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Giovanni Pulignano Ambulatorio per lo Scompenso Cardiaco I UO Cardiologia /UTIC

41 Congresso di Cardiologia Incontri con gli esperti Milano, 19 settembre 2007. “Gli aspetti che trascuriamo nel paziente con scompenso cardiaco: Esercizio fisico e scompenso cardiaco. Giovanni Pulignano Ambulatorio per lo Scompenso Cardiaco I UO Cardiologia /UTIC

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Giovanni Pulignano Ambulatorio per lo Scompenso Cardiaco I UO Cardiologia /UTIC

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  1. 41 Congresso di Cardiologia Incontri con gli esperti Milano, 19 settembre 2007 “Gli aspetti che trascuriamo nel paziente con scompenso cardiaco: Esercizio fisico e scompenso cardiaco Giovanni Pulignano Ambulatorio per lo Scompenso Cardiaco I UO Cardiologia /UTIC Dipartimento Cardiovascolare Az.Osp. S.Camillo-Forlanini

  2. Senni et al. On behalf of IN-CHF Investigators. Journal of Cardiac Failure Vol. 11 No. 4 2005

  3. ?

  4. VO2 training Esercizio e scompenso cardiaco Fattori periferici e centrali

  5. M. Piepoli, 1997

  6. Mechanisms to augment cardiac output (C.O.) in (A) healthy persons without HF and (B) patients with HF. Piña et al, Circulation March 4, 2003

  7. Cardio-Pulmonary eXercise (CPX) test Healthy subject CHF patient

  8. Relationship of LVEF and peak oxygen uptake Circulation 1993 87:VI-7

  9. Survival by peak VO2 in CHF 100 >21 Survival (%) 80 16-21 100 80 60 40 20 0 increase in peak VO2 decrease in peak VO2 60 Percent Survival 14-16 40 <14 n = 297 p = 0.0002 20 Francis, Heart 2000 0 0 10 20 30 40 50 60 70 Time (months) p < 0.05 Florea, EHJ 2000 0 5 10 15 20 25 30 35 40 Time (months)

  10. 100 < 27 80 27-33 60 34-42 40 > 43 n = 297 P < 0.0001 20 0 0 10 20 30 40 50 60 70 Time (months) Ventilatory Inefficiency in CHF: VE/VCO2 slope VE (L/min) Survival 140 120 100 80 60 Normal Moderate CHF 40 Severe CHF 20 0 0 1 2 3 4 5 6 (L/min) VCO 2

  11. Impaired Tolerance and Abnormal Responses to Exercise in CHF: Peripheral Factors 1. Blood flow ml/min reduced 2. Metabolism early lactic acid production phosphate depletion 3. Function Weakness, increased fatigue 4. Morphology: Quantity Loss of muscle mass (or bulk) Site Localised to legs or general abnormality Orientation and fibre position Quality Atrophy, damage and/or necrosis (apoptosis) Change of fibre type, myosin IIb

  12. Muscle Ergoreflex System: Anatomical Pathways

  13. Neural Reflex Activation in Heart Failure Ponikowski, Piepoli et al Circulation. 2001;104:2324-2330.)

  14. Detraining Training Effect of Exercise training on the Contribution of Muscle Ergoreflex to Exercise in Heart Failure vs Controls Piepoli et al. Circulation 1996;93: 940

  15. Cicoira MA et al. JACC 2001 Skeletal muscle mass independently predicts peak oxygen consumption and ventilatory response during exercise in noncachectic patients with chronic heart failure Massa muscolare scheletrica e tolleranza allo sforzo

  16. Piepoli et al Circulation 2006

  17. Modello fisiopatologico degli adattamentiindotti dal training fisico nello scompenso cardiaco Belardinelli R, Agostoni PG.

  18. Studi randomizzati sugli gli effetti del training nei pazienti con insufficienza cardiaca cronica.

  19. Principali adattamenti indotti dal trainingfisico nell’insufficienza cardiaca cronica. ParametroEffetto del Training VO2 picco + 12-26% VO2 alla AT + VE/CO2 ratio - 6-18% Durata esercizio + 17% Eur HF training Group . Eur Heart J 1998; 19:466-475 Pina IL. Circulation 2003; 107(8):1210-1225.

  20. Principali adattamenti indotti dal trainingfisico nell’insufficienza cardiaca cronica. • Adattamenti centrali • Ridotta progressione di stenosi coronariche – (30-45) • Dilatazione arteriosa coronarica endotelio-dipendente + (20-30) • Aumento della diffusione polmonare + (10-20) • Miglioramento della perfusione miocardica + (15-25) • Miglioramento del rilasciamento diastolico + (15-28) • Miglioramento della contrattilità + (15-25) • Miglioramento della funzione sistolica globale + (10-15)

  21. Principali adattamenti indotti dal trainingfisico nell’insufficienza cardiaca cronica. • Adattamenti periferici • Miglioramento del flusso muscolare + (12-30) • Aumento degli enzimi muscolari ossidativi + (15-30) • Aumento del volume di densità mitocondriale + (15-25) • Aumento delle fibre muscolari tipo I + (15-30) • Dilatazione arteriosa endotelio-dipendente + (15-40) • Attenuazione dell’ergoriflesso

  22. Effect of Exercise Training on Muscle Metabolism in CHF Adamopoulos et al. Physical Training in Heart Failure. JACC 1993;21:1101-1106.

  23. Training corrects endothelial dysfunction and improves exercise capacity in CHF Physical exercise increases in endothelium-dependent blood flow (A), whereas peripheral blood flow remained unchanged (B) in the control group. #P<0.05 vs beginning; *P<0.05 vs control. Hambrecht et al. Circulation 1998;98:2709

  24. S. Adamopoulos European Heart Journal (2001) 22, 791–797

  25. Aerobic training decreases B-type natriuretic peptide expression and adrenergic activation in patients with heart failure Improvements in patents in the exercise group *Compared with control group, which showed no changes BNP=B-type natriuretic peptide NT-proBNP=amino-terminal pro-brain natriuretic peptide Passino C et al. J Am Coll Cardiol 2006; 47:1835-1839.

  26. Conclusioni: in condizioni di stabilità, l’esercizio moderato, a lungo termine, non ha effetti negativi sul volume e sulla funzione del VS, ma anzi attenua il rimodellamento. Inoltre l’allenamento è sicuro ed efficace per aumentare la tolleranza all’esercizio e migliorare la qualità della vita. Circulation. 2003; 108: 554-559

  27. Haykowsky et al. JACC Vol. 49, No. 24, 2007

  28. Training and quality of life in CHF Afzal et al. Progress in Cardiovascular Diseases 1998

  29. Fattori predittivi di risposta positiva al training fisico nei pazienti con insufficienza cardiaca Wilson JR et al. Circlation 1996; 94: 1767-72

  30. Belardinelli R, Circulation. 1999;99:1173-1182.)

  31. ExTraMATCH Collaborative.Exercise training meta-analysis of trials in patients with chronic heart failure (ExTraMATCH) ExTraMATCH BMJ  2004;328:189

  32. K-M cumulative two year survival (top) and cumulative two year survival or free from admission hospital (bottom). ExTraMATCH BMJ  2004;328:189

  33. death .65 (.46 to .92)

  34. death/ Admission .72 (.56 to .93)

  35. HF-ACTION: Heart Failure: AControlled Trial Investigating Outcomes of Exercise TraiNing • 5-year, 3,000-patient NYHA II-IV, EF<35% randomized trial, • 50 U.S. and Canadian hospitals, • first large-scale prospective trial designed to determine whether exercise can reduce mortality and hospitalizations for patients with HF or any other disease • Ongoing enrolment • >2000 pts, >> male, low mean age, mild peak VO2 impairment Whellan DJ Am Heart J. 2007 Feb;153(2):201-11. Adams, Barcelona WCC 4 September 2006

  36. “ Despite ..benefits, a limitation of these investigations was the primary focus on males <60 years with impaired left ventricular systolic function”. • “Thus the role that exercise training may play in attenuating the HF-mediated decline in VO2peak in women >65 years of age with systolic or diastolic dysfunction remains unknown”. HAYKOWSKYJ ournal of Cardiac Failure Vol. 10 No. 2 2004

  37. Modalità • Durata • Frequenza • Intensità • Progressione • Sicurezza

  38. Relative and absolute contraindications European Heart Journal (2001) 22, 125–135 Working Group Report

  39. European Heart Journal (2001) 22, 125–135 Working Group Report Modality of exercise training programme in CHF • Aerobic exercise • Cycle ergometer • walking (<50-100 m/min) • out-door cycling? jogging ? Swimming ? • Calisthenic: flexibility, coordination, strength • Resistance • rhythmic, ie. 1:1 rate • small muscle: single limb • small repetition: 60”ex/120”recovery • 50-80% max voluntary capacity • Respiratory • inspiratory, (20-30% max capacity) 20-30min/d, 3-5 d/w • abdominal muscle • yoga

  40. European Heart Journal (2001) 22, 125–135 Working Group Report Aerobic Exercise. Cycle ergometer: Warm up 10’ – Conditioning phase 40’– Cool down 10’ • Interval training: short bouts of work phases followed by short recovery phases. • 30” exercise: 50-60% max ex capacity / 60” recovery (low load, 10W) • 10-12 work phases in 15-min training session • Max ex capacity: steep ramp test, 25W every 10” • Steady-state training • 10-60 min /d, 3-7 d/w • 40-80% peak VO2 (or peak HR or perceived exertion by Borg scale) • <3METS, 2-3 sessions/d, 5-10 min; >3METS 3-5 sessions, 20-30min Modality of exercise training programme in CHF

  41. European Heart Journal (2001) 22, 125–135 Working Group Report Modality of exercise training programme in CHF Aerobic Training: Phases of exercise progression 1. Initial stage: - 10-15min, 40%-50% pkVo2, 2. Improvement stage (>15d): - 15-20-30min, 50% -> 60% -> 70% pkVo2 3. Maintenance stage (>6m)

  42. European Heart Journal (2001) 22, 125–135 Working Group Report Safety of exercise training programme in CHF • Initial phase: in-hospital supervision • Pulmonary and cardiac O.E. • body weight and oedema • HR and BP monitoring • symptoms • Maintenance Phase: combination of supervised/ unsupervised training • selected group of patients • to favour adherence to prescription

  43. European Heart Journal (2001) 22, 125–135 Working Group Report Safety of exercise training programme in CHF

  44. Eur J Cardiovasc Prev Riabil 2005; 12:321-325

  45. Conclusioni: Il training nel paziente con scompenso cardiaco stabile: • Migliora la funzione vascolare periferica, muscolare e metabolica • Migliora la funzione respiratoria e del sistema nervoso autonomo • Questi effetti portano ad un significativo miglioramento della tolleranza all’esercizio e alla qualità della vita • Nessun deterioramento significativo dell’emodinamica centrale • Attenuazione dello sfavorevole rimodellamento del ventricolo sinistro • Migliori risultati con esercizio aerobico, intensità moderata (60%), personalizzato, lunga durata (mesi), con supervisione specialistica.

  46. Conclusioni:Problemi • Evidenza derivante da studi randomizzati con numero limitato di pazienti arruolati in centri altamente specializzati, >>maschi, età media 50-55 anni con interferenza di altri fattori (Hawthorne effect) • Mancanza di dati relativi a pazienti con diversi modelli fisiopatologici (SC diastolico, cpt. valvolare) • Diversità nei protocolli negli studi pubblicati • Bassa prescrizione ACE/ARB, BB o CRT • Risultati non sempre concordi in termini di QDV, tolleranza allo sforzo e sopravvivenza • Scarsità di fattori (clinici, di funzione ventricolare, ecc.) predittivi di miglioramento durante programma riabilitativo • Difficoltà organizzative

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