open access

Vol 12, No 3 (2017)
Review Papers
Published online: 2017-06-30
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Cirrhotic cardiomyopathy

Michalina Galas, Renata Główczyńska, Gabriela Parol
DOI: 10.5603/FC.2017.0052
·
Folia Cardiologica 2017;12(3):254-261.

open access

Vol 12, No 3 (2017)
Review Papers
Published online: 2017-06-30

Abstract

There is a specifi c heart disease associated with cirrhosis, named ‘cirrhotic cardiomyopathy’ (CCM). Essentials in the defi nition are a chronic cardiac dysfunction in cirrhotic patients, characterised by blunted contractile responsiveness to stress, and/or altered diastolic relaxation with electrophysiological abnormalities in the absence of other known cardiac disease. CCM is usually subclinical and is masked by reduced arterial pressure and hiperdynamic circulation and those characteristic hemodynamic changes are associated with portal hypertension. Decompensation of heart failure can develop under special condidions such as stress, volume overload, exercise and surgeries such as liver transplantation. Cirrhotic cardiomyopathy is often problem and correlates with the severity of cirrhosis. Prevalence of CCM remains still unknown. Heart failure is a cause of 7 to 23% of death after liver transplant.

Abstract

There is a specifi c heart disease associated with cirrhosis, named ‘cirrhotic cardiomyopathy’ (CCM). Essentials in the defi nition are a chronic cardiac dysfunction in cirrhotic patients, characterised by blunted contractile responsiveness to stress, and/or altered diastolic relaxation with electrophysiological abnormalities in the absence of other known cardiac disease. CCM is usually subclinical and is masked by reduced arterial pressure and hiperdynamic circulation and those characteristic hemodynamic changes are associated with portal hypertension. Decompensation of heart failure can develop under special condidions such as stress, volume overload, exercise and surgeries such as liver transplantation. Cirrhotic cardiomyopathy is often problem and correlates with the severity of cirrhosis. Prevalence of CCM remains still unknown. Heart failure is a cause of 7 to 23% of death after liver transplant.

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Keywords

cirrhotic cardiomyopathy, liver disease, portal hypertension, hyperdynamic circulation

About this article
Title

Cirrhotic cardiomyopathy

Journal

Folia Cardiologica

Issue

Vol 12, No 3 (2017)

Pages

254-261

Published online

2017-06-30

DOI

10.5603/FC.2017.0052

Bibliographic record

Folia Cardiologica 2017;12(3):254-261.

Keywords

cirrhotic cardiomyopathy
liver disease
portal hypertension
hyperdynamic circulation

Authors

Michalina Galas
Renata Główczyńska
Gabriela Parol

References (34)
  1. Iwakiri Y, Groszmann RJ. The hyperdynamic circulation of chronic liver diseases: from the patient to the molecule. Hepatology. 2006; 43(2 Suppl 1): S121–S131.
  2. Kowalski HJ, Abelmann WH. The cardiac output at rest in Laennec's cirrhosis. J Clin Invest. 1953; 32(10): 1025–1033.
  3. Zardi EM, Zardi DM, Chin D, et al. Cirrhotic cardiomyopathy. J Am Coll Cardiol. 2010; 56(7): 539–549.
  4. Timoh T, Protano MA, Wagman G, et al. A perspective on cirrhotic cardiomyopathy. Transplant Proc. 2011; 43(5): 1649–1653.
  5. Moller S, Henriksen JH. Cirrhotic cardiomiopathy. J Hepatol. 2010; 53(1): 179–190.
  6. Lee SS, Marty J, Mantz J, et al. Desensitization of myocardial beta-adrenergic receptors in cirrhotic rats. Hepatology. 1990; 12(3 Pt 1): 481–485.
  7. Barrière E, Tazi KA, Pessione F, et al. Role of small-conductance Ca2+-dependent K+ channels in in vitro nitric oxide-mediated aortic hyporeactivity to alpha-adrenergic vasoconstriction in rats with cirrhosis. J Hepatol. 2001; 35(3): 350–357.
  8. Glenn TK, Honar H, Liu H, et al. Role of cardiac myofilament proteins titin and collagen in the pathogenesis of diastolic dysfunction in cirrhotic rats. J Hepatol. 2011; 55(6): 1249–1255.
  9. Ceolotto G, Papparella I, Sticca A, et al. An abnormal gene expression of the beta-adrenergic system contributes to the pathogenesis of cardiomyopathy in cirrhotic rats. Hepatology. 2008; 48(6): 1913–1923.
  10. Wong F, et al. Cirrhotic cardiomyopathy. Hepatol Int. 2009(3): 294.
  11. Zardi EM, Zardi DM, Chin D, et al. Cirrhotic cardiomyopathy in the pre- and post-liver transplantation phase. J Cardiol. 2016; 67(2): 125–130.
  12. Myers RP, Lee SS. Cirrhotic cardiomyopathy and liver transplantation. Liver Transpl. 2000; 6(4 Suppl 1): S44–S52.
  13. Moller S, Henriksen JH. Cardiovascular complications of cirrhosis. Gut. 2008; 57(2): 268–278.
  14. Krag A, Bendtsen F, Mortensen C, et al. Effects of a single terlipressin administration on cardiac function and perfusion in cirrhosis. Eur J Gastroenterol Hepatol. 2010; 22(9): 1085–1092.
  15. Wong F, Villamil A, Merli M, et al. Prevalence of diastolic dysfunction in cirrhosis and its clinical significance. Hepatology. 2011; 54: 475A.
  16. Møller S, Wiese S, Halgreen H, et al. Diastolic dysfunction in cirrhosis. Heart Fail Rev. 2016; 21(5): 599–610.
  17. Sampaio F, Pimenta J, Bettencourt N, et al. Left atrial function is impaired in cirrhosis: a speckle tracking echocardiographic study. Hepatol Int. 2014; 8(1): 146–153.
  18. Nazar A, Guevara M, Sitges M, et al. LEFT ventricular function assessed by echocardiography in cirrhosis: relationship to systemic hemodynamics and renal dysfunction. J Hepatol. 2013; 58(1): 51–57.
  19. Karagiannakis DS, Papatheodoridis G, Vlachogiannakos J. Recent advances in cirrhotic cardiomyopathy. Dig Dis Sci. 2015; 60(5): 1141–1151.
  20. Carvalheiro F, Rodrigues C, Adrego T, et al. Diastolic Dysfunction in Liver Cirrhosis: Prognostic Predictor in Liver Transplantation? Transplant Proc. 2016; 48(1): 128–131.
  21. Lunzer MR, Newman SP, Bernard AG, et al. Impaired cardiovascular responsiveness in liver disease. Lancet. 1975; 2(7931): 382–385.
  22. Decaux G, Cauchie P, Soupart A, et al. Role of vagal neuropathy in the hyponatraemia of alcoholic cirrhosis. Br Med J (Clin Res Ed). 1986; 293(6561): 1534–1536.
  23. Bernardi M, Rubboli A, Trevisani F, et al. Reduced cardiovascular responsiveness to exercise-induced sympathoadrenergic stimulation in patients with cirrhosis. J Hepatol. 1991; 12(2): 207–216.
  24. Bernardi M, Calandra S, Colantoni A, et al. Q-T interval prolongation in cirrhosis: prevalence, relationship with severity, and etiology of the disease and possible pathogenetic factors. Hepatology. 1998; 27(1): 28–34.
  25. Pateron D, Beyne P, Laperche T, et al. Elevated circulating cardiac troponin I in patients with cirrhosis. Hepatology. 1999; 29(3): 640–643.
  26. Henriksen JH. Increased circulating pro-brain natriuretic peptide (proBNP) and brain natriuretic peptide (BNP) in patients with cirrhosis: relation to cardiovascular dysfunction and severity of disease. Gut. 2003; 52(10): 1511–1517.
  27. Saner FH, Neumann T, Canbay A, et al. High brain-natriuretic peptide level predicts cirrhotic cardiomyopathy in liver transplant patients. Transpl Int. 2011; 24(5): 425–432.
  28. Mohamed R, Forsey PR, Davies MK, et al. Effect of liver transplantation on QT interval prolongation and autonomic dysfunction in end-stage liver disease. Hepatology. 1996; 23(5): 1128–1134.
  29. Saner FH, Neumann T, Canbay A, et al. High brain-natriuretic peptide level predicts cirrhotic cardiomyopathy in liver transplant patients. Transpl Int. 2011; 24(5): 425–432.
  30. Henderson JM, Mackay GJ, Hooks M, et al. High cardiac output of advanced liver disease persists after orthotopic liver transplantation. Hepatology. 1992; 15(2): 258–262.
  31. Liu H, Lee SS. Acute-on-chronic liver failure: the heart and systemic hemodynamics. Curr Opin Crit Care. 2011; 17(2): 190–194.
  32. Henriksen JH, Bendtsen F, Hansen EF, et al. Acute non-selective beta-adrenergic blockade reduces prolonged frequency-adjusted Q-T interval (QTc) in patients with cirrhosis. J Hepatol. 2004; 40(2): 239–246.
  33. Sersté T, Melot C, Francoz C, et al. Deleterious effects of beta-blockers on survival in patients with cirrhosis and refractory ascites. Hepatology. 2010; 52(3): 1017–1022.
  34. Sampathkumar P, Lerman A, Kim BY, et al. Post-liver transplantation myocardial dysfunction. Liver Transpl Surg. 1998; 4(5): 399–403.

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