Mechanism of PTCRA-induced injury of the coronary microcircuration

长时间的胸痛和心动过缓是经皮冠状动脉腔内旋切术(PTCRA)中众所周知的并发症，这限制了其有效性。腺苷被认为与心肌缺血相关的心动过缓和心绞痛的感觉有关。然而，目前尚不清楚腺苷是否也与PTCRA中的胸痛和心动过缓有关。我们评估了腺苷P1受体拮抗剂氨茶碱对PTCRA相关的持续性胸痛和心动过缓的抑制作用。20例行PTCRA的劳力型心绞痛患者，术前静脉注射氨茶碱5 mg/kg(A组)或生理盐水10例(B组)。两组患者的特征(年龄、性别、冠状动脉危险因素、既往有心肌梗死史和用药情况)以及病变部位和形态相似。所有患者PTCRA均获得成功，两组患者在手术方式(毛刺/动脉比率、消融速度和消融时间)方面无显著差异。A组10例患者中无一例出现胸痛或心动过缓，而B组10例患者中有5例和4例出现胸痛和深部心动过缓(50次/分)(P<0.05)。两组患者术中血压和ΣST段抬高(ST段抬高总和)的变化相似。PTCRA术后两组冠状动脉远端P-选择素水平均升高。总之，氨茶碱不能减轻PTCRA期间心肌缺血的严重程度，部分原因可能是由于血小板的激活，但确实减轻了PTCRA相关的胸痛和心动过缓，可能是通过拮抗腺苷P1受体。氨茶碱预处理可使PTCRA更安全、更容易。

Prolonged chest pain and bradycardia are well known complications during percutaneous transiuminal coronary rotational atherectomy (PTCRA), which limit its usefulness. Adenosine has been implicated in myocardial ischemia-related bradycardia and the perception of anginal pain. However, it is not known whether adenosine is also responsible for chest pain and bradycardia during PTCRA.We assessed the inhibitory effect of aminophylline, an adenosine P1 receptor antagonist, on PTCRA-related prolonged chest pain and bradycardia. Of 20 patients with effort angina who underwent PTCRA, aminophylline (5mg/kg) was administered intravenously before the procedure in 10 patients (group A) or saline in the other 10 patients (group B). Patient characteristics (age, sex, coronary risk factors, presence of previous myocardial Infarction and medications) and the lesion location and morphology were similar between these two groups. PTCRA was successful in all patients and there was no significant difference in the procedure (burr/artery ratio, speed and duration of the ablation) between these two groups. In group A, none of 10 patients had chest pain or bradycardia during PTCRA.However , 5 and 4 of 10 patients in group B had chest pain and profound bradycardia (<50bpm) (p<0.05). The changes of blood pressure and ΣST-elevation (sum of ST segment elevations) on the electrocardiograms during PTCRA were similar between these two groups. Plasma levels of P-selectin in the distal coronary artery were increased after PTCRA in both two groups. In conclusion, aminophylline did not reduce the severity of myocardial ischemia during PTCRA, probably due, in part, to the platelet activation, but indeed reduced PTCRA-related chest pain and bradycardia probably by antagonizing the adenosine P1 receptor. The pretreatment with aminophylline may make PTCRA safer and easier.