Statin reload before off-pump coronary artery bypass graft: Effect on biomarker release kinetics

Statins confer protection from ischemia/reperfusion through various pathways including pleiotropic mechanisms. Following chronic administration, activation of intrinsic cellular mechanisms causes attenuation of these pleiotropic effects.

Since coronary artery bypass surgery (CABG) represents a reversible ischemia-reperfusion sequence, we assessed if statin reload is effective in patients undergoing off-pump CABG (n = 100) in limiting myocardial injury. Patients received loading dose of rosuvastatin (40 mg initiated 7 days before surgery) while nonloaded patients continued whatever statin dose they were receiving and served as controls. Cardiac biomarkers (Troponin-I, creatine kinase muscle/brain [CK-MB], and B-type natriuretic peptide [BNP]) were measured at 8, 24, and 48 h postoperatively. The primary end-point was the extent of perioperative myocardial injury (area under the curve [AUC]: AUC of each biomarker).

Despite similar baseline levels, all biomarkers at 8, 24, and 48 h were significantly lower in the loaded group. The AUC for each biomarker was also significantly lower in the loaded group (cTnI 37.96 vs. 70.12 ng. hr/ml, CK-MB 229.64 vs. 347.04 ng. hr/ml, and BNP 5257.56 vs. 15606.68 pg. hr/ml, all P < 0.001). Delta cTnI (change from baseline to peak level) (1.00 ± 1.34 vs. 2.25 ± 2.59), delta CK-MB (4.54 ± 5.89 vs. 10.68 ± 9.95), and delta BNP (120.41 ± 172.48 vs. 449.23 ± 790.95) all P < 0.001 were also significantly lower in the loaded group. Those loaded with rosuvastatin had lower inotrope duration (22.9 ± 23.33 vs. 31.26 ± 25.39 h, P = 0.04) and ventilator support time (16.94 ± 6.78 vs. 23.8 ± 20.53 h, P = 0.03).

In patients undergoing off-pump CABG, statin reload can "recapture" cardioprotection in patients already on statins with favorable effect on release kinetics of biomarkers and postoperative outcomes.