Changes of angiography-derived coronary microcirculatory resistance before and after drug-coated balloon treatment

Abstract

Abstract Background Drug coated balloon (DCB) is a treatment option for a lesion in a small coronary artery. The effect of DCB is proven in mechanistic and clinical outcomes, however, its influence on the microvascular function has not been elucidated. In addition, because there are differences in the types of drugs and coatings among different DCBs, their effects on microvascular function may vary. Angiography-derived microcirculatory resistance (AMR) is a novel angiographic parameter calculated from angiography-derived quantitative flow ratio and flow velocity estimation. AMR is reported to have a good correlation with the wire-based index of microvascular resistance. Purpose To investigate the AMR in coronary vessels treated with sirolimus or paclitaxel coated balloon. Methods This is a subanalysis of the TRANSFORM I (The TReAtmeNt of Small Coronary Vessels: MagicTouch Sirolimus Coated Balloon) trial. TRANSFORM I is a prospective, randomized, multi-center, open-label noninferiority trial conducted in Europe that enrolled 121 patients (126 vessels) with stabilized acute coronary syndrome or chronic coronary syndrome who had at least one de novo coronary artery lesion in a small coronary vessel. Patients were randomized 1:1 to treatment with the sirolimus coated balloon (SCB) or paclitaxel coated balloon (PCB). The SCB is coated with phospholipid encapsulated sirolimus nanocarrier, whereas the PCB is coated with crystalline paclitaxel. In this subanalysis, angiography at baseline and post-procedure were analyzed to calculate the AMR by an imaging core lab. Coronary microvascular dysfunction (CMD) was defined as AMR≧2.5 mmHg*s/cm. Results In the total of 126 vessels, 63 were included in each of the SCB and PCB group. Angiography both at baseline and post-procedure were analyzable for AMR in 59 vessels in SCB and in 59 vessels in PCB group. In SCB group, the median AMR increased significantly after procedure (baseline; 2.03 [1.58-2.42], post-procedure;2.21 [1.78-2.53], p=0.03). However, the proportion of vessels with CMD did not significantly change (baseline; 22.0% [13/59], post-procedure; 32.2% [18/59], p=0.19) (Figure). In the PCB group, the median AMR increased significantly after procedure (baseline; 2.22 [1.66-2.53], post-procedure;2.45 [1.93-2.96], p=0.003). Furthermore, the proportion of vessels with CMD significantly increased (baseline; 27.1% [16/59], post-procedure; 47.5% [28/59], p=0.046) (Figure). The AMR measurement was not significantly different between SCB and PCB at baseline (p=0.53), but it was significantly higher in PCB than in SCB at post-procedure (p=0.04). Conclusion After DCB treatment, AMR significantly increased in both arms. The proportion of the vessel with CMD after procedure did not significantly change in the SCB group but increased in the PCB group. The potential mechanism of increase in AMR after DCB treatment (e.g. embolization of small crystals) may warrant further investigation.Proportion of AMR≥2.5