摘要
目的研究接受直接经皮冠脉介入(PCI)治疗的急性ST段抬高型心肌梗死(STEMI)患者非梗死相关动脉(罪犯血管)病变进展的临床和冠脉造影相关因素。方法入选2006年1月至2009年12月接受直接PCI治疗的急性STEMI患者492例,进行12个月临床和造影随访。主要终点:临床驱动的非梗死相关动脉PCI治疗。测定血清儿茶酚胺(肾上腺素和去甲肾上腺素)和血清C-反应蛋白(CRP)水平,并对患者的临床和造影特点进行分析。结果 492例患者中,45例患者接受了临床驱动的非梗死相关动脉病变PCI治疗(研究组),447例患者未接受PCI治疗(对照组)。两组患者血清儿茶酚胺水平[肾上腺素(621.48±79.31)vs(268.14±73.26)pg/ml,P<0.01;去甲肾上腺素(6212.43±822.41)vs(3218.34±614.16)pg/ml,P<0.01],血清CRP水平[(3.29±1.31)vs(2.51±1.14)mg/dl,P<0.05],血清肌钙蛋白I(cTnI)峰值[(27.27±4.02)vs(16.12±3.23)ng/ml,P<0.01],血栓病变率(62.22%vs 23.04%,P<0.01),≥2支血管病变率(80.00%vs 46.09%,P<0.01),罪犯病变长度[(33.2±12.9)vs(28.1±13.1)mm,P<0.01]和复杂病变率(57.78%vs 36.02%,P<0.01)均有显著性差异。非罪犯血管狭窄程度与血清肾上腺素水平(r=0.95,P<0.01)、去甲肾上腺素水平(r=0.97,P<0.01)、CRP水平(r=0.83,P<0.05)、cTnI峰值(r=0.90,P<0.05)、血栓病变率(r=0.81,P<0.05)、≥2支血管病变率(r=0.84,P<0.05)、罪犯病变长度(r=0.95,P<0.01)和复杂病变率(r=0.96,P<0.01)存在显著的相关性。结论急性STEMI患者直接PCI术后的再次PCI主要是由于非罪犯病变进展所致。非罪犯病变进展可能涉及炎症和应激机制。
Objective To investigate the clinical and angiographic factors related to the progression of non- infarction-related artery （non-culprit vessel ） lesions in patients with acute ST-elevation myocardial infarction （STEMI） underwent primary percutaneous coronary intervention （PCI）. Methods A total of 492 consecutive patients with acute STEMI who underwent PCI from January 2006 to December 2009 were enrolled in present study. All of the patients received clinical and angiographic follow-up for 12 months. Primary endpoint： clinically driven non-culprit lesions PCI. The levels of serum catecholamine [ epinephrine （ E）, norepinephrine （NE） ] and C-reactive protein （CRP） were assayed. The clinical and angiographic features were analyzed. Results Of 492 patients, 45 underwent clinically driven Non-culprit lesions PCI （ study group）, 447 were free of revascularization （ control group）. There were significant differences in the levels of catecholamine [ E （621.48±79.31 ） vs （268.14 ± 73.26） pg/ml,P〈0.01; NE （6212.43 ±822.41） vs （3218.34 ±614.16） pg/ml ,P〈0.01],CRP[（3.29 ±1.31） vs （2.51 ± 1.14） mg/dl , P 〈 0. 05 ], cardiac troponin I （cTnI） peak value [ （ 27.27 ± 4.02） vs （ 16. 12± 3.23 ）ng/ ml,P 〈 0.01 ], thrombosis lesion rate （ （ 62.22% vs 23.04%, P 〈 0.05 ）, ≥ 2 vessel lesions rate （ 80.00% vs 46. 09%, P 〈 0. 01 ）, culprit lesion length [ （ 33.2 ± 12.9 ） vs （ 28.1 ± 13.1 ） mm, P 〈 0.01 ], and complex lesion rate（57.78% vs 36.02% ,P 〈0.01 ） between two groups. Correlation analysis showed that the stenosis degree of non-culprit vessel was significantly correlated with serum E （ r = 0.95, P 〈 0.01 ）, NE （ r = 0. 97, P 〈 0.01 ）, CRP （ r = 0.83, P 〈 0.05 ）, cTnI peak value （ r = 0.90, P 〈 0.05 ）, thrombosis lesion rate （ r = 0. 81, P 〈 0.05 ）, ≥ 2 vessel lesions rate （r = 0.84, P 〈 0.05 ）, culprit lesion length （ r = 0.95, P 〈 0.01 ）, and complex lesion rate （ r = 0. 96,P 〈 0.01 ）. Conclusions Recurrent PCI is mainly due to non-culprit lesions progression in patients with acute STEMI after primary PCI. Inflammation and stress mechanism may be involved in the progression of non-culprit lesions.
出处
《中国临床研究》
CAS
2013年第9期889-891,共3页
Chinese Journal of Clinical Research
