Myocardial protection by intracoronary nicardipine administration during percutaneous transluminal coronary angioplasty

To determine if the calcium antagonist nicardipine protects the myocardium against ischemia, myocardial lactate, hypoxanthine and prostanoid function was studied in 12 patients during percutaneous transluminal coronary angioplasty (PTCA). Values were obtained before balloon inflation and during 4 minutes after deflation. Intracoronary injection of 0.2 mg of nicardipine distal to the stenosis was done randomly before the first or second inflation; the other inflation served as a control. One minute after deflation, coronary sinus flow levels were similar during the nicardipine and control procedure (161 ± 61 vs 159 ± 72 ml/min); lactate (-9 ± 21% vs -17 ± 21%, p < 0.025) and hypoxanthine production (-107 ± 85% vs -218 ± 153%, p < 0.05) were less severe after nicardipine pretreatment than after control. All patients reverted to lactate extraction 4 minutes after inflation plus nicardipine infusion, whereas lactate was still produced 4 minutes after control inflation. No significant changes in thromboxane B₂ or prostacyclin levels were observed in the coronary sinus 1 minute after inflation, but higher arterial thromboxane B₂ values were observed after control inflation than after inflation with nicardipine infusion (median values 169 vs 78 pg/ml, p < 0.05). In conclusion, intracoronary infusion of nicardipine reduced signs of ischemia and alterations in prostanoid handling after coronary occlusion. The mechanisms of myocardial protection appeared unrelated to coronary sinus blood flow changes or to a systemic effect of nicardipine.