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Geschlechtsspezifische negative inotrope Wirkung von Übergewicht?

Gender-specific negative inotropic action of adipose tissue?

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Zeitschrift für Herz-,Thorax- und Gefäßchirurgie Aims and scope

Zusammenfassung

Fragestellung

Die Hypothese wurde geprüft, ob sich auf der Grundlage der Analyse isolierten menschlichen Myokards eine geschlechtsspezifische Beziehung zwischen Kontraktionsverhalten und Übergewicht nachweisen ließe.

Methoden

Rechtsatriale Muskelpräparate (0.5 x 6 mm) von 77 Frauen und 106 Männern, die sich einer aortokoronaren Bypassoperation unterzogen, wurden bei optimaler Länge elektrisch stimuliert. Wir bestimmten isometrische Kraftamplitude, passive Ruhekraft und Muskelquerschnitt der Präparate (Messbedingungen: 37 °C, Krebs-Henseleit-Lösung, optimale Länge, supramaximale Stimulation). Die Beziehung von Body-Mass-Index (BMI) und muskelphysiologischen Messwerten am menschlichen Myokardpräparat wurde unter Verwendung linearer Regressionsmodelle und deskriptiver Statistik analysiert.

Ergebnisse

Die Messwerte zeigten eine deutliche geschlechtsspezifische Reduk- tion der isometrischen Kraftamplitude (mN/mm2) und der bei optimaler Länge bestimmten passiven Ruhekraft (mN/mm2) mit zunehmendem BMI (p < 0.0001). Diese Effekte waren im atrialen Myokard von Frauen deutlich ausgeprägter als bei Männern (p < 0.0001).

Fazit

Die Daten zeigen am Modell des isolierten atrialen Myokards einen mit dem Anstieg des BMI assoziierten deutlichen negativ inotropen Effekt, der bei Frauen deutlich ausgeprägter erscheint.

Offensichtlich hat das Fettgewebe als endokrines Organ das Potenzial, durch Sekretion von Mediatoren einen direkten und signifikanten kardiodepressiven Einfluss auszuüben und kann so zur Entwicklung der Herzinsuffizienz übergewichtiger Patienten beitragen.

Abstract

Objectives

The hypothesis was tested, whether there is a gender-specific association between contractile performance and obesity based on the analysis of isolated human myocardium.

Methods

Right atrial muscle preparations (0.5 x 6 mm) of 77 female and 106 male patients undergoing coronary artery bypass surgery were electrically stimulated at optimal length. Isometric force amplitude (stimulation) and resting force (relaxation) were measured (measurement conditions: 37 °C, Krebs-Henseleit solution, optimal length, supramaximal electrical stimulation). The relationship between body mass index (BMI) and measured parameters was analyzed statistically by using a linear regression model and the student’s T test.

Results

There was a gender-specific decline in isometric force amplitude (mN/mm2) and resting force (mN/mm2) with increasing BMI (p < 0.0001). The effects were more pronounced in women (p < 0.0001).

Conclusions

The data seem to indicate that in isolated human myocardium there is a considerable negative inotropic effect of BMI and this effect is more pronounced in women. Adipose tissue thus may be interpreted as an endocrine organ with the potential to exert important cardio-depressant effects that may contribute to the development of heart failure in overweight patients.

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Literatur

  1. Atlantis E, Baker M (2008) Obesity effects on depression: systematic review of epidemiological studies. International Journal of Obesity 32:881–891

    Article  PubMed  CAS  Google Scholar 

  2. Borders TF, Rohrer JE, Cardarelli KM (2006) Gender-specific Disparities in obesity. J Community Health 31:57–68

    Article  PubMed  Google Scholar 

  3. Isozumi K (2004) Obesity as a risk factor for cerebrovascular disease Keio J Med 53:7–11

    Google Scholar 

  4. Gillum RF, Mussolino ME, Madans JH (2001) Body fat distribution, obesity, overweight and stroke incidence in women and men: the NHANES I Epidemiologic Follow-Up Study. Int J Obes Relat Metab Disord 25:628–638

    Article  PubMed  CAS  Google Scholar 

  5. He J, Ogden LG, Bazzano LA, Vupputuri S, Loria C, Whelton PK (2001) Risk factors for congestive heart failure in US men and women: NHANES I epidemiologic follow-up study. Arch Intern Med. 161(7):996–1002

    Article  PubMed  CAS  Google Scholar 

  6. Hubert HB, Feinleib M, McNamara PM, Castelli WP (1983) Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study. Circulation 67(5):968–977

    PubMed  CAS  Google Scholar 

  7. Kenchaiah S, Evans JC, Levy D, Wilson PW, Benjamin EJ, Larson MG, Kannel WB, Vasan RS (2002) Obesity and the risk of heart failure. N Engl J Med 1;347(5):305–313

    Article  PubMed  Google Scholar 

  8. Wong CY, O´Moore-Sullivan T, Leano R, Byrne N, Beller E, Marwick TH (2004) Alterations of the left ventricular myocardial characteristics associated with obesity. Circulation 110(19):3081–3087

    Article  PubMed  Google Scholar 

  9. Alpert MA (2001) Obesity cardiomyopath: pathophysiology and evolution of the clinical syndrome. Am J Med Sci 321(4):225–236

    Article  PubMed  CAS  Google Scholar 

  10. Lainscak M, Keber I, Anker SD (2006) Body composition changes in patients with systolic heart failure treated with beta blockers: a pilot study. Int J Cardiol 26;106(3):319–322

    Article  PubMed  Google Scholar 

  11. Kovacić D, Marinsek M, Gobec L, Lainscak M, Podbregar M (2008) Effect of selective and nonselective beta-blockers on body weight, insulin resistance and leptin concentration in chronic heart failure. Clin Res Cardiol 97(1):24–31

    Article  PubMed  CAS  Google Scholar 

  12. Lauer MS, Anderson KM, Kannel WB, Levy D (1991) The impact of obesity on left ventricular mass and geometry. The Framingham Heart Study. J Am Me Assoc 10; 266(2):231–236

    Article  CAS  Google Scholar 

  13. Zhou YT, Grayburn P, Karim A, Shimabukuro M, Higa M, Baetens D, Orci L, Unger RH (2000) Lipotoxic heart disease in obese rats: implications for human obesity. Proc Natl Acad Sci USA 15; 97(4):1784–1789

    Article  PubMed  CAS  Google Scholar 

  14. Krug AW, Erhart-Bornstein M (2005) Newly discovered endocrine functions of white adipose tissue: possible relevance in obesity-related diseases. Cell Mol Life Sci 62(12):1359–1362

    Article  PubMed  CAS  Google Scholar 

  15. Kershaw EE, Flier JS (2004) Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 89(6):2548–2556

    Article  PubMed  CAS  Google Scholar 

  16. Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (1994) Positional cloning of the mouse obese gene and its human homologue. Nature 1; 372(6505):425–432

    Article  PubMed  CAS  Google Scholar 

  17. Doehner W, Pflaum CD, Rauchhaus M, Godsland IF, Egerer K, Cicoira M, Florea VG, Sharma R, Bolger AP, Coats AJ, Anker SD, Strasburger CJ (2001) Leptin, insulin sensitivity and growth hormone binding protein in chronic heart failure with and without cardiac cachexia. Eur J Endocrinol 145(6):727–735

    Article  PubMed  CAS  Google Scholar 

  18. Lyva F, Anker SD, Egerer K, Stevenson JC, Kox WJ, Coats AJ (1998) Hyperleptinaemia in chronic heart failure. Relationships with insulin. Eur Heart J 19(10):1547–1551

    Article  Google Scholar 

  19. Staiger H, Häring HU (2005) Adipocytokines: fat-derived humoral mediators of metabolic homeostasis. Exp Clin Endocrinol Diabetes 113(2):67–79

    Article  PubMed  CAS  Google Scholar 

  20. Sharma V, McNeill JH (2005) The emerging roles of leptin and ghrelin in cardiovascular physiology and pathophysiology. Curr Vasc Pharmacol 3(2):169–180

    Article  PubMed  CAS  Google Scholar 

  21. Nickola MW, Wold LE, Colligan PB, Wang GJ, Samson WK, Ren J (2000) Leptin attenuates cardiac concentration in rat ventricular myocytes. Role of NO. Hypertension 36(4):501–505

    PubMed  CAS  Google Scholar 

  22. Holycross BJ, Radin MJ (2002) Cytokines in heart failure: potential interactions with angiotensin II and leptin. Mol Interv 2(7):424–427

    Article  PubMed  CAS  Google Scholar 

  23. Davos CH, Doehner W, Rauchhaus M, Cicoira M, Francis DP, Coats AJ, Clark AL, Anker SD (2003) Body mass and survival in patients with chronic heart failure without cachexia: the importance of obesity. J Card Fail 9(1):29–35

    Article  PubMed  Google Scholar 

  24. Engeli S, Negrel R, Sharma AM (2000) Physiology and Pathophysiology of the adipose tissue reninangiotensin system. Hypertension 35(6):1270– 1277

    PubMed  CAS  Google Scholar 

  25. Lefroy DC, Crake T, Del Monte F, Vescovo G, Dalla Libera L, Harding S, Poole-Wilson PA (1996) Angiotensin II and contraction of isolated myocytes from human, guinea pig, and infarcted rat hearts. Am J Physiol 270(6 Pt 2):H2060–2069

    PubMed  CAS  Google Scholar 

  26. Doehner W, Anker SD (2008) Beta blockers and glucose metabolism in chronic heart failure: friend or foe? Clin Res Cardiol 97(1):21–23

    Article  PubMed  CAS  Google Scholar 

  27. Regitz-Zagrosek V, Lehmkuhl E, Weickert MO (2006) Gender differences in the metabolic syndrome and their role for cardiovascular disease. Clin Res Cardiol 95(3):136–147

    Article  PubMed  CAS  Google Scholar 

  28. Lainscak M, Doehner W, Anker SD (2007) Metabolic disturbances in chronic heart failure: a case for the “macho” approach with testosterone?! Eur J Heart Fail 9(1):2–3

    Article  PubMed  CAS  Google Scholar 

  29. Kaplan N (1989) The deadly quartet: upper body obesity, glucose intolerance, hypertriglyceridemia, hypertension. Arch. Intern. Med. 149:1514–1520

    Article  PubMed  CAS  Google Scholar 

  30. Vahl CF, Bonz A, Hagl C, Timek T, Herold U, Fuchs H, Kochsiek N, Hagl S (1995) Cardioplegia on the contractile apparatus level: evaluation of a new concept for Myokardial preservation in perfused pig hearts. Thorac Cardiovasc Surg 43(4):185–193

    Article  PubMed  CAS  Google Scholar 

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Authors and Affiliations

  1. Klinik für Herz-, Thorax- und Gefäßchirurgie, Universität Mainz, Mainz, BRD

    Katja Denk, J. Albers, N. Kayhan, D. Ister, L. Hakami, U. Mehlhorn, A. Peivandi & C.-F. Vahl

  2. Klinik für Anästhesiologie, Universität Mainz, Mainz, BRD

    C. Werner

  3. II Medizinische Klinik (Kardiologie), Universität Mainz, Mainz, BRD

    T. Münzel

  4. Klinik für Herz-, Thorax- und Gefäßchirurgie, Johannes Gutenberg-Universität Mainz, Langenbeckstraße1, 55131, Mainz, BRD

    Katja Denk

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  1. Katja Denk
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  2. J. Albers
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  3. N. Kayhan
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  4. D. Ister
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Corresponding author

Correspondence to Katja Denk.

Additional information

Dr. med. Katja Denk, Jahrgang 1979, studierte Humanmedizin an der Universität Ulm. Seit Januar 2006 ist sie Assistenzärztin in der Abteilung für Herz-, Thorax- und Gefäßchirurgie der Johannes Gutenberg-Universität Mainz.

Interessenkonflikt. Der korrespondierende Autor gibt an, dass kein Interessenkonflikt besteht.

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Denk, K., Albers, J., Kayhan, N. et al. Geschlechtsspezifische negative inotrope Wirkung von Übergewicht?. Z Herz- Thorax- Gefäßchir 22, 250–256 (2008). https://doi.org/10.1007/s00398-008-0662-0

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  • DOI: https://doi.org/10.1007/s00398-008-0662-0

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