Tomai F, Crea F, Gaspardone A, Versaci F, Esposito C, Chiariello L, Gioffrè P A
Servizio Speciale di Diagnosi e Cura di Emodinamica, Italy.
J Am Coll Cardiol. 1993 Dec;22(7):1892-6. doi: 10.1016/0735-1097(93)90775-v.
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.
Anecdotal experimental 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.
We randomly allocated 48 consecutive patients undergoing coronary angioplasty into two groups. In Group A the second 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.
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 Groups 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).
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 repeated 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.
本研究旨在确定冠状动脉血管成形术期间患者所经历的心脏疼痛是否受以下因素调节：1）冠状动脉壁的伸展；2）缺血预处理的相关机制。
轶事性实验观察表明，冠状动脉壁的伸展是足以引发心脏疼痛的一种刺激。此外，近期实验研究表明，心绞痛疼痛的介质腺苷似乎在缺血预处理的发生过程中起重要作用。
我们将48例连续接受冠状动脉血管成形术的患者随机分为两组。A组第二次球囊扩张的压力高于第一次；B组前两次扩张的球囊压力水平相同。在每个扩张期结束时，测量12导联体表心电图（ECG）和冠状动脉内ECG上ST段移位的平均值（±1标准差）。同时，使用视觉模拟量表获取心脏疼痛的严重程度。
两组患者第二次球囊扩张期间的平均ST段移位均显著小于第一次扩张期间（A组：12.8±9.3 vs. 18.5±11.9 mm，p<0.001；B组：13.7±10.1 vs. 21.3±13.9 mm，p<0.001）。然而，但A组第二次扩张期间心脏疼痛的严重程度大于第一次扩张期间（40.8±32.7 vs. 26.9±27.2 mm，p<0.01），而B组则较轻（23.1±20.7 vs. 32.9±29.6 mm，p<0.05）。然而，在后一组中，在对平均ST段移位进行归一化后，第一次和第二次扩张期间的疼痛严重程度相似（2.1±2.4 vs. 2.7±3.6，p=无显著性差异）。
在冠状动脉血管成形术期间，患者所经历的心脏疼痛部分由冠状动脉壁的伸展引起。如果在重复冠状动脉闭塞期间伸展保持在恒定水平，则心脏疼痛完全由心肌缺血的严重程度预测，因此似乎不受缺血预处理相关机制的直接调节。
