Impact of primary percutaneous coronary intervention on blood perfusion in nonculprit artery in patients with anterior ST elevation myocardial infarction

Abstract

Background Recent studies have demonstrated that epicardial flow in nonculprit arteries, which has been assumed to be normal, was slowed in the setting of ST-elevation myocardial infarction (STEMI). However, the impact of primary percutaneous coronary intervention (PCI) on blood perfusion in nonculprit arteries in patients with STEMI has not been clarified. The purpose of this study was to investigate the impact of primary PCI on blood perfusion in nonculprit arteries in patients with STEMI and correlated clinical factors. Methods A total of 117 patients with anterior wall STEMI, the culprit artery being the left anterior descending artery (LAD), undergoing primary PCI (the study group) and 100 patients with normal coronary angiography (the control group) were enrolled. To observe the differences of corrected TIMI frame count (cTFC) and myocardial blush grade (MBG) before and after primary PCI in both culprit and nonculprit arteries, the left circumflex coronary artery (LCX), cTFC and MBG in the LAD and LCX were measured in the study group and control group. The study group was divided into three groups; reflow in the culprit artery group (the R group), no reflow in culprit artery group (the NR group), and no reflow in both the culprit artery and nonculprit artery group (the NRB group) according to MBG grade. The level of serum C-reactive protein (CRP), catecholamine, and fibroblast growth factor-21 (FGF21) were assayed. The clinical and angiographic characteristics were also analyzed. Results cTFC (28.1±24.3 vs. 20.3±19.3, P <0.05) and MBG in the LCX were different in the study group compared to the control group before primary PCI. cTFC (25.2±22.3 vs. 28.1±24.3, P <0.05) and the MBG level in the LCX were improved after successful primary PCI, but were not recovered to the normal level. Patients with no reflow in the culprit artery had a higher incidence of no-reflow in the nonculprit artery (78% vs. 19%, P <0.0001), and the levels of CRP ((3.29±1.31) mg/dl vs. (2.51±1.14) mg/dl vs. (2.93±1.07) mg/dl, P <0.05, respectively), catecholamine ((epinephrine (693.48±89.78) pg/ml vs. (398.12±93.28) pg/ml vs. (562.54±96.22) pg/ml, P <0.0001, respectively), and norepinephrine ((7012.43±932.47) pg/ml vs. (4012.34±814.16) pg/ml vs. (5549.03±912.65) pg/ml, P <0.0001, respectively)) in the NRB group were higher than those in the R group and NR group. The level of FGF21 ((0.299±0.093) ng/ml vs. (0.612±0.071) ng/ml vs. (0.428±0.074) ng/ml, P <0.0001 respectively) in the NRB group was lower than that in the R group and NR group. Conclusions The blood perfusion in the nonculprit artery may be impaired in patients with STEMI. Although nonculprit artery perfusion may be improved after successful primary PCI, it is still lower than that in the control group, and may be involved in inflammation and spasms.