Türkoğlu Caner, Gür Mustafa, Şeker Taner, Selek Şahbettin, Koçyiğit Abdurrahim
aDepartment of Cardiology, Yenimahalle Training and Research Hospital, Ankara bDepartment of Cardiology, Adana Numune Training and Research Hospital, Adana cDepartment of Cardiology, Osmaniye State Hospital, Osmaniye dDepartment of Clinical Biochemistry, School of Medicine, Bezmi-Alem University, İstanbul, Turkey.
Coron Artery Dis. 2016 Dec;27(8):690-695. doi: 10.1097/MCA.0000000000000416.
Left ventricular (LV) remodeling is an important pathophysiological event that develops following acute myocardial infarction and causes LV systolic dysfunction. Mechanisms such as apoptosis, necrosis, and oxidative stress play an important role in LV remodeling.
This study aimed to determine the relationship between the development of LV remodeling and the apoptosis marker M30 in patients with anterior ST-segment elevation myocardial infarction (STEMI) who were treated with primary percutaneous coronary intervention (PCI).
This retrospective study included 255 consecutive patients (210 men, 45 women, mean age 54.9±11.8 years) with anterior STEMI who were treated with primary PCI. Blood samples were obtained from each patient at admission and 24 h after admission for measurements of M30, M65, oxidative parameters, and biochemical parameters. Transthoracic echocardiography was performed in each patient within 24 h of infarction and 6 months after infarction. LV remodeling was defined as greater than or equal to 20% increase in end-diastolic volume 6 months after primary PCI. The patients were divided into two groups on the basis of 6 months of post-primary PCI follow-up findings: LV remodeling group and non-LV remodeling group.
In all, 60 patients received LV remodeling and 195 did not receive LV remodeling at 6 months after primary PCI. Total oxidative stress, M30 and M65 levels, and the oxidative stress index were significantly higher and the total antioxidant capacity and M65/M30 ratio were lower in the LV remodeling group (P<0.05, for all). Brain natriuretic peptide, M30, and oxidative stress index were independent predictors of LV remodeling (P<0.05 for all). Receiver operating characteristic curve analysis showed that the M30 cut-off value for predicting LV remodeling was 144.9 U/l (80% sensitivity and 77% specificity, P<0.001).
In patients with anterior STEMI treated with primary PCI, the apoptosis marker M30 might be useful for predicting LV remodeling and subsequent LV systolic dysfunction.
左心室(LV)重构是急性心肌梗死后发生的重要病理生理事件,可导致左心室收缩功能障碍。细胞凋亡、坏死和氧化应激等机制在左心室重构中起重要作用。
本研究旨在确定接受直接经皮冠状动脉介入治疗(PCI)的前壁ST段抬高型心肌梗死(STEMI)患者左心室重构的发生与凋亡标志物M30之间的关系。
本回顾性研究纳入了255例连续接受直接PCI治疗的前壁STEMI患者(210例男性,45例女性,平均年龄54.9±11.8岁)。在入院时及入院后24小时采集每位患者的血样,用于检测M30、M65、氧化参数和生化参数。在梗死24小时内及梗死后6个月对每位患者进行经胸超声心动图检查。左心室重构定义为直接PCI术后6个月舒张末期容积增加大于或等于20%。根据直接PCI术后6个月的随访结果将患者分为两组:左心室重构组和非左心室重构组。
直接PCI术后6个月,共有60例患者发生左心室重构,195例未发生左心室重构。左心室重构组的总氧化应激、M30和M65水平以及氧化应激指数显著更高,而总抗氧化能力和M65/M30比值更低(均P<0.05)。脑钠肽、M30和氧化应激指数是左心室重构的独立预测因素(均P<0.05)。受试者工作特征曲线分析显示,预测左心室重构的M30临界值为144.9 U/l(灵敏度80%,特异度77%,P<0.001)。
在接受直接PCI治疗的前壁STEMI患者中,凋亡标志物M30可能有助于预测左心室重构及随后的左心室收缩功能障碍。