Effect of small-amplitude electrical activity on myocardial preservation in the cold potassium-arrested heart

Recent reports indicate that small-amplitude electrical activity may be present in the cold potassium-arrested heart. Twenty-four mongrel dogs were placed on cardiopulmonary bypass and cooled to a rectal temperature of 26°C. Myocardial preservation was provided with a combination of systemic hypothermia 26°C. Potassium (20 mEq/L) crystalloid cardioplegic solution (10 ml/kg) infused initially and every 30 minutes during 90 minutes of ischemic arrest, and topical hypothermia. Myocardial temperature was maintained between 8° and 10° C. Electrical activity and transmural myocardial temperature were monitored with specially designed plunge electrodes. Left ventricular stroke work index, cardiac index, and maximum rate of rise of left ventricular pressure were measured before bypass and 45 minutes after ischemic arrest. Biopsy specimens were taken before bypass and at 15 and 45 minutes after ischemic arrest. The specimens were used to measure adenosine triphosphate and to analyze electron microscopic ultrastructure. Small-amplitude electrical activity was present in 16 of 24 animals during cardioplegic arrest. Cardiac index decreased 18 ml/min/kg (not significant), left ventricular stroke work index fell by 0.28 ± 0.1 gm-m/beat/kg (p < 0.007), and maximum rate of rise of left ventricular pressure decreased 409 mm Hg/sec (p < 0.01) in the eight animals without small-amplitude electrical activity. Adenosine triphosphate concentration was unchanged and electron microscopic ultrastructure was well preserved. In contrast, small-amplitude electrical activity (16 animals) resulted in a decrease in cardiac index of 67 ml/min/kg (p < 0.001), a decrease in left ventricular stroke work index of 0.79 ± 0.8 gm-m/beat/kg (p < 0.001), and a fall in maximum rate of rise of left ventricular pressure of 775 mm Hg/sec (p < 0.001). Adenosine triphosphate concentration decreased from 25 to 21 μmol/gm (p < 0.04) and electron microscopic ultrastructure was poorly preserved (p < 0.001). This study demonstrates that small-amplitude electrical activity in the cardioplegia-arrested heart at 10° C impairs myocardial preservation.