Heartfailure

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Heartfailure

  1. 1. 2012 Focused Update ACCF/AHA/ESC/HFA Guidelinesfor the Diagnosis and Management of Heart Failure in Adults Update in the management of heart failure 2012
  2. 2. Walls have ears Sir THOMAS LEWIS ,1933
  3. 3. Change before you have to Jack Welch Better a low dose than no dose
  4. 4. - Patients with acute heart failure frequentlydevelop chronic heart failure.- Patients with chronic heart failure frequentlydecompensate acutely. ESC Guidelines - update
  5. 5. ESC Guidelines - update
  6. 6. Diagnosis of heart failure 2012
  7. 7. New York Heart Association functional classification based on severity of symptoms and physical activity
  8. 8. heart failure 2012
  9. 9. ESC Guidelines - update
  10. 10. Symptoms and signs typical of heart failure 2012
  11. 11. heart failure 2012
  12. 12. ESC Guidelines - update
  13. 13. heart failure 2012
  14. 14. heart failure 2012
  15. 15. ACC-AHA
  16. 16. heart failure 2012
  17. 17. Stages of Heart FailureAt Risk for Heart Failure:STAGE A High risk for developing HFSTAGE B Asymptomatic LV dysfunctionHeart Failure:STAGE C Past or current symptoms of HFSTAGE D End-stage HF
  18. 18. Stages of Heart Failure• Designed to emphasize preventability of HF• Designed to recognize the progressive nature of LV dysfunction
  19. 19. Mechanisms and Models in Heart Failure1.The "cardiorenal model" :as a problem of excessive salt andwater retention that was caused by abnormalities of renal bloodflow2. The "hemodynamic model " :to arise largely as a result ofabnormalities of the pumping capacity of the heart andexcessive peripheral vasoconstriction3. The ―neurohormonal hypothesis‖: a theory to explain themechanism of disease progression in heart failure4. The biomechanical model :many device-based therapies thatconcurrently affect LV pump performance and LV remodeling(eg, cardiac resynchronization) are beneficial Douglas L. Mann, MD; Michael R. Bristow; Mechanisms and Models in Heart Failure CIRCULATION,2005
  20. 20. ESC Guidelines - update
  21. 21. heart failure 2012
  22. 22. ESC Guidelines - update
  23. 23. heart failure 2012
  24. 24. heart failure 2012
  25. 25. Atrial fibrillation2012
  26. 26. heart failure 2012
  27. 27. heart failure 2012
  28. 28. heart failure 2012
  29. 29. Algorithm for the diagnosis of Heart Failure or Left Ventricular DysfunctionSuspected LV dysfunction because of signs Suspected Heart Failure because of symptoms and signs NormalAssess presence of cardiac disease by ECG, X-ray or Heart failure or LV dysfunctionNatriuretic peptides ( where available) unlikely Tests abnormal Normal Imaging by Echocardiography (Nuclear angiography Heart failure or LV dysfunction or MRI where available) unlikely Tests abnormal Additional diagnostic testsAssess aetiology, degree, precipitating factors andtype of cardiac dysfunction Where appropriate (e.g. coronary angiography) Choose therapy ESC Guidelines
  30. 30. ESC Guidelines - update
  31. 31. ESC Guidelines - update
  32. 32. ESC Guidelines - update
  33. 33. ESC Guidelines - update
  34. 34. ESC Guidelines - update
  35. 35. Chronic Heart Failure; Drugs That Reduce Mortality; Improve Symptoms, or Might HarmReduce Mortality; Must Try to Use1. ACE inhibitors or ARBs2. ß-Blockers3. Spironolactone or eplerenone4. Isosorbide-hydralazine (in some)Improve Symptoms; Use According to Clinical Judgment1. Diuretics2. Digoxin (low dose)3. Nitrates4. Ion for anemia5. Metabolically active agents (consider)May be Harmful; Use Cautiously After Due Consideration1. Inotropes and inotropic dilators2. Antiarrhythmics, except ß-Blockers and amiodarone3. Calcium channel blockers4. High-dose digoxin Drugs for the Heart, 7th, 2009
  36. 36. Drugs for the Heart, 7th, 2009
  37. 37. ACE-i. Mechanism of ActionVASOCONSTRICTION VASODILATATION ALDOSTERONE PROSTAGLANDINS VASOPRESSIN Kininogen tPA SYMPATHETIC Kallikrein Angiotensinogen RENIN Angiotensin I BRADYKININ A.C.E. Inhibitor Kininase IIANGIOTENSIN II Inactive Fragments
  38. 38. ACE Inhibitors – In Whom and When? Indications: • Potentially all patients with heart failure • First-line treatment (along with beta-blockers) in NYHA class I–IV heart failure Contra-indications: • History of angioedema • Bilateral renal artery stenosis • Significant renal dysfunction (creatinine >2.5 mg/dL or 221 µmol/L) • Serum potassium concentration (K+ >5.0 mmol/L) • Severe aortic stenosis • Symptomatic or severe asymptomatic hypotension (SBP <90 mmHg) Drug interactions to look out for: • K+ supplements/ K+ sparing diuretics (including spironolactone) • NSAIDs* • AT1-receptor blockers *avoid unless essentialMcMurray J, Cohen-Solal A, Dietz R, Eichhorn E, Erhardt L, Hobbs R, Maggioni A, Pina I, Soler-Soler J, Swedberg K ESC Guidelines - update
  39. 39. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — ACE INHIBITORS —ACE Inhibitors – How to Use • Start with a low dose • Double dose at not less than two weekly intervals • Aim for target dose or, failing that, the highest tolerated dose • Remember some ACE inhibitor is better than no ACE inhibitor • Monitor blood chemistry (urea, creatinine, K+) and blood pressure • When to stop up-titration/down-titration – see PROBLEM SOLVINGMcMurray J, Cohen-Solal A, Dietz R, Eichhorn E, Erhardt L, Hobbs R, Maggioni A, Pina I, Soler-Soler J, Swedberg K
  40. 40. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — ACE INHIBITORS — ACE Inhibitors – Advice to Patient • Explain expected benefits (see WHY?) • Treatment is given to improve symptoms, to prevent worsening of heart failure and to increase survival • Symptoms improve within a few weeks to a few months • Advise patients to report principal adverse effects (i.e. dizziness/symptomatic hypotension, cough)McMurray J, Cohen-Solal A, Dietz R, Eichhorn E, Erhardt L, Hobbs R, Maggioni A, Pina I, Soler-Soler J, Swedberg K
  41. 41. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — ACE INHIBITORS — ACE Inhibitors – Problem SolvingCough: • Cough is common in patients with heart failure, many of whom have smoking-related lung disease • Cough is also a symptom of pulmonary oedema, which should be excluded if a new or worsening cough develops • ACE inhibitor-induced cough rarely requires treatment discontinuation • If a very troublesome cough develops (e.g. one stopping the patient sleeping) and can be proven to be due to ACE inhibition (i.e. it recurs after ACE inhibitor withdrawal and rechallenge), substitution with an AT1-receptor blocker can be considered McMurray J, Cohen-Solal A, Dietz R, Eichhorn E, Erhardt L, Hobbs R, Maggioni A, Pina I, Soler-Soler J, Swedberg K
  42. 42. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — ACE INHIBITORS —ACE Inhibitors – Problem Solving (continued) Worsening renal function: • Some increase in urea (blood urea nitrogen), creatinine and K+ is to be expected after initiation; if the increase is small and asymptomatic no action is necessary • An increase in creatinine of up to 50% above baseline, or 3 mg/dL (266 µmol/L), whichever is the smaller, is acceptable • An increase in K+ 6.0 mmol/L is acceptable • If urea, creatinine or K+ rise excessively, consider stopping concomitant nephrotoxic drugs (e.g. NSAIDs), other K+ supplements/ K+ retaining agents (triamterene, amiloride) and, if no signs of congestion, reducing the dose of diuretic • If greater rises in creatinine or K+ than those outlined above persist, despite adjustment of concomitant medications, halve the dose of ACE inhibitor and recheck blood chemistry; if there is still an unsatisfactory response, specialist advice should be sought McMurray J, Cohen-Solal A, Dietz R, Eichhorn E, Erhardt L, Hobbs R, Maggioni A, Pina I, Soler-Soler J, Swedberg K
  43. 43. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — ACE INHIBITORS —ACE Inhibitors – Problem Solving (continued) Worsening renal function (cont.): • If K+ rises to >6.0 mmol/L, or creatinine increases by >100% or to above 4 mg/dL (354 µmol/L), the dose of ACE inhibitor should be stopped and specialist advice sought • Blood chemistry should be monitored serially until K+ and creatinine have plateaued NOTE: it is very rarely necessary to stop an ACE inhibitor and clinical deterioration is likely if treatment is withdrawn; ideally, specialist advice should be sought before treatment discontinuationMcMurray J, Cohen-Solal A, Dietz R, Eichhorn E, Erhardt L, Hobbs R, Maggioni A, Pina I, Soler-Soler J, Swedberg K
  44. 44. Role of Angiotensin II in Vascular Disease Blocking the RAAS with ACE inhibitors and ARBs Chung, Unger., Am J Hypertens 1999;12:150S–156S
  45. 45. Renin-Angiotensin MechanismBeta-blocker ACEI ARB renal juxtaglomerular BRAUNWALDS HEART DISEASE
  46. 46. Benefits of RAAS Blockade for Renal Protection Haemodynamic effects  Reduction in systemic BP  Reduction in glomerular capillary pressure  Reduction in proteinuria Angiotensin II Non-haemodynamic effects  Stimulation of extracellular matrix degradation  Inhibition of macrophage/monocyte infiltration
  47. 47. Potential Mechanisms whereby Angiotensin II Receptor Blockers (ARBs) Interact with Peroxisome Proliferator-activated Receptor Gamma (PPAR ) Angiotensin II ARB AT2 AT1 ARB L RA p300 Anti-diabetic PPAR RxR Anti-hypertensive Anti-inflammatory PPRE Gene 5’ 3’Acta Diabetologia (2005) 42:S26-S32
  48. 48. Morbidity and Mortality along the Cardiovascular Continuum Remodeling Ventricular Dilation Myocardial Congestive Infarction Heart Failure CAPRICORN Atherosclerosis ISIS 1 MERIT-HF End-Stage and LVH BHAT CIBIS Heart Disease TIMI-II and Death Risk Factors MAPHY COPERNICUS Diabetes UKPDS Death HypertensionAdapted from Dzau V, Braunwald E. Am Heart J. 1991;121:1244-1263.
  49. 49. Acute renal failure for ACE
  50. 50. Opie 2008 Positively inotropic Tachycardia DromotropicAC : adenyl cyclase ; Gs : stimulatory protein G; PKA ; protein kinase A ; P :phosphorylatePDE : phosphodiesterase ; Ach : acetylcholine LH. Drug for the Heart. Elsevier Saunders 2009, 7th ed p.3 Opie
  51. 51. Cardiac effects of beta-blockers Interacting drugs Nodal depression by Negative chronotropic Negative dromotropic Anti- arrhythmic Negative inotropic Anti-ischemicOpie LH. Drug for the Heart. Elsevier Saunders 2009
  52. 52. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — BETA BLOCKERS —Beta Blockers – In Whom and When?Cautions/seek specialist advice: • Severe (NYHA Class IV) heart failure • Current or recent (<4 weeks) exacerbation of heart failure (e.g. hospital admission with worsening heart failure) • Heart block or heart rate <60 beats/min • Persisting signs of congestion – raised jugular venous pressure, ascites, marked peripheral oedema Drug interactions to look out for: • verapamil/diltiazem (should be discontinued) • amiodarone
  53. 53. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — BETA BLOCKERS —Beta Blockers – How to Use• Start with a low dose• Double dose at not less than two-weekly intervals• Aim for target dose or, failing that, the highest tolerated dose• Remember some beta-blocker is better than no beta-blocker• Monitor HR, BP, clinical status (symptoms, signs – especially signs of congestion, and body weight)• Check blood chemistry 1–2 weeks after initiation and 1–2 weeks after final dose titration• A specialist heart failure nurse may assist with patient education, follow-up (in person/by telephone) and dose up-titration• When to down-titrate/stop up-titration – see PROBLEM SOLVING
  54. 54. Heart Failure: A Firm Indication for beta Blockade – Titration and Doses of DrugsBeta Blockers First Dose 3rd Week 5th-6th Week Final DoseCarvedilol 3.125 6.25 2 12.5 2 25 2Metoprolol SR 25 50 100 200Bisoprolol 1.25 3.75 5.0 10.0Nebivolol 1.25 2.5 5.0 10 Drugs for the Heart, 7th, 2009
  55. 55. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — BETA BLOCKERS —Beta Blockers – Which and What Dose? Starting dose Target dose bisoprolol 1.25 mg od 10 mg od carvedilol 3.125 mg bd 25–50 mg bd metoprolol CR/XL 12.5–25 mg od 200 mg od od = once daily; bd = twice daily
  56. 56. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — BETA BLOCKERS —Beta Blockers – Problem SolvingWorsening symptoms/signs (e.g. increasing dyspnoea,fatigue, oedema, weight gain):• If increasing congestion, double the dose of diuretic and/or halve the dose of beta-blocker (if increasing diuretic does not work)• If marked fatigue (and/or bradycardia – see below), halve the dose of beta-blocker (rarely necessary)• Review patient in 1–2 weeks; if not improved, seek specialist advice• If serious deterioration, halve the dose of beta-blocker or stop this treatment (rarely necessary); seek specialist advice
  57. 57. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — BETA BLOCKERS —Beta Blockers – Problem Solving (continued)Low heart rate:• If <50 beats/min and worsening symptoms – halve the dose of beta-blocker or, if severe deterioration, stop beta-blocker (rarely necessary)• Review need for other heart-rate slowing drugs (e.g. digoxin, amiodarone, diltiazem)• Arrange ECG to exclude heart block• Seek specialist advice
  58. 58. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — BETA BLOCKERS —Beta Blockers – Problem Solving (continued)Asymptomatic low blood pressure:• Does not usually require any change in therapySymptomatic hypotension:• If dizziness, light-headedness and/or confusion and a low blood pressure occur, reconsider need for nitrates, calcium channel blockers and other vasodilators• If no signs/symptoms of congestion, consider reducing diuretic dose• If these measures do not solve problem, seek specialist adviceNOTE: Beta-blockers should not be stopped suddenly unless absolutely necessary (there is a risk of a ‘rebound’ increase in myocardial ischaemia/infarction and arrhythmias); ideally specialist advice should be sought before treatment discontinuation
  59. 59. Aldosterone Inhibitors Spironolactone ALDOSTERONECompetitive antagonist of the -aldosterone receptor(myocardium, arterial walls, kidney)• Retention Na+ • Collagen Edema deposition• Retention H2O Fibrosis• Excretion K+ - myocardium Arrhythmias• Excretion Mg2+ - vessels
  60. 60. The Renin-Angiotensin-Aldosterone SystemWeber K. N Engl J Med 2001;345:1689-1697
  61. 61. The Renin-Angiotensin-Aldosterone (RAA) System Kidneys Adrenal cortex Liver secretes secrete secretes angiotensinogen renin aldosterone Angiotensin converting Blood Renin enzyme (ACE) Angiotensinogen Angiotensin I Angiotensin II Aldosterone NA+ retention Growth Vascular H2O retention factor Sympathetic smooth muscle K+ excretion stimulation activation constriction Mg+ excretion
  62. 62. Điều hòa ngược trong bài tiết Aldosterone Afferent Arteriole AngiotensinogenGlomerulus Renin _ _ A-I “Short Volume Loop” Converting Enzyme Efferent Arteriole A-II Na reabsorption K excretion Cortical Collecting _ Adrenal Duct K
  63. 63. Extraadrenal Production of Aldosterone by Endothelial and Vascular Smooth-Muscle Cells in an Intramyocardial Coronary Artery Weber K. N Engl J Med 2001;345:1689-1697
  64. 64. Heart Failure Angiotensinogen Renin Angiotensin I ACE ACEI reduces Angiotensin II levels Angiotensin II ACTH K+ Elevated Other ALDOSTERONE Na+ Verospirone & Eplerenone blocks Aldosterone at receptors Pathologic Fluid retention Hypokalemia,LVH/myocardial And edema Hypomagnesemia, fibrosis arrhythmias Morbidity Mortality
  65. 65. Role of Aldosterone in CV DiseaseAngiotensin II–K+ –ACTH- Norepinephrine – Serotonin – Endothelin-NO Aldosterone Kidneys Brain Blood Vessels Heart +SNS Na+ reabsorption Blood Cytokine Activation K+ excretion Pressure Vascular Inflammation Cardiac Hypertrophy Endothelial Dysfunction Myocardial fibrosis Hypertension Vascular Injury LV Hypertrophy Ventricular Remodeling End-stage renal disease, MI, HF, Arrhythmias
  66. 66. Aldosterone in Heart Failure
  67. 67. Aldosterone in Heart Failure Aldosterone  K+  Mg++  Arterial compliance  LV  Fibrosis  Baroreceptor function  Na+ mass  Norepinephrine uptake &  Norepinephrine Uptake  Endothelial function fibrosis  PAI-1  Heart rate variability  Ischemic Edema  Remodeling  Arrhythmia Events Progression of HF Sudden cardiac death
  68. 68. Aldosterone Antagonists Non-diuretic doses RALES trial  Spironolactone  Class III-IV EPHESUS trial  Eplerenone  Low EF after MI
  69. 69. Randomized Aldactone Evaluation Study (RALES) 1.00 0.95 0.90 0.85 0.80 0.75 Probability 0.70 Spironolactone of Survival 0.65 0.60 p< 0.001 0.55 Placebo 0.50 0.45 0.00 0 3 6 9 12 15 18 21 24 27 30 33 36 MonthsPitt et al. N Engl J Med. 1999;341(10):709-717.
  70. 70. EPHESUS Total deaths  478 eplerenone  554 placebo CV deaths  407 eplerenone  483 placebo
  71. 71. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — SPIRONOLACTONE—Spironolactone – In Whom and When? Indications: • Potentially all patients with symptomatically moderately severe or severe heart failure • Second-line therapy (after ACE inhibitors and beta-blockers) in patients with NYHA class III–IV heart failure Cautions/seek specialist advice: • Significant renal dysfunction (creatinine >221 µmol/L or 2.5 mg/dL) • Significant hyperkalaemia (K+ >5.0 mmol/L)
  72. 72. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — SPIRONOLACTONE—Spironolactone – How to Use • Start at 25 mg once daily • Check blood chemistry at 1, 4, 8 and 12 weeks; 6, 9 and 12 months; 6 monthly thereafter • If K+ rises to between 5.5 and 6.0 mmol/L, or creatinine rises to 2.5 mg/dL (221 µmol/L), reduce dose to 25 mg on alternate days and monitor blood chemistry closely • If K+ rises to >6.0 mmol/L, or creatinine to >4.0 mg/dL (354 µmol/L), stop spironolactone and seek specialist advice
  73. 73. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — SPIRONOLACTONE—Spironolactone – Advice to Patient • Explain expected benefits (see WHY?) • Treatment is given to improve symptoms, prevent worsening of heart failure and to increase survival • Symptom improvement occurs within a few weeks to a few months of starting treatment • Avoid NSAIDs not prescribed by a physician (self-purchased ‗over the counter‘ treatment, e.g. ibuprofen) • Temporarily stop spironolactone if diarrhoea and/or vomiting occur and contact physician
  74. 74. Practical Recommendations for Heart Failure Treatment: Putting Guidelines into Practice — SPIRONOLACTONE—Spironolactone – Problem Solving Worsening renal function/hyperkalaemia: • See HOW TO USE section • Major concern is hyperkalaemia (K+ >6.0 mmol/L) though this was uncommon in RALES; a high-normal K+ may be desirable in heart failure patients, especially if taking digoxin • It is important to avoid other K+ retaining drugs (e.g. K+ sparing diuretics) and nephrotoxic agents (e.g. NSAIDs) • Some ‗low salt‘ substitutes have a high K+ content • Male patients may develop breast discomfort and/or gynaecomastia
  75. 75. Diuretics Thiazides Inhibit active exchange of Cl-NaCortex in the cortical diluting segment of the ascending loop of Henle K-sparing Inhibit reabsorption of Na in the distal convoluted and collecting tubule Loop diureticsMedulla Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle Loop of Henle Collecting tubule
  76. 76. Diuretic Therapy Renal Reabsorption of Na ( Hypomagnesemia and Mg)Hyponatremi Saluresis & a Diuresis Plasma Volume Cardiac Renal Blood PRA Output Flow Postural GFR Distal Ca++ Aldosterone hypotension Reabsorption Pre-renal Proximal Kaliuresis Azotemia Reabsorption Hyper- (?) CLUric acid CLcalcium Hypokalemia cholesterole mia Hyperuricemia Hypercalcemia Glucose Tolerence Kaplan’s Clinical Hypertension , 2006
  77. 77. Thiazides, Loop Diuretics. Adverse Effects • K+, Mg+ (15 - 60%) (sudden death ???) • Na+ • Stimulation of neurohormonal activity • Hyperuricemia (15 - 40%) • Hypotension. Ototoxicity. Gastrointestinal. Alkalosis. MetabolicSharpe N. Heart failure. Martin Dunitz 2000;43Kubo SH , et al. Am J Cardiol 1987;60:1322MRFIT, JAMA 1982;248:1465Pool Wilson. Heart failure. Churchill Livinston 1997;635
  78. 78. Diuretic Resistance • Neurohormonal activation • Rebound Na+ uptake after volume loss • Hypertrophy of distal nephron • Reduced tubular secretion (renal failure, NSAIDs) • Decreased renal perfusion (low output) • Altered absortion of diuretic • Noncompliance with drugsBrater NEJM 1998;339:387Kramer et al. Am J Med 1999;106:90
  79. 79. Managing Resistance to Diuretics • Restrict Na+/H2O intake (Monitor Natremia) • Increase dose (individual dose, frequency, i.v.) • Combine: furosemide + thiazide / spiro / metolazone • Dopamine (increase cardiac output) • Reduce dose of ACE-i • UltrafiltrationMotwani et al Circulation 1992;86:439
  80. 80. ESC Guidelines - update
  81. 81. Vasodilators VENOUS Venous Nitrates Vasodilatation Molsidomine MIXED Calcium antagonists -adrenergic Blockers ACE-I, ARBs K+ channel activators Nitroprusside Arterial ARTERIAL Vasodilatation Minoxidil Hydralazine
  82. 82. NITRATES HEMODYNAMIC EFFECTS1- VENOUS VASODILATATION Pulmonary congestion Ventricular size Preload Vent. Wall stress MVO22- Coronary vasodilatation Myocardial perfusion3- Arterial vasodilatation • Cardiac output Afterload • Blood pressure4- Others
  83. 83. ESC Guidelines - update
  84. 84. ESC Guidelines - update
  85. 85. Mechanism of action of digoxin. Digoxin inhibits Na+/K+ ATPase. As a consequence of an increasedintercellular Na+ concentration, Ca2+ extrusion (via Na+/Ca2+ exchange) is reduced. The result is an increasein cellular Ca2+.
  86. 86. Digitalis -Na-K ATPase Na+ Na-Ca Exchange K+ Na+ Ca++ Myofilaments Ca++ K+ Na+ CONTRACTILITY
  87. 87. Digitalis. Mechanism of ActionBlocks Na+ / K+ ATPase => Ca+ +• Inotropic effect• Natriuresis• Neurohormonal control - Plasma Noradrenaline - Peripheral nervous system activity - RAAS activity - Vagal tone - Normalizes arterial baroreceptors NEJM 1988;318:358
  88. 88. Digitalis. Clinical Effects• Improve symptoms• Modest reduction in hospitalization• Does not improve survival
  89. 89. Digitalis. Indications• When no adequate response to ACE-i + diuretics + beta-blockers AHA / ACC Guidelines 2001• In combination with ACE-i + diuretics if persisting symptoms ESC Guidelines 2001• AF, to slow AV conductionDose 0.125 to 0.250 mg / day
  90. 90. Digoxin. Contraindications• Digoxin toxicity• Advanced A-V block without pacemaker• Bradycardia or sick sinus without PM• PVC’s and VT• Marked hypokalemia• W-P-W with atrial fibrillation
  91. 91. ESC Guidelines - update
  92. 92. Device Therapy1.Implantable Cardioverter- Defibrillators (ICD)2.Cardiac Resynchronization Therapy or Biventricular Pacing3.Ventricular Assist Devices
  93. 93. CRT: cardiac resynchronization therapy
  94. 94. ESC Guidelines - update
  95. 95. Chronic Heart Disease Aims of treatmentPrevention Prevention and / or controlling of disease leading to cardiac dysfunction and heartdisease Prevention of progression to heart failure once cardiac dysfunction is establishedMorbidity Maintenance or improvement in quality of life Avoid re-admissionsMortality Increased duration of lifeNon-pharmacological management The ESC Guidelines for the Diagnosis & Treatment of Chronic Heart Failure
  96. 96. General advice and measuresPatient and family education-Explain what HF is and why symptoms occur-Causes of HF-How to recognize symptoms and what to do when they occur-Daily self-weighing and what to do in case of weight gain-Rationale for treatments-Importance of adhering to pharmacological and non-pharmacological prescriptions-Refrain from smoking-PrognosisDrug counselling-Effects-Doses and times of administration-Side-effects and adverse effects-What to do in case of skipped doses-Self-management The ESC Guidelines for the Diagnosis & Treatment of Chronic Heart Failure
  97. 97. General advice and measures (continued…)Dietary and social habits-Control sodium intake when necessary (e.g. some patients with advanced HF)-Avoid excessive fluid intake (e.g. >1.5 L/day) in severe HF-Avoid excessive alcohol fluid intake-Reduce weight in obese patients-Assess malnutrition and cardiac cachexiaRest and exercise-Rest recommended only in AHF or decompensated CHF-Encourage daily physical activities that do not induce symptoms-Recommended exercise training programme in stable NYHA class II-III patients-Work counselling Sexual activity-Phosphodiesterase-5 inhibitors are not recommended in advance heart failure. It used, they should be avoided < 24-48 h of nitrate intake depending on agent. The ESC Guidelines for the Diagnosis & Treatment of Chronic Heart Failure
  98. 98. General advice and measures (continued…)Travelling- Discourage long journeys, high altitudes, very hot or humid placesVaccinations- Advice on immunizations-Immunization for influenza is widely usedDrugs to avoid or use with caution-Non-steroidal anti-inflammatory drugs (NSAIDs) & coxibs-Class I anti-arhythmics-Calcium-antagonists-Tricyclic antidepressants-Lithium-Corticosteroids The ESC Guidelines for the Diagnosis & Treatment of Chronic Heart Failure
  99. 99. ESC Guidelines - update
  100. 100. 50 – 60% < 5%. Normal blood pressure: Vasodilators Reduced blood pressure : Inotropics or vasopressors 20%,Dec G.W. Management of Acute Decompensated Heart Failure. Curr Probl Cardiol 2007; 32: 319 - 366
  101. 101. http://www.biomerieux-diagnostics.com/servlet/srt/bio/clinical-diagnostics/dynPage?node=Heart_Failure
  102. 102. Ventricular Stretch Enzyme corin T ½ 1.5 to 2 hours T ½ 20 minutes Heart Failure Clin 2 (2006)-291-298
  103. 103. The prognostic power of BNP &ø Troponins 30–70% of patients hospitalized with AHFS have detectable plasma levels of cardiac troponin( Troponin I or Troponin T*) Associated with a 2-fold increase in postdischarge mortality and a 3-fold increase in rehospitalization rate elevated cTnI and elevated BNP identified patients with advanced HF with a markedly increased risk of death (12-fold increase) ** * Gheorghiade M et al. Circulation 2005; 112: 3958 – 3968 ** Horwich TB et al. Circulation 2003; 108: 833 - 838
  104. 104. Gheorghiade M et al. Circulation 2005; 112: 3958 – 3968
  105. 105. Predictor PointsElevated NT-proBNP 4Interstitial edema on chest X-ray 2Orthopnea 2Absence of fever 2Current loop diuretic use 1Age > 75 years 1Rales on lung examination 1Absence of cough 1 A total score of ≥ 6 has a highInterpretation predictive accuracy for the diagnosis of acute HF http://www.biomerieux-diagnostics.com/servlet/srt/bio/clinical- diagnostics/dynPage?node=Heart_Failure
  106. 106. Diagnosis of acute HF
  107. 107. Evaluationand Management of Heart Failure
  108. 108. B-type Natriuretic Peptide (BNP) BNP is a neurohormone secreted by the myocardium in response to stretch Elevated BNP levels are associated with elevated ventricular filling pressures Large variation in “normal” or optimal level  Obesity  Age  Gender
  109. 109. BNP Levels in Patients With Dyspnea Secondary to COPD or CHF 1200 1076 +/- 138 1000 p < 0.001 BNP pg/mL 800 600 400 86 +/- 39 200 0 COPD CHF N=56 N=94 Cause of DyspneaDao Q et al, JACC 2001
  110. 110. BNP Levels for Types of Lung Disease 207 272Morrison KL et al, JACC 2002
  111. 111. How do I monitorresponse to treatment?
  112. 112. Echocardiography Once the diagnosis of heart failure due to systolic dysfunction is established, repeat echocardiography is indicated only  For significant change in functional status  To assess response to beta blockade
  113. 113. Uses of BNP levels DIAGNOSIS  Levels less than 100 pg/ml generally exclude a cardiac cause of dyspnea PROGNOSIS  Failure to lower BNP level during hospitalization suggests an increased risk of early readmission  Elevation of BNP during hospitalization suggests increased mortality
  114. 114. Uses of BNP levels On admission During course of therapy When euvolemic  Clinically  By right heart catheterization On discharge
  115. 115. BNP Predicts Outcome 1506BNP Level 690 2009 2 •Of the 72 patients admitted with CHF, 22 endpoints occurred •In these patients BNP increased by a mean of 233 pg/ml, p<0.001 •In patients without death or readmission BNP decreased by 215 pg/ml •The last BNP level measured was the strongest predictor of events, if the level was <1200 (in this population) 90% chance of no adverse events
  116. 116. BNP Concentration for the Prediction of Clinical Events CHF Death, Hospitalization, or ED visit 50% 45 40 35 30 BNP > 480 pg/ml 25 RR CHF death 20 24.1 15 BNP 230-480 pg/ml 10 5 BNP < 230 pg/ml 0 0 20 40 60 80 100 120 140 160 180 DaysHarrison A, et al, Annals of Emergency Medicine 2002
  117. 117. Conclusions• NT-Pro BNP & BNP are valuable adjuncts for the diagnosis & prognosis of decompensated HF in patients with dyspnea• Elevated natriuretic levels in the absence of HF may often represent other acute or chronic heart disease including ischemia• Additional applications may include risk stratification in patients with renal disease

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