links treatments that are appropriate at each stage of HF • It is intended to complement not substitute NYHA, which subjectively gauges severity of symptoms

  36. Staging of HF

  37. Staging of HF and Therapy

  38. Stage A of HF and Therapy • High risk of developing HF. • Control systolic and diastolic BP (Class I Level of evidence A) • Adequate control of DM. (not yet shown to reduce subsequent HF) • Treatment of lipid disorders in accordance with guidelines as patients with atherosclerotic disease are likely to develop HF (Class I Level of evidence B) • Treat Thyroid disease (Class I Level of evidence C) • Periodic evaluation for signs and symptoms of HF (Class I Level of evidence C)

  39. Stage A of HF and Therapy • Avoidance of cardiotoxic agents and behaviors such as smoking, illicit drug use and alcohol consumption.(Class I Level of evidence C) • Ionizing radiation to mediastinum and chemotherapeutic agents such as anthracyclines, high dose cyclophosphamide and the monoclonal agent trastuzumab. • Control ventricular rate of tachyarrhythmias (Class I Level of evidence B) • ACE inhibition in patients with history of atherosclerotic vascular disease, DM, HBP and associated cardiovascular risk factors (Class I Level of evidence B)

  40. Stage B of HF and Therapy • LV dysfunction without HF symptoms. • Patients with AMI should receive thrombolytic or undergo PTCA to decrease risk of developing HF. ACEI regardless of EF and even if ischemic episode is remote (Class I Level of evidence A) and /or beta-blocker regardless of EF (Class I Level of evidence A) improve survival. • Long term use of ACEI has been shown to delay onset of HF symptoms in patients with low EF independently of MI or not (Class I Level of evidence B) • Beta blockers independent of whether the patient has had MI should be given in low LVEF (Class I Level of evidence B)

  41. Stage B of HF and Therapy • Valve replacement or repair for patients with hemodynamically significant stenosis or regurgitation (Class I Level of evidence B) • Long term treatment with vasodilators in severe aortic regurgitation has not been shown to reduce risk of HF or death (Class IIb Level of evidence B) • Treatment with digoxin in asymptomatic patient with LV dysfunction who are in sinus rhythm is not recommended (Class III Level of evidence C)

  42. Stage C of HF and Therapy • LV dysfunction with current or prior symptoms. • Sodium restriction. • Daily weight. • Influenza and pneumococcal vaccination. • Physical activity exercise program. (Class IIa Level of evidence A) • Avoidance of NSAIDs (including COX2), calcium channel blockers ( except amlodipine) and antiarrhythmic agents (except amiodarone). (Class I Level of evidence B) • Monitor potassium (3.8-5.2mmol per L) and magnesium. • Patient education and close supervision.

  43. Stage C of HF and Therapy

  44. Stage C of HF and Therapy • Diuretics. For fluid retention. (Class I Level of evidence A) • Inhibit reabsorption of sodium or chloride at specific sites in the renal tubule. • Loop diuretics excrete up to 20-25% Na, enhance free water clearance and remain effective unless severe renal impairment. • No long term studies effects on morbidity and mortality are not known • Produce symptomatic relief more rapidly than any other drug. • Risk of use is electrolyte depletion, hypotension and azotemia.

  45. Stage C of HF and Therapy • ACE inhibitors. (Class I Level of evidence A) • Not only interferes with RAS but potentates action of kinins and kinin-mediated prostaglandin. • Alleviate symptoms, improve clinical status, reduce risk of death and of hospitalization. • Contraindicated if angioedema or pregnant . • Fluid retention can blunt effects and fluid depletion can potentate adverse effects (Hypotension, hyperkalemia, renal failure) • Cough. All other causes must be excluded medication withdrawn with improvement after 1-2 weeks and reappearance after rechallenge with another ACEI.

  46. Stage C of HF and Therapy • Beta-blockers principally inhibit effects of sympathetic nervous system and should be given to all patients with symptoms (Class I Level of evidence A) • Alleviate symptoms, improve clinical status, reduce risk of death and of hospitalization. • Diuretics are needed to maintain sodium balance and prevent fluid retention that can accompany initiation of beta-blocker. • Should be given only if no or only minimal evidence of fluid retention and no recent use of intravenous positive inotropic agent.

  47. Stage C of HF and Therapy • Beta-blockers • A patient who has been using medication for more than 3 months and has acute decompensation should not be taken off medication and diuretics should be adjusted. If decompensation is cause due to hypoperfusion then medication should be stopped and positive inotropic agent that doesn’t mediate its effects through beta receptor is preferred. • Side effects include fatigue, fluid retention,bradychardia, heart block, and hypotension. • Should not be given to patients with hyperactive airway disease yet should be given to COPD patients.

  48. Stage C of HF and Therapy • Digitalis (Class I Level of evidence A) • Inhibits Na-K ATPase • In cardiac cells causing increased contractility • Vagal afferent fibers sensitize carotid baroreceptor which reduces sympathetic out flow of CNS • Kidney reduces renal tubular reabsorption of Na which leads to suppression of of renin secretion • Improves symptoms, exercise tolerance and quality of life yet little effect on mortality • Dose should be of 0.125-0.25mg QD, without loading and lower if patient is over age 70, has renal impairment or low lean body mass • Serum levels are followed for purpose of toxicity and not to guide therapy

  49. Stage C of HF and Therapy • Spironolactone (Class IIa Level of evidence B) • Low doses reduced risk of mortality in patents with current or recent class IV symptoms • Effects were most marked in those taking digitalis and beta blockers • Role in mild to moderate HF not clear and use cannot be recommended • Risk of hyperkalemia and painful gynecomastia

  50. Stage C of HF and Therapy • Angiotensin receptor blocker • Should not be considered superior or equivalent to ACEI (Class III Level of evidence B) • Added to therapy before a beta-blocker (Class III Level of evidence A) • Should not be added to therapy if taking an ACEI and beta-blocker • Should be given if ACEI intolerant (Class IIa Level of evidence A)

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