Mehta Hetal H, Morris Mackenzie, Fischman David L, Finley John J, Ruggiero Nicholas, Walinsky Paul, McCarey Melissa, Savage Michael P
Cardiac Catheterization Laboratory, Thomas Jefferson University Hospital, 111 South 11th Street, Gibbon Building, Ste 6210, Philadelphia, PA 19107 USA.
J Invasive Cardiol. 2019 Mar;31(3):42-45. doi: 10.25270/jic/18.00250. Epub 2018 Dec 15.
An under-recognized cause of chest pain, the coronary slow-flow (CSF) phenomenon is characterized by delayed coronary opacification during diagnostic angiography in the absence of epicardial coronary artery disease (CAD). Given its angiographic resemblance to no-reflow during percutaneous coronary intervention, a condition associated with microvascular spasm responsive to calcium-channel blockers, we hypothesized that spontaneous CSF may similarly be reversed by intracoronary (IC) nicardipine.
The effect of IC nicardipine was evaluated in 30 patients. CSF was defined as spontaneously delayed flow (<TIMI 3) during diagnostic coronary angiography in the absence of obstructive epicardial CAD or other conditions associated with impaired flow. Nicardipine was administered as a 200 μg IC bolus, after which repeat angiography was performed. Coronary flow before and after nicardipine was evaluated by TIMI flow grade and corrected TIMI frame count (TFC) assessments.
The study population consisted of 22 men and 8 women (mean age, 54 ± 11 years). Clinical presentation was rest angina in 21 patients (70%). At baseline, CSF with <TIMI 3 flow was observed in 49 vessels. TFC was prolonged (>27) in 68/90 vessels (76%). IC nicardipine produced markedly accelerated coronary filling, which was corroborated by TFC analysis. TFC was 47 ± 17 before vs 15 ± 5 after nicardipine (P<.001). All vessels demonstrated TIMI 3 flow and TFC <28 after nicardipine treatment.
IC nicardipine appears highly effective in reversing spontaneous CSF. These findings implicate microvascular spasm in the pathogenesis of CSF. Future studies of oral calcium-channel blockers in the long-term management of CSF are needed.
冠状动脉慢血流（CSF）现象是胸痛的一个未被充分认识的原因，其特征是在诊断性血管造影时冠状动脉显影延迟，而不存在心外膜冠状动脉疾病（CAD）。鉴于其血管造影表现与经皮冠状动脉介入治疗时的无复流相似，后者是一种与对钙通道阻滞剂有反应的微血管痉挛相关的情况，我们推测冠状动脉内（IC）尼卡地平可能同样能逆转自发性CSF。
对30例患者评估IC尼卡地平的效果。CSF定义为在诊断性冠状动脉造影时，在无阻塞性心外膜CAD或其他与血流受损相关疾病的情况下，自发出现的血流延迟（<TIMI 3级）。尼卡地平以200μg冠状动脉内推注给药，之后进行重复血管造影。通过TIMI血流分级和校正的TIMI帧计数（TFC）评估来评价尼卡地平前后的冠状动脉血流。
研究人群包括22名男性和8名女性（平均年龄54±11岁）。21例患者（70%）临床表现为静息性心绞痛。基线时，在49支血管中观察到CSF且血流< TIMI 3级。68/90支血管（76%）的TFC延长（>27）。冠状动脉内尼卡地平使冠状动脉充盈明显加快，TFC分析证实了这一点。尼卡地平治疗前TFC为47±17，治疗后为15±5（P<0.001）。尼卡地平治疗后所有血管均显示TIMI 3级血流且TFC<28。
冠状动脉内尼卡地平似乎对逆转自发性CSF非常有效。这些发现提示微血管痉挛在CSF的发病机制中起作用。需要进一步开展关于口服钙通道阻滞剂对CSF长期治疗的研究。
