Your SlideShare is downloading. ×
Hc 01 intro heart failure verwey
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Hc 01 intro heart failure verwey

237
views

Published on

Published in: Health & Medicine

0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total Views
237
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
8
Comments
0
Likes
0
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. Chronic Heart FailureHarriette F. Verwey, MD,PhD Dept of cardiology LUMC June 2010
  • 2. Heart Failure
  • 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. Definition• Heart Failure is a clinical syndrome including circulatory congestion or inadequate tissue perfusion, due to abnormal heart function and associated neurohormonal abnormalities
  • 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. The progression of Heart FailureHo et al., Epidemiology of Congestive Heart Failure
  • 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. Ischemic Heart Disease• Myocardial infarction: scar tissue• Chronic ischaemia : diffuse regional wall abnormalities. » Hybernation » Stunning
  • 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. Cardiomyopathies• Primarily in the Heart – Genetic – Infectious disease – Metabolic disorders – Toxic – Endocrine – Infiltrative disease: Amyloid; rheumatoid disease (MCTD); LE – Ageing – Idiopathic
  • 25. Valvular heart disease• Valve stenosis: Aortic valve stenosis• Valve incompetence: Mitral valve regurgitation » Aortic valve regurgitation
  • 26. Rhythm and conduction abnormalities• Tachycardia and bradycardia• Heart block
  • 27. Distribution of LVEF among women and men enrolled in the Euro Heart Survey Hogg K et al. JACC 2004;43:317-27
  • 28. Kaplan-Meier Survival curves for Pts with Heart Failure and Preserved orreduced Ejection Fraction N Engl J Med 2006;355:260-9
  • 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. Definition• Heart Failure is a clinical syndrome including circulatory congestion or inadequate tissue perfusion, due to abnormal heart function and associated neurohormonal abnormalities
  • 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. Determinants of Ventricular Function Contractility Preload Afterload Stroke Volume
  • 33. Determinants of Ventricular Function Contractility Preload Afterload Stroke Volume• Synergistic LV Contraction• Wall Integrity Heart Rate• Valvular Competence Cardiac Output
  • 34. 2) Frank Starling curve Pressure-volume curves for the intact ventricle
  • 35. Relation pressure vs ECG
  • 36. Neuro Hormonal Activation Mechanism Hormonal Systems SNS RAAS VasopressinNormal Cardiovascular Homeostasis
  • 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. Compensatory Mechanisms:Sympathetic Nervous System Decreased MAP↑Sympathetic Nervous System ↑Contractility Tachycardia Vasoconstriction  ↑TPR ↑SV x ↑HR 
  • 39. Downloaded from: Heart Disease (on 4 April 2006 11:06 AM) © 2005 Elsevier
  • 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. 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. 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. Hemodynamic Basis for HF Symptoms LVEDP  Left Atrial Pressure  Pulmonary Capillary Pressure  Pulmonary Congestion
  • 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. 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. Compensatory Mechanisms:Renin-Angiotensin-Aldosterone (RAAS) Renin-Angiotensin-Aldosterone (↓ renal perfusion) Salt-water retention Sympathetic Thirst Vasoconstriction Augmentation  ↑TPR ↑SV x ↑HR 
  • 47. Other Neurohormones Natriuretic Pepetides ANP BNP CNP Vasodilating Actions
  • 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. - 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. 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. 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. 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. Downloaded from: Heart Disease (on 4 April 2006 11:06 AM) © 2005 Elsevier
  • 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. 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. 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. ECG at the first visit
  • 58. Downloaded from: Heart Disease (on 12 September 2005 09:10 PM) © 2005 Elsevier
  • 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. EchocardiographyUltrasoundFast, availableFunction:Structural abnormalitiesIschaemia / infarctionValve diseaseHaemodynamic implications
  • 61. 2D-echo 4 chamber view
  • 62. 2D-echo 2 chamber view
  • 63. 2D-echoShort axis view
  • 64. 3D-echo ®LV functie contrast acquisitions ) detection on 4D Automatic border (TomtTec volume
  • 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. 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. 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. Nucleaire imaging techniekSPECT scan “Mibi of Myoview” / PET scanRadioactiviteitMeestal beschikbaar, complexe techniekIschemie / infarct, hartfunctie, innervatie
  • 69. Nuclear ischaemia / infarction Myoview scan: normal
  • 70. Nuclear scan: ischaemia / infarction myoview scan: ischaemia
  • 71. Nuclear scan: ischaemia / infarction myoview scan: myocardial infarction
  • 72. Techniques, FDG• FDG: marker of glucose utilization Hypoperfused myocardium with FDG uptake = viable Maddahi et al. J Nucl Med 1994
  • 73. Techniques,Thallium-201• Early uptake is perfusion• Late uptake is cellmembrane integrity
  • 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. Ischemic CMP ΔLVEF post-revascularization N=355 pts with LVEF <35%30% 58% 12%EF EF EF
  • 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. MRI scanMagneet golvenMatig-redelijk beschikbaarComplexe techniekGeen metaal (pm, ICD)FunctieStructurele afwijkingenIschemie / infarctBeoordeling myocard
  • 78. FUTURE MRI: ONE-STOP SHOP!coronaries valve lesions LV function: rest - dobu grafts Lamb, de Roos, Bax viability
  • 79. A B C RCA LADD E F LAD RCA LCXLCX
  • 80. A B C RCA LADD E F LCXLCX RCA LAD
  • 81. Coronair angiografieAcuut myocard infarct