Elective coronary angioplasty with 60 s balloon inflation does not cause peroxidative injury.

Background: The aim of this study was to evaluate the ongoing controversial issue of whether ischemia/reperfusion during elective coronary angioplasty evokes myocardial peroxidative injury.

Design: We measured indicators of free radical damage to lipids (free malondialdehyde) and proteins (sulphydryl groups) in coronary sinus blood in 19 patients with stable angina who were undergoing elective angioplasty for isolated stenosis of the proximal left anterior descending coronary artery. Ischemia induced by 60 s balloon inflations was confirmed by lactate washout into coronary sinus after deflation, with immediate and 1 min samples. Peroxidative injury was assessed from washout of (a) malondialdehyde measured directly by high performance liquid chromatography and (b) reduced sulphydryl groups, inverse marker of protein oxidative stress.

Results: Mean lactate concentration immediately after each deflation increased by 120-150% of the initial value, confirming ischemia and showing that blood originated largely from the ischemic region. Lack of myocardial production of malondialdehyde was confirmed by (a) no arteriovenous differences in individual basal concentrations (aortic, range 0.33-12.03 nmol mL-1, mean 7.82; coronary sinus blood, range 0.52-15.82 nmol mL-1, mean 8.18), and (b) after deflations, mean concentrations were not significantly different from preocclusion value. There was no decrease in concentration of sulphydryl groups throughout angioplasty.

Conclusion: Elective coronary angioplasty with 60 s balloon inflations is a safe procedure that does not induce peroxidative myocardial injury as assessed by methods used in the present study.