‘Myocardial Depression’ or’ septic Cardiomyopathy’?

  • K. Werdan
  • A. Oelke
  • U. Müller-Werdan


’septic acute myocarditis’ in the pre-antibiotic era was a purulent disease of the heart. Nowadays, non-specific pathomorphological and pathohistological alterations characterize the myocardium of patients whose hearts have failed in septic shock. For decades, septic myocardial depression in animal models was attributed to the release of cardiodepressant factors into the blood stream, while the existence of human septic myocardial depression was only unequivocally proven in the early 1980s by the group of Parrillo [1], who had examined patients in the ICU with nuclear imaging techniques. Since then, experimental and clinical evidence has accumulated arguing for a more complex alteration of the heart in sepsis than exclusive myocardial depression. The concept of a “septic cardiomyopathy” was proposed [2], which emphasizes alterations of cardiac cellular phenotype as a basis of organopathy in response to a variety of agents acting on heart cells, like bacterial toxins and endogenous cytokines, hormones, mediators, and cardiodepressant factors. Not only is impairment of complex intrinsic heart function a consequence, but regulation of cardiac function is also severely disturbed due to excessive autonomic dysfunction [3].


Septic Shock Heart Rate Variability Severe Sepsis Mean Arterial Pressure Brain Natriuretic Peptide 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Parrillo JE (1989) The cardiovascular pathophysiology of sepsis. Ann Rev Med 40: 469–485PubMedGoogle Scholar
  2. 2.
    Müller-Werdan U, Reithmann C, Werdan K (1996) Cytokines and the Heart: Molecular Mechanisms of Septic Cardiomyopathy. Landes Bioscience, AustinGoogle Scholar
  3. 3.
    Schmidt H, Müller-Werdan U, Werdan K (2008) The consequences of cardiac autonomic dysfunction in multiple organ dysfunction syndrome. In: Vincent JL (ed) 2008 Yearbook of Intensive Care and Emergency Medicine. Springer, Heidelberg, pp 55–64CrossRefGoogle Scholar
  4. 4.
    Pilz G, McGinn P, Boekstegers P, Kääb S, Weidenhöfer S, Werdan K (1994) Pseudomonas sepsis does not cause more severe cardiovascular dysfunction in patients than non-pseudomonas sepsis. Circ Shock 42: 174–182PubMedGoogle Scholar
  5. 5.
    Levy RJ, Piel DA, Acton PD, et al (2005) Evidence of myocardial hibernation in the septic heart. Crit Care Med 33: 2752–2756CrossRefPubMedGoogle Scholar
  6. 6.
    Elliott P, Andersson B, Arbustini E, et al (2008) Classification of the cardiomyopathies: a position statement from the European Society Of Cardiology Working Group On Myocardial and Pericardial Diseases. Eur Heart J 29: 270–276CrossRefPubMedGoogle Scholar
  7. 7.
    Spies C, Haude V, Fitzner R, et al (1998) Serum cardiac troponin T as a prognostic marker in early sepsis. Chest 113: 1055–1063CrossRefPubMedGoogle Scholar
  8. 8.
    Wu AHB (2001) Increased troponin in patients with sepsis and septic shock: myocardial necrosis or reversible myocardial depression? Intensive Care Med 27: 959–961CrossRefGoogle Scholar
  9. 9.
    Brueckmann M, Huhle G, Lang S, et al (2005) Prognostic value of plasma N-Terminal probrain natriuretic peptide in patients with severe sepsis. Circulation 112: 527–534CrossRefPubMedGoogle Scholar
  10. 10.
    Charpentier J, Luyt C-E, Fulla Y, et al (2004) Brain natriuretic peptide: A marker of myocardial dysfunction and prognosis during severe sepsis. Crit Care Med 32: 660–665CrossRefPubMedGoogle Scholar
  11. 11.
    Witthaut R, Busch C, Fraunberger P, et al K (2003) Plasma atrial natriuretic peptide and brain natriuretic peptide are increased in septic shock: impact of interleukin-6 and sepsisassociated left ventricular dysfunction. Intensive Care Med 29: 1696–1702CrossRefPubMedGoogle Scholar
  12. 12.
    McLean AS, Huang SJ (2006) Intensive care echocardiography. In: Vincent JL (ed) 2006 Yearbook of Intensive Care and Emergency Medicine. Springer, Heidelberg, pp 131–141CrossRefGoogle Scholar
  13. 13.
    Cotter G, Moshkovitz Y, Kaluski E, et al (2003) The role of cardiac power and systemic vascular resistance in the pathophysiology and diagnosis of patients with acute congestive heart failure. Eur J Heart Failure 5: 443–451CrossRefGoogle Scholar
  14. 14.
    Maeder M, Ammann P, Kiowski W, Rickli H (2005) B-type natriuretic peptide in patients with sepsis and preserved left ventricular ejection fraction. Eur J Heart Fail 7: 1164–1167CrossRefPubMedGoogle Scholar
  15. 15.
    Müller-Werdan U, Buerke M, Ebelt H (2006) Septic cardiomyopathy — A not yet discovered cardiomyopathy? Exp Clin Cardiol 11: 226–236PubMedGoogle Scholar
  16. 16.
    Levy RJ (2007) Mitochondrial dysfunction, bioenergetic impairment, and metabolic downregulation in sepsis. Shock 28: 24–28CrossRefPubMedGoogle Scholar
  17. 17.
    Cinel I, Nanda R, Dellinger RP (2008) Cardiac dysfunction in septic shock. In: Vincent JL (ed) Yearbook of Intensive Care and Emergency Medicine. Springer Heidelberg, pp 43–54CrossRefGoogle Scholar
  18. 18.
    Zorn-Pauly K, Pelzmann B, Lang P, et al (2007) Endotoxin impairs the human pacemaker current If. Shock 28: 655–661PubMedGoogle Scholar
  19. 19.
    Dhainaut JF, Hughebaert M-F, Monsallier JF, et al (1987) Coronary hemodynamics and myocardial metabolism of lactate, free fatty acids, glucose, and ketones in patients with septic shock. Circulation 75: 533–541PubMedGoogle Scholar
  20. 20.
    Dhainaut J-F, Pinsky MR, Nouria S, Slomka F, Brunet F (1997) Right ventricular function in human sepsis — A thermodilution study. Chest 112: 1043–1049.CrossRefPubMedGoogle Scholar
  21. 21.
    Varriale P, Ramaprasad S (1995) Septic cardiomyopathy as a cause of long QT syndrome. J Electrocardiology 28: 327–329CrossRefGoogle Scholar
  22. 22.
    Prondzinsky R, Stache N, Witthaut R, et al (1997) Multiorgan-failure (MOF) with and without sepsis: differences in incidence and pattern of detected arrhythmias. Crit Care 1 (Suppl 1): P30CrossRefGoogle Scholar
  23. 23.
    Knotzer H, Mayr A, Ulmer H, et al (2000) Tachyarrhythmias in a surgical intensive care unit: a case-controlled epidemiologic study. Intensive Care Med 26: 908–914CrossRefPubMedGoogle Scholar
  24. 24.
    Müller-Werdan U, Engelmann H, Werdan K (1998) Cardiodepression by tumor necrosis factor α. Eur Cytokine Netw 9: 689–691PubMedGoogle Scholar
  25. 25.
    Müller-Werdan U, Werdan K (2000) Immune modulation by catecholamines — a potential mechanism of cytokine release in heart failure? Herz 25: 271–273CrossRefPubMedGoogle Scholar
  26. 26.
    Müller-Werdan U, Jacoby J, Loppnow H, et al (1999) Noradrenaline stimulates cardiomyocytes to produce interleukin-6, indicative of a proinflammatory action, which is suppressed by carvedilol. Eur Heart J 20 (Suppl):P1721 (abst)Google Scholar
  27. 27.
    Godin P J, Buchman T G (1996) Uncoupling of biological oscillators: a complementary hypothesis concerning the pathogenesis of multiple organ dysfunction syndrome. Crit Care Med 24: 1107–1116CrossRefPubMedGoogle Scholar
  28. 28.
    Schmidt H, Muller-Werdan U, Hoffmann T, et al (2005) Autonomic dysfunction predicts mortality in patients with multiple organ dysfunction syndrome of different age groups. Crit Care Med 33: 1994–2002CrossRefPubMedGoogle Scholar
  29. 29.
    Tracey K J (2007). Physiology and immunology of the cholinergic antiinflammatory pathway. J Clin Invest 117: 289–296CrossRefPubMedGoogle Scholar
  30. 30.
    Godin P J, Fleisher L A, Eidsath A, et al (1996) Experimental human endotoxemia increases cardiac regularity: results from a prospective, randomized, crossover trial. Crit Care Med 24: 1117–1124.CrossRefPubMedGoogle Scholar
  31. 31.
    Baruscotti M, Bucchi A, & Difrancesco D (2005) Physiology and pharmacology of the cardiac pacemaker (”funny”) current. Pharmacol Ther 107: 59–79CrossRefPubMedGoogle Scholar
  32. 32.
    Ludwig A, Zong X, Hofmann F, & Biel M (1999) Structure and function of cardiac pacemaker channels. Cell Physiol Biochem 9: 179–186CrossRefPubMedGoogle Scholar
  33. 33.
    Schmidt H, Saworski J, Werdan K, Muller-Werdan U (2007) Decreased beating rate variability of spontaneously contracting cardiomyocytes after co-incubation with endotoxin. J Endotoxin Res 13: 339–342CrossRefPubMedGoogle Scholar
  34. 34.
    Kurata Y, Hisatome I, Imanishi S, Shibamoto T (2002) Dynamical description of sinoatrial node pacemaking: improved mathematical model for primary pacemaker cell. Am J Physiol Heart Circ Physiol 283: H2074–2101Google Scholar
  35. 35.
    Sakr Y, Reinhart K, Vincent JL, et al (2006) Does dopamine administration in shock influence outcome? Results of the Sepsis Occurrence in Acutely Ill Patients (SOAP) Study. Crit Care Med 34: 589–597CrossRefPubMedGoogle Scholar
  36. 36.
    Cunha-Goncalves D, Perez-de-Sa V, Dahm P, Grins E, Thörne J, Blomquist S (2007) Cardiovascular effects of levosimendan in the early stages of endotoxemia. Shock 28: 71–77CrossRefPubMedGoogle Scholar
  37. 37.
    Takeuchi K, del Nido PJ, Ibrahim AE, et al (1999) Vesnarinone and amrinone reduce the systemic inflammatory response syndrome. J Thorac Cardiovasc Surg 117: 375–381CrossRefPubMedGoogle Scholar
  38. 38.
    Wagner DR, McTiernan C, Sanders VJ, Feldman AM (1998) Adenosine inhibits lipopolysaccharide-induced secretion of tumor necrosis factor-a in the failing human heart. Circulation 97: 521–524PubMedGoogle Scholar
  39. 39.
    Suzuki T, Morisaki H, Serita R, et al (2005) Infusion of the beta-adrenergic blocker esmolol attenuates myocardial dysfunction in septic rats. Crit Care Med 33: 2294–2301CrossRefPubMedGoogle Scholar
  40. 40.
    De Backer D, Creteur J, Preiser JC, Dubois MJ, Vincent JL (2002) Microvascular blood flow is altered in sepsis. Am J Respir Crit Care Med 166: 98–104CrossRefPubMedGoogle Scholar
  41. 41.
    Elebute EA, Stoner HB (1983) The grading of sepsis. Br J Surg 70: 29–31CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2009

Authors and Affiliations

  • K. Werdan
    • 1
  • A. Oelke
    • 1
  • U. Müller-Werdan
    • 1
  1. 1.Department of Medicine III Universitätsklinikum HalleMartin-Luther-University Halle-WittenbergHalle/SaaleGermany

Personalised recommendations