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Ann Thorac Surg 1997;63:598-599
© 1997 The Society of Thoracic Surgeons
Division of Cardiovascular Thoracic Surgery, The University of British Columbia, 700 W 10th Ave, Floor C Suite 314, Vancouver, Bc V5z 4e5 Canada
To the Editor:
Robert Guyton and his associates at Emory have contributed greatly to our understanding of myocardial protection. I therefore read their recent article in The Annals comparing the effects of different cardioplegic solutions and temperatures on microvascular reactivity with interest [1]. There are some specifics in their report that I would appreciate them reviewing and discussing further.
From the methods and Table 1 it appears that the potassium concentration of their crystalloid solution was 100 mEq/L, whereas the potassium concentration of the blood solution (one part crystalloid solution to four parts blood = [100 + 20]/5) would have been in the 24 mEq/L range. Early clinical and subsequent animal studies of Lam's solution and high-potassium Melrose formulations documented severe myocardial damage when high potassium concentration solutions were infused into the heart [2]. I suspect that any potassium concentration greater than 50 mEq/L may be deleterious. Could the loss of endothelium-dependent relaxation in the crystalloid-infused animals in the present study be due to a higher potassium concentration than in the blood cardioplegic groups?
Loss of endothelium-dependent relaxation is an important complication of cardioplegic arrest that is present after infusion of some crystalloid formulations, for example, high-magnesium–including St. Thomas' 2 solution, but has not been demonstrated after infusion of formulations mimicking extracellular electrolyte concentrations plus a modestly elevated potassium level [3, 4]. Loss of endothelium-dependent relaxation may occur after infusion of both blood and crystalloid cardioplegic solutions with 20 times the normal extracellular concentration of potassium and might not be present after infusion of Murphy, Pan-Chih, and Guyton's [1] crystalloid solution if the potassium concentration was in the usual clinical arrest range of four to five times physiologic. Have they performed additional studies that might resolve these questions?
Two other concerns relate to the low temperature of 4.8°C reached by the myocardium in both of the hypothermic study groups and detrimental effects of the use of topical ice slush [5] when several intrapericardial cardiac jacketing devices are available to maintain controlled hypothermia. The majority of clinical and animal studies have demonstrated persistent metabolic and functional dysfunction after myocardial temperature has decreased to less than 7° to 10°C [6, 7], and myocardial stunning (transient early delay in functional recovery) is observed clinically when myocardial temperatures in the 4° to 5°C range are occasionally accidentally achieved. Could some of the microvascular dysfunction observed be due to avoidable hypothermic injury?
References
Department of Cardiothoracic Surgery, Emory University Hospital, Rm 3220, 1365 Clifton Rd, Atlanta, Ga 30322
To the Editor:
My colleagues and I appreciate very much the letter of Dr Tyers concerning our article. Doctor Tyers' careful reading of our article points out a potentially very confusing error in the table. The cold crystalloid group received cardioplegia with 20 mEq of potassium chloride added to the 1 L of isolyte (approximate final potassium concentration, 24 mEq/L). The two blood groups received cardioplegia that was a 4:1 mixture of blood with the crystalloid component identified in Table 1 (100 mEq/L) leading also to a final potassium concentration of approximately 24 mEq/L. Therefore, both groups of animals received essentially the same potassium concentration in the cardioplegic solution. Similar solutions have been used for crystalloid cardioplegia previously in our laboratory (references 5, 6, and 14 in our article). We regret the error made in the table and appreciate Dr Tyers' attention to detail in reading this article. We fully agree with him that, if the potassium concentration had been 100 mEq/L, this would be potentially damaging to the endothelium.
It is also certainly possible that low temperatures reached in the myocardium in the hypothermic groups may have led to endothelial injury. This is one of the threats of hypothermic cardioplegia as the endothelium is exposed to the very lowest temperatures when infusion hypothermia is used and the cardioplegia being infused is cooled with an ice bath. Although the external cooling jackets may maintain global myocardial temperature at 10° to 15°C, the endothelium will still be exposed to very cold temperatures if this type of infusion hypothermia is used.
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