Mechanisms of cardiac pain during coronary angioplasty

Objectives. This study was conducted to establish whether the cardiac pain patients experience during coronary angioplasty is modulated by 1) the stretching of the coronary artery wall, and 2) the mechanisms responsible for the ischemic preconditioning. Background. Anecdotal experiment observations indicate that stretching of the coronary artery wall is a stimulus adequate to cause cardiac pain. Furthermore, recent experimental studies indicate that adenosine, a mediator of the anginal pain, appears to play an important role in the genesis of ischemic preconditioning. Methods. We randomly allocated 48 consecutive patients undergoing coronary angioplasty into two groups. In Group A the secondm balloon inflation was performed at a higher level than the first; in Group B the first two inflations were performed at the same level of balloon pressure. The mean values (±1 SD) of ST segment shift on the surface 12-lead electrocardiogram (ECG) and the intracoronary ECG were measured at the end of each inflation period. Severity of cardiac pain was also obtained at the same time by using a visual analog scale. Results. The mean ST segment shift during the second balloon inflation was significantly less than that during the first inflation in both groups of patients (12.8 ± 9.3 vs. 18.5 ± 11.9 mm, p < 0.001 and 13.7 ± 10.1 vs. 21.3 ± 13.9 mm, p < 0.001, respectively, in Group A and B). Yet, the severity of cardiac pain during the second inflation was greater than that during the first inflation in Group A (40.8 ± 32.7 vs. 26.9 ± 27.2 mm, p < 0.01), whereas it was lesser in Group B (23.1 ± 20.7 vs. 32.9 ± 29.6 mm, p < 0.05). However, in the latter group, pain severity after normalization for the mean ST segment shift was similar during the first and second inflations (2.1 ± 2.4 vs. 2.7 ± 3.6, p = NS). Conclusions. During coronary angioplasty, the cardiac pain experienced by patients is caused in part by stretching of the coronary artery wall. If the stretching is maintained at a constant level during coronary occlusions, the cardiac pain is entirely predicted by the severity of myocardial ischemia and therefore does not appear to be directly modulated by the mechanisms responsible for the ischemic preconditioning.