Effects of Shen-Yuan-Dan on Periprocedural Myocardial Injury and the Number of Peripheral Blood Endothelial Progenitor Cells in Patients with Unstable Angina Pectoris Undergoing Elective Percutaneous Coronary Intervention

Objectives. We aimed to investigate the effects of Shen-Yuan-Dan (SYD), a Chinese medicine preparation, on periprocedural myocardial injury (PMI) and the number of peripheral blood endothelial progenitor cells (EPCs) in patients with unstable angina pectoris (UA) who underwent elective percutaneous coronary intervention (PCI). Methods. Patients were randomly divided into the experimental (group A) and control (group B) groups through the random number table method. In group A, patients concurrently received the conventional western treatment and SYD orally (4 capsules/time, 3 times/d, from 3 d before surgery to 7 d after surgery). In group B, patients received conventional Western medicine treatment. Both groups underwent coronary angiography, and patients undergoing PCI were eventually included in the study. The following patient data were collected: incidence of PMI, serum CK-MB content before PCI, 4 h, 24 h, and 7 d after PCI, number of CD45dim/-CD34+CD309+ peripheral venous EPCs, and number of CD184 coexpressed EPCs. The incidence of adverse reactions and 30-day major adverse cardiovascular events (MACEs) were also recorded. Results. Sixty-two patients were finally included in this study, with 32 and 30 in groups A and B, respectively. In group A, the number of peripheral blood EPCs and the number of CD184 coexpressed EPCs at 1 h before surgery were higher than those at 3 d before surgery (37.24 ± 25.20 vs. 22.78 ± 9.60/ml; P < 0.001 and 23.38 ± 15.30 vs. 13.54 ± 8.08/ml; P < 0.001 , resp.). The number of peripheral blood EPCs and number of CD184 coexpressed EPCs at 4 h after surgery were lower than those at 1 h before surgery (25.30 ± 11.90 vs. 37.24 ± 25.20/ml; P = 0.019 and 15.38 ± 8.78 vs. 23.38 ± 15.30/ml; P = 0.013 , resp.), but there was no difference at 24 h and at 7 d after surgery in comparison with that at 1 h before surgery ( P > 0.05 ). In group B, compared with that at 1 h before surgery, there existed a decline in the number of EPCs in peripheral blood and the number of CD184 coexpressed EPCs at 4 h after surgery, but without a statistical difference ( P > 0.05 ). Comparing both groups, it was found that the incidence of PMI in group A was lower (6.25% vs. 26.67%; P = 0.04 ), and the serum CK-MB content at 4 and 24 h after surgery was also lower than that in group B (17.33 ± 5.83 vs. 20.38 ± 4.32 U/l; P = 0.048 and 15.79 ± 5.32 vs. 19.10 ± 4.93 U/l; P = 0.030 , resp.). The number of EPCs in peripheral blood and the number of CD184 coexpressed EPCs in group A were higher than those in group B at 1 h before surgery (37.24 ± 25.20 vs. 22.36 ± 12.26/ml; P = 0.034 and 23.38 ± 15.30 vs. 13.12 ± 14.62/ml; P = 0.013 , resp.). In addition, there were no obvious adverse reactions and no 30-day MACEs in both groups during the trial. Conclusion. SYD can reduce PMI and promote the mobilization of EPCs in the perioperative period of elective PCI in patients with UA.

Impact of Periprocedural Myocardial Injury and Infarction Definitions on Long-Term Mortality After Chronic Total Occlusion Percutaneous Coronary Intervention

Background: The prognostic implications of biomarker elevation following percutaneous coronary intervention (PCI) of chronic total occlusion (CTO) lesions remain controversial. This study assessed the association of periprocedural myocardial injury and clinically relevant definition of periprocedural myocardial infarction with subsequent outcomes after CTO-PCI. Methods: We enrolled consecutive patients between January 2010 and December 2013 who underwent CTO-PCI at a large-volume center with serial CK-MB (creatine kinase–myocardial band) or cTnI (cardiac troponin I) measurements. The primary outcome was 5-year cardiovascular death. Results: A total of 2616 patients (2691 CTOs) with postprocedural CK-MB or cTnI undergoing PCI recanalization were included, per-lesion technical success rate was 74.4%. Postprocedural CK-MB and cTnI elevation occurred in 5.6% and 65.5% patients, respectively. For 2485 patients with serial CK-MB measurements, only postprocedural peak CK-MB ≥5× upper reference limit was associated with increased 5-year cardiovascular death (adjusted hazard ratio, 9.88 [95% CI, 3.06–31.9]). In contrast, for 1233 patients with serial cTnI measurements, no such association was present in any threshold. The Society for Cardiovascular Angiography and Interventions definition of periprocedural myocardial infarction was associated with 5-year cardiovascular death (adjusted hazard ratio, 8.45 [95% CI, 3.58–20.0]), whereas the ARC-2 (Academic Research Consortium-2) and fourth UDMI (Universal Definition of Myocardial Infarction) were not. Conclusions: In a large cohort of CTO-PCI, moderate to high levels of peak postprocedural CK-MB were prognostically significant, whereas such association was not observed in postprocedural cTnI. The Society for Cardiovascular Angiography and Intervention criteria (but not ARC-2 and fourth UDMI) were identified as clinically relevant periprocedural myocardial infarction definition following CTO-PCI.

Peripheral Artery Tonometry Reveals Impaired Endothelial Function before Percutaneous Coronary Intervention in Patients with Periprocedural Myocardial Injury

Background. Periprocedural myocardial injury (PMI) is a most common complication of percutaneous coronary intervention (PCI). Microembolization and inflammation underlying PMI could lead to coronary microvascular dysfunction (CMD) and vice versa. Reactive hyperemia index (RHI) assessed by peripheral artery tonometry (PAT) has been considered as a noninvasive method to assess endothelial function and CMD, which could be useful to predict PMI. Methods. 268 patients suspected with stable coronary artery disease (CAD) and scheduled for elective coronary angiography were enrolled. RHI was measured by using the Endo-PAT2000™ device before angiography. The association among RHI, PMI, and cardiovascular events was further assessed. Results. In this cohort, 189 patients (70.5%) were diagnosed with CAD and 119 patients (44.4%) underwent drug-eluting stent (DES) implantation. Compared with patients without CAD, CAD patients had lower RHI (1.88 ± 0.55 vs. 2.02 ± 0.58, P < 0.05 ). Patients with PMI had a lower RHI before angiography (1.75 ± 0.37 vs. 1.95 ± 0.50, P < 0.05 ). Receiver operating characteristic curve analysis of RHI revealed an area under the curve (AUC) of 0.61, with a sensitivity of 62.7% and specificity of 50.0% to predict PMI. Moreover, we found that CAD patients with RHI ≤ 1.81 had a higher incidence of composite cardiac events after stenting (adjusted hazard ratio (HR) 3.31, 95% confidence interval (CI) 1.07–10.22, P < 0.05 ). Conclusions. RHI assessment through PAT could be a promising method to predict PMI before the procedure. RHI is associated with increased risk of long-term adverse cardiac events after DES implantation.

Colchicine to Prevent Periprocedural Myocardial Injury in Percutaneous Coronary Intervention: The COPE-PCI Pilot Trial

Background: Periprocedural myocardial infarction and injury (PM-injury) are the most common complications of percutaneous coronary intervention (PCI) and are associated with future adverse cardiac events. Inflammation plays a pivotal role in the development of PM-injury. In this randomized pilot trial, we assessed the effect of an anti-inflammatory medication colchicine on periprocedural myocardial injury. Methods: Patients undergoing PCI for stable angina or non–ST-segment–elevation myocardial infarction were randomized to oral colchicine (1 mg followed by 0.5 mg 1 hour later) or placebo, 6 to 24 hours preprocedure. Blood samples were taken immediately pre- and 24-hours post-PCI. The primary outcome, periprocedural myocardial infarction, was defined by an increase in post-PCI troponin >5×99th% upper reference limit when the pre-PCI troponin was normal, or >20% increase in post-PCI troponin when the pre-PCI troponin was raised, including supporting evidence of new myocardial ischemia. Major PM-injury was defined as per periprocedural myocardial infarction without supporting evidence of new myocardial ischemia. Minor PM-injury was defined by post-PCI troponin increase >99th% upper reference limit but ≤5×99th% upper reference limit. Results: A total of 196 patients met inclusion criteria and were randomized. One hundred twenty-one patients were excluded (no PCI, unstable troponin before PCI, or poor-quality measurements) leaving a study population of 75 patients. Thirty-six patients were randomized to colchicine and 39 to placebo preprocedure. Forty-four presented with non–ST-segment–elevation myocardial infarction and 31 with stable angina. High-sensitive (hs) troponin-I pre-PCI was similar between treatment groups (colchicine: 79 ng/L [4–1336] versus placebo: 35 [5–448], P =0.42). Absolute change in hs-troponin-I (calculated as 24-hour post-PCI minus pre-PCI measurements) was significantly lower in the colchicine group: 59 (1–221) versus placebo: 166 (53–530), P =0.02. No patients developed periprocedural myocardial infarction in either group. Significantly fewer patients developed major PM-injury: 11 (31%) versus 21 (54%), P =0.04 or minor PM-injury: 21 (58%) versus 33 (85%), P =0.01, if given colchicine pre-PCI. Conclusions: In this randomized pilot trial, colchicine given 6 to 24 hours pre-PCI reduces periprocedural myocardial injury. Registration: URL: https://www.anzctr.org.au ; Unique identifier: ACTRN12615000485538.