The Journal of Thoracic and Cardiovascular Surgery, Vol 91, 684-689, Copyright © 1986 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Effect of small-amplitude electrical activity on myocardial preservation in the cold potassium-arrested heart
RW Landymore, AE Marble, A Trillo, M MacAulay, G Faulkner and C Cameron
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
degrees C. Myocardial preservation was provided with a combination of
systemic hypothermia 26 degrees 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 degrees and 10 degrees 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 less than 0.007),
and maximum rate of rise of left ventricular pressure decreased 409 mm
Hg/sec (p less than 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 less than 0.001), a decrease in left
ventricular stroke work index of 0.79 +/- 0.8 gm- m/beat/kg (p less than
0.001), and a fall in maximum rate of rise of left ventricular pressure of
775 mm Hg/sec (p less than 0.001). Adenosine triphosphate concentration
decreased from 25 to 21 mumol/gm (p less than 0.04) and electron
microscopic ultrastructure was poorly preserved (p less than 0.001). This
study demonstrates that small- amplitude electrical activity in the
cardioplegia-arrested heart at 10 degrees C impairs myocardial
preservation.
