Alterations in regional myocardial function after heterogeneous cardioplegia.

Coronary stenoses lead to heterogeneous delivery of cardioplegic solution during cardiac operations. This situation was simulated by occlusion of the circumflex artery during cardioplegic infusion in canine right heart bypass preparations. Regional myocardial function (systolic shortening by sonomicrometer) was often diminished, despite preservation of global function. The correlation between recovery of circumflex regional function and recovery of stroke work or dP/dt (at constant aortic pressure, heart rate, and left atrial pressure) was poor (r = 0.17 and 0.07). The response of damaged regions to hemodynamic manipulations was studied. Increases in afterload after arrest did not lead to further deterioration of damaged regions. Volume loading (cardiac output 2 to 5 L/min) improved regional function even in severely damaged, bulging regions (p less than 0.05). Regional distensibility (delta length/delta left atrial pressure) decreased by 41% (p less than 0.02) in regions with poor protection and by 22% (p less than 0.01) in regions with good cardioplegic protection. There was also an increase in resting length (p less than 0.001) in both circumstances (5.2% and 3.7%). These changes in diastolic properties have not always been apparent in other experimental studies with less precise hemodynamic control. Heterogeneous cardioplegia causes heterogeneous changes in both diastolic distensibility and systolic function. These changes are poorly detected by examination of global ventricular function.

Calcium-channel blockade as an adjunct to heterogeneous delivery of cardioplegia.

The clinical situation of heterogeneous cardioplegia was simulated in a canine model by temporary ligation of the circumflex coronary artery during a three-hour interval of cardioplegic arrest. Nifedipine and lidoflazine, administered prior to aortic clamping, were evaluated as adjuncts to cold (2 degrees C) crystalloid cardioplegia. Assessment was made of regional function (sonomicrometer systolic shortening) and of global function by measuring left atrial (LA) pressure at constant cardiac output (CO), aortic pressure, and heart rate, and by measuring stroke work at constant LA pressure, aortic pressure, and heart rate. Among 14 control dogs, only 7 could achieve a CO of 5 liters per minute following cardioplegic arrest. Left anterior descending coronary arterial systolic shortening recovered to only 86% of prearrest values (p less than 0.05), circumflex coronary arterial systolic shortening recovered only 28% (p less than 0.01), stroke work recovered 59% (p less than 0.01), and LA pressure was 6.7 mm Hg higher (p less than 0.01) than prior to cardioplegic arrest. Lidoflazine provided no statistically significant benefit in these animals (N = 4). However, dogs given nifedipine (N = 6) had very little change in left anterior descending coronary arterial systolic shortening (99% recovery), stroke work (93% recovery), and LA pressure (delta = 0.4 mm Hg). None of these changes was statistically significant. There was some deterioration in circumflex coronary arterial systolic shortening (56% recovery; p less than 0.05). All 6 dogs given nifedipine achieved a CO of 5 L/min following cardioplegic arrest. Clinical cardioplegia is typically heterogeneous cardioplegia. Calcium-channel blockade appears to be useful in this situation.