Hc 01 intro heart failure verwey

611 views

Published on

Published in: Health & Medicine
0 Comments
1 Like
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
611
On SlideShare
0
From Embeds
0
Number of Embeds
51
Actions
Shares
0
Downloads
29
Comments
0
Likes
1
Embeds 0
No embeds

No notes for slide

Hc 01 intro heart failure verwey

  1. 1. Chronic Heart FailureHarriette F. Verwey, MD,PhD Dept of cardiology LUMC June 2010
  2. 2. Heart Failure
  3. 3. Content• Chronic Heart Failure References. ESC guidelines: Eur J Heart Fail 2008;10:933-989 ACC/AHA guidelines : J Am Coll Card 2009;53(15)
  4. 4. Definition• Heart Failure is a clinical syndrome including circulatory congestion or inadequate tissue perfusion, due to abnormal heart function and associated neurohormonal abnormalities
  5. 5. Definition of Heart Failure (HF)• HF is a clinical syndrome in which the patient have the following features – Symptoms typical of HF • Breathlessness at rest or on exercise, fatigue, tiredness, ankle swelling – Signs typical of HF • Tachycardia , tachypnoea, rales, pleural effusion, raised venous pressure etc – Objective evidence of structural or functional abnormality of the heart at rest • Cardiomegaly, S3,cardiac murmurs, abnormality on echo, raised natriuretic peptides
  6. 6. Epidemiology of CHF• ESC population: > 900 million in 51 countries• Prevalence of HF : 15 million• Prevalence of asymptomatic LV dysfunction: 15 million• Estimated prevalence ~ 4 % of the population and increases with age – Ageing of the population – Success of treatment of heart disease – Hypertension – Diabetes – Success of treatment in pts with malignancies – Obesitas• Prognosis is poor: overall survival at 4 years is 50 %• HF : 5 % of acute hospital admissions/ 10 % of pts in hospital beds and ~ 2% of national expenditure on health
  7. 7. Prevalence of HF by Age and Gender • HF afflicts 10 out of every 1,000 over age 65 in the U.S. United States 1988-94 10 Percent of Population Males 8 Females 6 4 2 0 20-24 25-34 35-44 45-54 55-64 65-74 75+Source: NHANES III (1988-94), CDC/NCHS and the American Heart Association
  8. 8. Annual absolute mortality in the E.U. for different pathologies ovary cancer bowel cancer prostate cancer breast cancer colon/rectum cancer lung cancerall cancers combined heart failuremyocardial infarctionsudden cardiac death 0 100000 200000 300000 400000 500000 600000 700000 800000 •( Murdoch RD et al. Importance of heart failure as a cause of death. Eur H J 1998;19 )
  9. 9. The mortality from heart failure is as bad as , or even worsethan, that of many common cancers J. McMurray, H. Dargie, Chronic Heart Failure
  10. 10. Netherlands• Prevalence: 250.000 pts• Incidence : 20.000 pts annually• 10 % of the population > 75 years• Poor prognosis due to progression of HF and sudden cardiac death• 14 % of total hospital admissions for heart disease ( 8% of all types of heart and vessel)
  11. 11. Prevalence of HF in relation to age The Rotterdam Study• 55-64 year: 0.9%• 65-74 year: 4.0%• 75-84 year: 9.7%• >84 year: 17.4% Bleumink GS et al. Quantifying the heart failure epidemic. The Rotterdam Study. Eur. Heart J 2004:25:1614-19.
  12. 12. Life-time risk for HF The Rotterdam Study• 55 year: 30.2%• 65 year: 30.3%• 75 year: 28.7%• 85 year: 23.1%
  13. 13. NYHA Class Class I Class II Class III Class IV Moderate Asymptomatic Mild symptomatic Symptomatic symptomatic heart failure heart failure heart failure heart failure ejection fraction with ordinary at rest with less than (EF) <40% exertion ordinary exertionAdvisory Council to Improve Outcomes Nationwide in Heart Failure. Consensus recommendations for the management of chronicheart failure. Am J Cardiol. 1999;83(2A).
  14. 14. Ondanks maximale medicatie 100 10 SurvivalAnnual survival (%) 75 Hospitalizations / year 50 1 25 Hospitalization 0 .1 I II III IV NYHA CLASS •With the progress of the disease hospitalizations become frequent
  15. 15. NYHA II NYHA III 12% 26% CHF Other SCD 24% 59% CHF64% Other 15% SCD NYHA IV 33% CHF Other SCD 56% 11% MERIT-HF studie. Lancet 1999;353: 2001-07
  16. 16. Incidence of intraventricular conduction disturbances Gemiddelde HF 3-5 Severe Heart Failure class III/ IV populatie 1,2 15% IVCD NCD IVCD 30% NCD 70% 85% 1,2: Am H J 2002:; 143: 412-7/ Circ 2000; 102 ( 18 suppl II) 3-5: Am J Card 1993; 71: 720-6; Circ 1997; 95: 2660-7; Eur H J 2000;21:1246- 50
  17. 17. Heart Failure Definition A Complex Clinical Syndrome in which the heart is incapable of in which the heart is incapable of maintaining maintaining a cardiac output adequate toaccommodate the metabolic requirements an adequate venous return. ( E . Braunwald 1997)
  18. 18. Classification of HF• To the onset: – acute/ transient/ chronic• Based on LV function: – HF with low ejection fraction: Systolic Heart Failure – HF with preserved ejection fraction: Diastolic Heart Failure• Clinical syndrome: – Forward vs backward failure
  19. 19. Etiology of Heart Failure What causes Heart Failure ? Ischemic Heart Disease Hypertension, Idiopathic Cardiomyopathy, Infections Injury to the heart(viral myocarditis,Chagas’ disease), Toxins (alcohol,cytotoxic drugs), Valvular Disease, Prolonged Arrhythmias Loss of a critical quantity of functioning myocardial cells
  20. 20. The progression of Heart FailureHo et al., Epidemiology of Congestive Heart Failure
  21. 21. The HF Syndrome ( Different Profiles) Systolic and Diastolic Diastolic Dysfunction and Dysfunction systolic function preserved 70% 30% (EF > 40 %) (EF > 40 %) (EF < 40%)1 Lilly, L. Pathophysiology of Heart Disease. Second Edition p 200
  22. 22. Ischemic Heart Disease• Myocardial infarction: scar tissue• Chronic ischaemia : diffuse regional wall abnormalities. » Hybernation » Stunning
  23. 23. Hypertension• Related to Diastolic Heart Failure: cardiac hypertrophy and cardiac fibrosis• Diagnosis: echocardiography • Left ventricular hypertrophy » Measurements of the IVS and LVPW thickness • Left ventricular mass: risk for CVD » Male: ≥ 125 g/ m 2 » Female: ≥ 110 g/ m 2 • Concentric versus eccentric hypertrophy • Cardiac fibrosis • LV ejection fraction: > 45 % • Diastolic function
  24. 24. Cardiomyopathies• Primarily in the Heart – Genetic – Infectious disease – Metabolic disorders – Toxic – Endocrine – Infiltrative disease: Amyloid; rheumatoid disease (MCTD); LE – Ageing – Idiopathic
  25. 25. Valvular heart disease• Valve stenosis: Aortic valve stenosis• Valve incompetence: Mitral valve regurgitation » Aortic valve regurgitation
  26. 26. Rhythm and conduction abnormalities• Tachycardia and bradycardia• Heart block
  27. 27. Distribution of LVEF among women and men enrolled in the Euro Heart Survey Hogg K et al. JACC 2004;43:317-27
  28. 28. Kaplan-Meier Survival curves for Pts with Heart Failure and Preserved orreduced Ejection Fraction N Engl J Med 2006;355:260-9
  29. 29. Type hartfalen• HF + low EF: systolic HF • HF + normal EF: diastolic• Younger HF• Males • Older• Ischemic heart disease • Females• Less comorbidity • Hypertension• Cardiologist • More comorbidities• Evidence based medicine • GP/ internal med (RCT) • Treatment: ?
  30. 30. Definition• Heart Failure is a clinical syndrome including circulatory congestion or inadequate tissue perfusion, due to abnormal heart function and associated neurohormonal abnormalities
  31. 31. Cardiac Output• Cardiac output is the amount of blood that the ventricle ejects per minute Cardiac Output = HR x SV 4-8 liters / min 60-100 ml
  32. 32. Determinants of Ventricular Function Contractility Preload Afterload Stroke Volume
  33. 33. Determinants of Ventricular Function Contractility Preload Afterload Stroke Volume• Synergistic LV Contraction• Wall Integrity Heart Rate• Valvular Competence Cardiac Output
  34. 34. 2) Frank Starling curve Pressure-volume curves for the intact ventricle
  35. 35. Relation pressure vs ECG
  36. 36. Neuro Hormonal Activation Mechanism Hormonal Systems SNS RAAS VasopressinNormal Cardiovascular Homeostasis
  37. 37. Pathophysiology of HF Compensatory mechanisms and secondary damage Tri gg er i 60% njur y Compensatory mechanismsEjectionFraction Secondary damage 20% Time Asymptomatic Symptomatic
  38. 38. Compensatory Mechanisms:Sympathetic Nervous System Decreased MAP↑Sympathetic Nervous System ↑Contractility Tachycardia Vasoconstriction  ↑TPR ↑SV x ↑HR 
  39. 39. Downloaded from: Heart Disease (on 4 April 2006 11:06 AM) © 2005 Elsevier
  40. 40. Compensatory MechanismsNeurohormonal ActivationMany different hormone systems are involved inmaintaining normal cardiovascular homeostasis,including:• Sympathetic nervous system (SNS)• Renin-angiotensin-aldosterone system (RAAS)• Vasopressin (a.k.a. antidiuretic hormone, ADH)
  41. 41. Neurohormonal stimulation• Actication of the Sympathetic nervous system: • Tachycardia • Increased Oxygen demand: ischaemia • Fibrosis • Increased cell death: apoptosis • Vasoconstriction • Activation of RAAS• Activation of the Renin Angiotensin Aldosteron System • Retention of Sodium and H2O • Increased Aldosteron secretion • Vasoconstriction
  42. 42. Left Ventricular DysfunctionVolume Pressure Loss of ImpairedOverload Overload Myocardium Contractility LV Dysfunction EF < 40%  Cardiac  End Systolic Volume Output  End Diastolic Volume Hypoperfusion Pulmonary Congestion
  43. 43. Hemodynamic Basis for HF Symptoms LVEDP  Left Atrial Pressure  Pulmonary Capillary Pressure  Pulmonary Congestion
  44. 44. Sympathetic Activation in Heart Failure ↑ CNS sympathetic outflow  Cardiac sympathetic  Sympathetic activity activity to kidneys + peripheral vasculature 1- 2- 1- Activation 1- 1- receptors receptors receptors of RAS Myocardial toxicity Vasoconstriction Increased arrhythmias Sodium retention Disease progressionPacker. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.
  45. 45. Compensatory Mechanisms:Renin-Angiotensin-Aldosterone (RAAS) Angiotensinogen Renin Angiotensin I Angiotensin Converting Enzyme Angiotensin II AT I receptor ! Vasoconstriction Vascular remodeling Oxidative Stress LV remodeling Cell Growth Proteinuria
  46. 46. Compensatory Mechanisms:Renin-Angiotensin-Aldosterone (RAAS) Renin-Angiotensin-Aldosterone (↓ renal perfusion) Salt-water retention Sympathetic Thirst Vasoconstriction Augmentation  ↑TPR ↑SV x ↑HR 
  47. 47. Other Neurohormones Natriuretic Pepetides ANP BNP CNP Vasodilating Actions
  48. 48. Short- and Longterm results of activation of the neurohormonal system• Retention of sodium and water: Increase of preload: Congestion• Vasoconstriction: increase of afterload• SNS stimulation: increased oxygen expenditure• Hypertrophy: cell death
  49. 49. - Combined 1-, 1- en 2-blockade at heart failure (1) - CNS:  sympathetic activation  Cardiac sympathetic activitation  Renal and peripheral vascular& sympathetic activitation  1-  2-receptoren 1-receptoren receptoren Hypertrophy and myocyte death, Vasoconstriction &Na+- dilatation, ischaemia and retention arrhythmia Packer (1998)
  50. 50. Renine Angiotensin Aldosteron Systeem  Vasoconstriction Non-ACE Pathways  Oxidative stress (bijv. chymase)  Cellgrowth  Na+ /H2O retention  Sympathic activation Angiotensinogen renin Angiotensin I AT1 ACE Angiotensin II Aldosteron AT2 Cough, InactiveAngio-edema Bradykinin  Vasodilatation metabolites Benefits?  Antiproliferative effectsSiragy, Am J Cardiol 1999:84;3S-8S; Fogari, Blood Pressure, 2001:10;6-15 Fogari, 2001:10;6-  (kinines)Pfeffer, data gepresenteerd tijdens Scientific Sessions AHA, Orlando 2003Fogari, Blood Pressure, 2001:10;6-15Fogari, 2001:10;6-  NO release
  51. 51. Angiotensine II and end organ damage CVA Atherosclerosis* Vasoconstriction Vasculaire hypertrophy Hypertension Endothelial dysfunction MIAII receptor AT 1 LV hypertrophy Fibrosis Heart fail Death Remodeling GFR Proteinurie Renal fail Aldosteron release Glomerulaire sclerosis * Rouleau J., data gepresenteerd tijdens WCC, Sydney 2002
  52. 52. Renine Angiotensin Aldosteron Systeem  Vasoconstriction Non-ACE Pathways  Oxidative stress (bijv. chymase)  Cellgrowth  Na+ /H2O retention  Sympathic activation Angiotensinogen renin Angiotensin I AT1 ACE Angiotensin II Aldosteron AT2 Cough, InactiveAngio-edema  Bradykinin metabolites  Vasodilatation Benefits?  Antiproliferative effectsSiragy, Am J Cardiol 1999:84;3S-8S; Fogari, Blood Pressure, 2001:10;6-15 Fogari, 2001:10;6-  (kinines)Pfeffer, data gepresenteerd tijdens Scientific Sessions AHA, Orlando 2003Fogari, Blood Pressure, 2001:10;6-15Fogari, 2001:10;6-  NO release
  53. 53. Downloaded from: Heart Disease (on 4 April 2006 11:06 AM) © 2005 Elsevier
  54. 54. Symptoms of Heart Failure• Reduced cardiac output • Decreased circulation: fatigue; dyspnea; mental disturbancy. Loss of apetite. Sleep disorders • Vasoconstriction: pale, clammy skin • Decrease in urine output• Retention of Sodium and fluid • Increased JVP • Pulmonary congestion • Ankle edema • Hepatomegaly
  55. 55. Diagnosis of HF• Careful assessement of symptoms • Pitfalls: elderly and obese patients • Poor relation between symptoms and severity of cardiac dysfunction • Alertness, nutritional status, weight• Careful physical examination • Bloodpressure/ pulse pressure • Fluid overload • Heart: murmurs • Lungs: respiratory rate; rales, pleural effusion• Severity of HF: NYHA classification/ Killip classification and Forestor classification• Diagnostic tests
  56. 56. Additional diagnostic tests• Electrocardiogram• Laboratory tests• X Ray• Echocardiography• Exercise tests ( 6 minute walk tests)• Nuclear imaging• Coronary and ventriculography• MRA• MSCT• Holter monitoring• Myocardial biopsy: suspected infiltrative diseases e.g. amyloid; sarcoid; haemochromatosis; restrictive cardiomyopathy and eosinophylic myocarditis
  57. 57. ECG at the first visit
  58. 58. Downloaded from: Heart Disease (on 12 September 2005 09:10 PM) © 2005 Elsevier
  59. 59. Echocardiography• Distinction between systolic versus diastolic dysfunction – HFPEF: diastolic dysfunction – Presence of signs & symptoms of HF – Presence of normal or only mildly abnormal LVEF≥45-50 % – Evidence of abnormal LV relaxation or diastolic stiffness• Ejection fraction; RWM; valvular disease; filling status of the ventricle• TOE: inadequate TTE; complicated valvular pts; endocarditis; CHD; suspection of thrombus in LAA in pts with AF
  60. 60. EchocardiographyUltrasoundFast, availableFunction:Structural abnormalitiesIschaemia / infarctionValve diseaseHaemodynamic implications
  61. 61. 2D-echo 4 chamber view
  62. 62. 2D-echo 2 chamber view
  63. 63. 2D-echoShort axis view
  64. 64. 3D-echo ®LV functie contrast acquisitions ) detection on 4D Automatic border (TomtTec volume
  65. 65. Prediction of mortality and morbidity with a 6-minute walk test in patients with LVD 12 10,23 p<0.02 10 Mortality % 7,88 8 6 4,19 2,99 4 2 0 level 1 level 2 level 3 level 4 n=176 n=241 n=215 n=201 Distance Walked, m, by Performance Level
  66. 66. Patients hospitalized % 50 40,91 40 33,61 27,44 30 22,16 19,9 20 11,2 10 3,72 1,99 0 level 1 level 2 level 3 level 4 Distance Walked, m, by Performance Level Total hospitalized Hospitalized for Congestive Heart Failure P<0.001 P<0.01
  67. 67. Six-minute walk performance in patients with moderate-to-severe heart failure 1/2 3/4Opasich, et al. Eur Heart J 2001;22:488-196
  68. 68. Nucleaire imaging techniekSPECT scan “Mibi of Myoview” / PET scanRadioactiviteitMeestal beschikbaar, complexe techniekIschemie / infarct, hartfunctie, innervatie
  69. 69. Nuclear ischaemia / infarction Myoview scan: normal
  70. 70. Nuclear scan: ischaemia / infarction myoview scan: ischaemia
  71. 71. Nuclear scan: ischaemia / infarction myoview scan: myocardial infarction
  72. 72. Techniques, FDG• FDG: marker of glucose utilization Hypoperfused myocardium with FDG uptake = viable Maddahi et al. J Nucl Med 1994
  73. 73. Techniques,Thallium-201• Early uptake is perfusion• Late uptake is cellmembrane integrity
  74. 74. (Reverse) remodeling n=50 pts, Tl-201 imaging Pre-CABG Post-CABGEDVI (ml/m2) <0.01 100 <0.01 80 60 40 viable nonviable DalleMule J et al. EJCTS 2002
  75. 75. Ischemic CMP ΔLVEF post-revascularization N=355 pts with LVEF <35%30% 58% 12%EF EF EF
  76. 76. Improvement of LVEF 50 45 37 36 36 40percentage 30 20 10 0 LVEF pre LVEF post LVEF pre LVEF post Viable + Viable -
  77. 77. MRI scanMagneet golvenMatig-redelijk beschikbaarComplexe techniekGeen metaal (pm, ICD)FunctieStructurele afwijkingenIschemie / infarctBeoordeling myocard
  78. 78. FUTURE MRI: ONE-STOP SHOP!coronaries valve lesions LV function: rest - dobu grafts Lamb, de Roos, Bax viability
  79. 79. A B C RCA LADD E F LAD RCA LCXLCX
  80. 80. A B C RCA LADD E F LCXLCX RCA LAD
  81. 81. Coronair angiografieAcuut myocard infarct

×