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Eur J Cardiothorac Surg 2001;20:424-425
© 2001 Elsevier Science NL


Letter to the Editor

Role of the cardiac lymph system in myocardial fluid balance

Uwe Mehlhorna, Hans J. Geisslera, Glen A. Laineb, Steven J. Allenc

a Clinic for Cardiothoracic Surgery, University of Cologne, Joseph-Stelzmann-Strasse 9, 50924 Cologne, Germany
b Michael E. DeBakey Institute for Comparative Cardiovascular Science, Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, TX, USA
c Center for Microvascular and Lymphatic Studies, Department of Anesthesiology, The University of Texas–Houston Medical School, Houston, TX, USA

Received 19 April 2001; accepted 30 April 2001.

Corresponding author. Tel.: +49-221-478-6043; fax: +49-221-478-5906
e-mail: uwe.mehlhorn{at}medizin.uni-koeln.de

We read with interest the Letter to the Editor by Konuralp et al. [1] in response to the original article by Vazquez-Jimenez et al. [2] as well as Vazquez-Jimenez’ reply to the letter [3] regarding the cardiac lymph system. We fully agree with the authors’ statements regarding the importance of the cardiac lymph system in open-heart surgery [1] and that investigation of the cardiac lymph system is mandatory for the understanding of many cardiac diseases’ pathophysiologies [3]. However, we were somewhat surprised about the statement by Konuralp et al. that the knowledge on cardiac lymphatics is very limited [1]. This is incorrect as the relevance of the cardiac lymph system under normal and various pathological conditions has been investigated in many studies that can not all be quoted in this letter. For the interested reader we suggest our recent review articles [46]. In addition, Konuralp et al. raise several questions regarding the role of the cardiac lymph system in myocardial protection or superior venous cava pressure elevation [1]. As a matter of fact, our group and others have investigated these very issues.

1. Role of the myocardial lymph system in myocardial protection

We have shown in a dog model that organized cardiac contraction is the major determinant of myocardial lymphatic function and that cardioplegic arrest virtually stops myocardial lymph flow [7,8]. This myocardial lymph flow cessation was at least in part responsible for myocardial edema formation during both intermittent cold crystalloid [7] or continuous warm blood cardioplegia [8] and was associated with cardiac dysfunction post cardiopulmonary bypass (CPB). In addition, we have demonstrated that myocardial edema resolution following CPB and cardioplegic arrest can be enhanced by pharmacologically augmenting cardiac contractility which improves myocardial lymphatic function [9]. Further, we showed that myocardial lymphatic function can be maintained, thereby avoiding myocardial edema and cardiac dysfunction, if ‘minimal cardiac contractions’ are maintained on CPB using continuous coronary perfusion with warm oxygenated blood enriched with the ultra short-acting ß-blocker esmolol [10]. These experimental data have recently been confirmed in clinical studies demonstrating the efficacy of the ‘ß-blocker-technique’ for myocardial protection on CPB as compared to Bretschneider [11] or Buckberg cardioplegia [12] as well as in emergency revascularization after failed PTCA [13].

2. Impact of superior venous cava pressure elevation on myocardial fluid balance

Superior venous cava (SVC) pressure elevation results in myocardial edema formation associated with cardiac dysfunction for the following reasons: As myocardial lymph ultimately drains into the central venous system via the thoracic duct [5], central venous pressure elevation impedes fluid removal from the cardiac interstitium via myocardial lymphatics [46,14]. In addition, increased central venous pressure increases coronary sinus pressure, and thus, coronary microvascular pressure which enhances fluid filtration out of the coronary microvasculature into the cardiac interstitium [46,14]. Both factors act in concert leading to myocardial edema formation associated with cardiac dysfunction. This has been shown by our group and others [46,1417].

In conclusion, a lot of information about myocardial fluid balance under normal and pathological conditions has been elucidated over the past 60 years. However, further investigation is required to improve our knowledge and to generate new strategies for optimized patient care.

References

  1. Konuralp C., diz M., Ünal M. Importance of the cardiac lymphatic system in open heart surgery. Eur J Cardio-thorac Surg 2001;19:372-373.[Free Full Text]
  2. Vazquez-Jimenez J.F., Seghaye M.C., Qing M., Liakopoulos O.J., Rosenbaum M.L., Messmer B.J. Cannulation of the cardiac lymphatic system in swine. Eur J Cardio-thorac Surg 2000;18:228-232.[Abstract/Free Full Text]
  3. Vazquez-Jimenez J.F. Reply to Konuralp et al.. Eur J Cardio-thorac Surg 2001;19:374.[Free Full Text]
  4. Allen S.J. The pathophysiology of myocardial edema. Principles of myocardial fluid balance. Curr Opin Anesthesiol 1994;7:12-17.
  5. Laine G.A., Mehlhorn U., Davis K.L., Allen S.J. Myocardial interstitium and lymphatics: pathophysiology and effects on cardiac function. In: Reed R.K., McHale N.G., Bert J.L., Winlove C.P., Laine G.A., eds. Interstitium, connective tissue and lymphatics. London: Portland Press, 1995:271-282.
  6. Geissler H.J., Allen S.J. Myocardial fluid balance: pathophysiology and clinical implications. Thorac Cardiovasc Surg 1998;46(Suppl 2):242-247.
  7. Mehlhorn U., Davis K.L., Burke E.J., Adams D., Laine G.A., Allen S.J. Impact of cardiopulmonary bypass and cardioplegic arrest on myocardial lymphatic function. Am J Physiol 1995;268:H178-H183.[Abstract/Free Full Text]
  8. Mehlhorn U., Allen S.J., Adams D.L., Davis K.L., Gogola G.R., de Vivie E.R., Laine G.A. Normothermic continuous antegrade blood cardioplegia does not prevent myocardial edema and cardiac dysfunction. Circulation 1995;92:1940-1946.[Abstract/Free Full Text]
  9. Allen S.J., Geissler H.J., Davis K.L., Gogola G.R., Warters R.D., de Vivie E.R., Mehlhorn U. Augmenting cardiac contractility hastens myocardial edema resolution following cardiopulmonary bypass and cardioplegic arrest. Anesth Analg 1997;85:987-992.[Abstract]
  10. Mehlhorn U., Allen S.J., Adams D.L., Davis K.L., Gogola G.R., Warters R.D. Cardiac surgical conditions induced by ß-blockade: effect on myocardial fluid balance. Ann Thorac Surg 1996;62:143-150.[Abstract/Free Full Text]
  11. Mehlhorn U., Sauer H., Kuhn-Régnier F., Südkamp M., Dhein S., Eberhardt F., Grond S., Horst M., Hekmat K., Geissler H.J., Warters R.D., Allen S.J., de Vivie E.R. Myocardial ß-blockade as an alternative to cardioplegic arrest during coronary artery surgery. Cardiovasc Surg 1999;7:549-557.[Medline]
  12. Kuhn-Regnier F., Natour E., Dhein S., Dapunt O., Geissler H.J., Larose K., Görg C., Mehlhorn U. Beta-blockade versus Buckberg blood-cardioplegia in coronary bypass operation. Eur J Cardio-thorac Surg 1999;15:67-74.[Abstract/Free Full Text]
  13. Hekmat K., Clemens R.M., Mehlhorn U., Geissler H.J., Kuhn-Regnier F., de Vivie E.R. Emergency coronary artery surgery after failed PTCA: myocardial protection with continuous coronary perfusion of ß-blocker-enriched blood. Thorac Cardiovasc Surg 1998;46:333-338.[Medline]
  14. Laine G.A., Allen S.J. Left ventricular myocardial edema. Lymph flow, interstitial fibrosis, and cardiac function. Circ Res 1991;68:1713-1721.[Abstract/Free Full Text]
  15. Davis K.L., Mehlhorn U., Laine G.A., Allen S.J. Myocardial edema, left ventricular function, and pulmonary hypertension. J Appl Physiol 1995;78:132-137.[Abstract/Free Full Text]
  16. Mehlhorn U., Davis K.L., Laine G.A., Geissler H.J., Allen S.J. Myocardial fluid balance in acute hypertension. Microcirculation 1996;3:371-378.[Medline]
  17. Pratt J.W., Schertel E.R., Schaefer S.L., Esham K.E., McClure D.E., Heck C.F., Myerowitz P.D. Acute transient coronary sinus hypertension impairs left ventricular function and induces myocardial edema. Am J Physiol 1996;271:H834-H341.[Abstract/Free Full Text]




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