Thorac Cardiovasc Surg 1985; 33(4): 235-238
DOI: 10.1055/s-2007-1014128
© Georg Thieme Verlag Stuttgart · New York

Protection of the Hypertrophied Human Heart by Adjusting Regional Myocardial Temperature to a Safe Level

H. H. Scheld1 , G. Görlach1 , J. Mulch1 , T. Podzuweit2 , R. Höge1 , F. W. Hehrlein1 , W. Schaper2
  • 1Department of Cardiovascular Surgery, University of Giessen, FRG
  • 2Max-Planck-Institute for Physiological and Clinical Research, Division of Experimental Cardiology, Bad Nauheim, FRG
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Publikationsverlauf

1985

Publikationsdatum:
19. März 2008 (online)

Summary

Uneven distribution of temperature and the persistence of electro-mechanical activity after aortic cross-clamping are 2 factors limiting the myocardial protection during cardioplegic arrest, especially in hypertrophied hearts which are known to be extremely vulnerable to ischemia.

In the present study regional myocardial temperature (T) was continuously controlled, and the time until arrest occurred (&;t) was determined in 61 patients undergoing aortic valve replacement. In addition, the myocardial Contents of high energy phosphates and lactate were assessed.

Three different cardioplegic Solutions were employed: In the first group we used Bretschneider Solution (Br), in the second group St. Thomas' solution (St), and in the third group the so-called “Hamburg cardioplegia” (H). During cardiac arrest the regional myocardial temperature was adjusted to temperatures not exceeding 15 °C by intermittent infusions of cold cardioplegic Solution. We found a positive correlation between left ventricular muscle mass (LVMM) and &;t. A negative correlation existed between LVMM and adenosine triphosphate (ATP) contents at the end of the ischemic period. The cooling characteristics and At were significantly longer and the cooling to 15 °C was less rapid when H was used. Adenosine-triphosphate contents were well preserved during ischemia in all 3 groups.

We conclude that all 3 cardioplegic Solutions tested protect the hypertrophied myocardium adequately if the regional myocardial temperature does not increase above 15 °C during cardiac arrest. Hearts with a higher LVMM showed a decreased myocardial ATP content at the end of the ischemic period. Therefore, the LVMM may limit myocardial protection.

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