心肌梗死后心力衰竭患者经不同剂量培哚普利治疗后心肌能量消耗水平的变化

目的:以心肌能量消耗水平作为评价指标,探讨不同剂量培哚普利对于心肌梗死后心力衰竭患者的疗效影响。方法:112例心肌梗死后心力衰竭患者均采用培哚普利治疗方案,根据剂量大小分为常规剂量组52例和靶剂量组60例,计算并比较两组治疗前后心脏左室射血分数(LVEF)、心肌能量消耗水平(MEE)等指标,并采用Killip分级标准评价临床。结果:靶剂量组LVEF、LVFS、cESS和MEE改善效果均要优于常规剂量组(P<0.05)。靶剂量组总有效率91.7%,高于对照组的82.7%(χ~2=9.462,P<0.05)。结论:(1)培哚普利对改善心肌梗死后心力衰竭患者心肺功能疗效确切;(2)相较于常规剂量,靶剂量培哚普利更能显著降低心肌能耗水平,改善左室收缩功能,建议患者适时调增培哚普利剂量以促进作用释放。     

高、低两种剂量培哚普利治疗心肌梗死后心力衰竭的临床效果比较

目的:比较高、低两种剂量培哚普利治疗心肌梗死后心力衰竭的临床效果。方法:选取78例心肌梗死后心力衰竭患者作为观察对象。所有患者均给予培哚普利治疗,按随机数字表法将其分为低剂量组(4 mg/d)和高剂量组(8 mg/d)各39例。比较两组治疗前后血生化指标[血浆脑钠肽(BNP)、心型脂肪酸结合蛋白(H-FABP)、血钾、血肌酐(Scr)]、心功能[左心室舒张末内径(LVEDD)、左心室收缩末内径(LVESD)、左心室射血分数(LVEF)、短轴收缩率(FS)]及心肌能量消耗指标[心肌能量消耗水平(MEE)、左心室收缩末周向室壁应力(cESS)]情况。结果:治疗后,高剂量组BNP、H-FABP、LVEDD、LVESD、MEE、cESS水平均低于低剂量组,LVEF、FS水平均高于低剂量组,差异均有统计学意义(P<0.05);两组血钾、Scr水平相比,差异无统计学意义(P>0.05)。结论:高剂量培哚普利治疗心肌梗死后心力衰竭的效果优于低剂量治疗效果。     

心肌梗死后心力衰竭患者经不同剂量培哚普利治疗后心肌能量消耗水平的变化

目的探讨心肌梗死后心力衰竭患者给予不同剂量培哚普利治疗12个月后经无创超声心动图评估的心脏结构指标及心
肌能量消耗（MEE）水平变化及其意义。方法选取心肌梗死后不同程度心力衰竭患者63例,分别给予培哚普利治疗,根据长期
口服剂量水平分为常规剂量组（N,培哚普利4mg）和靶剂量组（H,培哚普利8mg）。治疗前及治疗12个月后分别用多普勒成像
技术测量心脏结构指标、左室收缩功能指标（左室短轴缩短率LVFS,左室射血分数LVEF）,计算左室收缩末周向室壁应力
（cESS）、MEE。入组前及治疗后分别于清晨采集外周静脉血,检测NT-proBNP及血肌酐。结果治疗前两组间各指标比较差异
均无统计学意义（P>0.05）。治疗后两组间比较,N组心脏结构指标（主动脉内径AD、左室收缩末期内径LVIDs、左室质量指数
LVMI、左房内径LA）、心肌能量消耗指标（cESS、MEE）及lgNT-proBNP大于H组,收缩功能指标（LVFS、LVEF）低于H组,差异
具有统计学意义（P<0.05）。与治疗前比较,H组治疗后心脏结构指标、心肌能量消耗指标及lgNT-proBNP均明显降低,收缩功
能指标明显升高;N组治疗后与治疗前比较,除PWTs、LVFS外其他各指标间变化均有统计学意义（P<0.05）。双变量相关分析
显示,MEE与lgNT-proBNP呈正相关关系（P<0.01）。结论心肌梗死后心力衰竭患者经过12个月不同剂量培哚普利治疗,均抑
制了心肌重构,改善了左室收缩功能,降低了NT-proBNP及心肌能量消耗水平;高剂量培哚普利治疗较低剂量能更明显地抑制
心肌重构,改善左室收缩功能,降低NT-proBNP及心肌能量消耗水平。
     

培哚普利对心力衰竭患者心肌肌钙蛋白Ⅰ水平的影响

目的探讨培哚普利对心力衰竭(HF)患者心肌肌钙蛋白Ⅰ(cTnI)的影响及cTnI作为评价HF不同治疗方案效果的价值.方法对62例HF患者在测定血清cTnI后,随机分为常规治疗组30例(利尿剂、洋地黄)和培哚普利组32例(利尿剂、洋地黄、培哚普利),治疗5周后复查cTnI.采用超声心动图测定治疗前后左室射血分数(LVEF).结果常规组,治疗前后c附分别为1.16±0.86μg/L,及cTnI 0.35±0.19μg/L(P＜0.01);培哚普利组治疗前后cTnI分别为1.28±0.98μg/L,及0.23±0.17μg/L(P＜0.01).治疗后培哚普利组cTnI水平比常规组显著降低(P＜0.05).常规组治疗前后LVEF分别为:0.30±0.061及0.38±0.065(P＜0.05);培哚普利组治疗前后LVEF分别为:0.29±0.071及0.45±0.076(P＜0.01);培哚普利组LVEF改善优于常规治疗组(P＜0.05).结论培哚普利降低HF患者cTnI水平优于常规治疗,表明培哚普利有明显的抑制心肌损伤作用;提示cTnI作为评价HF的不同治疗方案的疗效有一定意义.     

培哚普利应用于心肌梗死后心力衰竭治疗的效果研究

目的探讨心肌梗死后心力衰竭运用培哚普利治疗的临床效果。方法选择2017年1月至2018年1月期间我院收治的心肌梗死后心力衰竭患者92例为研究对象,根据数字随机法将其分为两组,两组均采用培哚普利治疗,其中给予对照组常规剂量,而观察组则运用大剂量,对两组的治疗效果进行比较分析。结果治疗前,两组的MEE、cESS、LVEFS以及LVEF比较无差异(P 0.05);治疗后,与对照组相比,观察组的LVEFS、MEE、LVEF以及cEES均改善明显,组间对比差异显著(P 0.05);相比较对照组而言,观察组的治疗有效率高,组间比较有显著差异(P0.05);同时,两组的Cr、NT-proBNP水平对比有统计学意义(P0.05)。结论临床上给予心肌梗死后心力衰竭患者大剂量培哚普利治疗可以改善心功能。     

培哚普利对慢性心力衰竭患者血清CTn-I的影响

目的 观察慢性心力衰竭患者血清肌钙蛋白I（cardiac troponi I,CTn-I）水平及其与左室射血分数（left ven-tricular ejection fraction,LVEF）的相关性和培哚普利对它的影响及临床意义。方法 （1）64例慢性心力衰竭患者,男42例,女22例,均对治疗方案知情同意。根据纽约心脏协会心功能分级标准,心功能Ⅲ级45例,心功能Ⅳ级19例。随机将入选患者分为两组,常规治疗组32例和培哚普利组32例。选择同期本院门诊健康体检者30例为对照组,男19例,女11例;（2）常规治疗组接受心力衰竭的常规治疗,培哚普利组在常规治疗的基础上加用培哚普利2～6 mg,治疗随访6周。（3）采用电化学免疫发光法测定血清CTn-I水平,应用彩色心脏超声仪测定心功能指标左室射血分数LVEF,两组比较、且与健康对照组比较,并进行组间均数t检验及相关性分析分析。结果 血清CTn-I水平心力衰竭患者明显高于对照组（P〈0.01）,升高的程度随着心功能的恶化而明显,常规治疗组及培哚普利组治疗后血清CTn-I水平均显著降低（P〈0.05）,而培哚普利降低更明显（P〈0.01）,左室射血分数两组治疗后均较治疗前升高,以培哚普利组升高幅度更明显（P〈0.01）。结论 血清CTn-I与心力衰竭的发生发展有关,培哚普利可降低血清CTn-I水平,改善心功能,培哚普利有抑制心肌损伤,改善心室重塑作用。     

培哚普利对慢性心力衰竭患者血浆miR-423-5p的调控及对心功能的影响

目的 探讨不同剂量培哚普利对慢性心力衰竭患者血浆miR-423-5p表达的影响及与心功能之间的相关性。 方法 选取慢性心力衰竭患者75例,随机分为常规组(常规药物治疗)、小剂量组(常规药物+4 mg/d培哚普利)和大剂量组(常规药物+8 mg/d培哚普利),每组25例。选取同期健康查体心功能正常人群25例(正常对照组)。经药物治疗4周,检测各组治疗前后左室舒张末内径(LVEDD)、左室射血分数(LVEF)、氨基末端脑利钠肽前体(NT-proBNP)及血浆miR-423-5p的表达水平。 结果 基线水平常规组、小剂量组、大剂量组LVEF的表达均显著低于正常对照组(P<0.05),LVEDD、NT-proBNP及血浆miR-423-5p的表达均显著高于正常对照组(P<0.05);治疗4周后常规组、小剂量组、大剂量组LVEF的表达均较治疗前显著升高(P<0.05),LVEDD、NT-proBNP、血浆miR-423-5p的表达均较治疗前显著降低(P<0.05);治疗后小剂量组和大剂量组LVEF的表达均显著高于常规组(P<0.05),LVEDD、NT-proBNP、血浆miR-423-5p的表达均显著低于常规组(P<0.05);同时,与小剂量组比较,大剂量组LVEF、LVEDD、NT-proBNP、血浆miR-423-5p的表达水平变化呈显著差异(P<0.05)。 结论 培哚普利可以降低慢性心力衰竭患者血浆miR-423-5p的表达水平,进而改善左室功能,其改善程度与药物剂量呈正相关。     

环磷腺苷葡胺联合培哚普利对慢性心力衰竭患者氧化应激指标的影响

目的:探讨环磷腺苷葡胺联合培哚普利治疗慢性心力衰竭的临床效果。方法:选择2015年9月—2017年3月我院收治的慢性心力衰竭患者140例,随机分为两组,各70例。给予对照组患者常规抗心衰治疗,观察组在此基础上采用环磷腺苷葡胺联合培哚普利治疗,比较两组患者氧化应激治疗水平及心功能改善情况。结果:治疗后观察组CAT、SOD及GSH-Px水平均高于对照组,MDA低于对照组,差异有统计学意义(P<0.05);治疗后观察组LVEDD、LVESD指标水平均低于对照组,LVEF高于对照组,差异有统计学意义(P<0.05)。结论:给予慢性心力衰竭患者环磷腺苷葡胺联合培哚普利治疗可有效减轻其氧化应激反应,并改善心功能,临床用药安全可靠。     

卡托普利和培哚普利对急性心肌梗死患者血压及心率的影响

目的研究卡托普利和培哚普利对急性心肌梗死患者血压和心率的影响。方法采用随机对照平行的前瞻性研究,将66例发病36小时内的急性心肌梗死患者随机分为卡托普利组33例（剂量6．25—12．5rag）和培哚普利组（剂量2—4mg）33例治疗48小时,监测给药前2小时及给药后48小时的无创血压及心率。结果给药48小时后两组血压、心率及低血压发生率均无显著性差异（P〉0．05）,卡托普利组最大血压下降值较培哚普利组显著增大（P〈0．05）。结论急性心肌梗死患者36小时内使用卡托普利和培哚普利是安全的,但培哚普利血压波动幅度较小,更适合于急性心肌梗死患者。     

不同剂量ACEI对收缩性心力衰竭患者血浆BNP水平的影响

目的 观察不同剂量培哚普利对收缩性心力衰竭患者血浆B型利钠肽(BNP)水平及6 min步行试验结果 的影响.方法 28例在该院住院治疗的收缩性心力衰竭患者治疗前及治疗后3个月检测血浆BNP及6 min步行试验,前3个月给予培哚普利4 mg/d,后3个月给予培哚普利8 mg/d;探讨ACEI对血浆BNP水平及6 min步行试验结果 有无影响.结果 服药后血浆BNP水平较服药前下降明显(P＜0.01),服药后6 min步行试验距离较服药前增加明显(P＜0.01),服培哚普利8mg 3个月者血浆BNP水平较服培哚普利4mg 3个月者下降明显(P＜0.01),服培哚普利8 mg 3个月者6 m/n步行试验距离较服培多普利4 mg 3个月者明显增加(P＜0.01).结论 服8 mg比服4 mg培哚普利能更好地降低心衰患者血浆BNP水平,改善患者症状.     

磁共振心肌灌注成像评价心肌梗死PTCA治疗前后心肌存活

目的 评价磁共振心肌灌注成像(MRMPI) 检测心肌梗死存活心肌的作用. 方法 选择心肌梗死患者51 例.采用1.5 T MR扫描仪,反转恢复快速小角度激励( IR-turbo FLASH) 序列,全部患者均在静脉注射钆喷替酸葡甲胺(Gd-DTPA) 0.1 mmol/kg、MRMPI 首过期及5~30 min 延迟期成像.21 例行静息、负荷99锝单光子发射计算机体层摄影术( single photon emission computed tomography, SPECT) 进行对照研究.首过期行短轴面成像,延迟期行短轴面及长轴面成像.结果 51例心肌梗死患者,42 例(82.3%) 首过期显示灌注减低;50 例(98%) 延迟增强.在21例168个心肌段SPECT诊断无活性心肌段48个,MRMPI 示梗死区均有延迟增强,SPECT诊断存活心肌段120 个,MRMPI 示97段无延迟增强.以静息、负荷99m锝SPECT 作为参考标准,MRMPI 的敏感度、特异度分别为100%、80.8%. 结论 MRMPI 可有效地检测心肌梗死的存活和非存活心肌,以及其程度和范围.     

Acute myocardial infarction due to myocardial bridge

Myocardial bridge (MB) is regarded as a common anatomic variant rather than a congenital condition anomaly,defined as the intramyocardial course of a portion of the coronary artery.It was first mentioned by Rayman in 1737 and first described by Grainicianu in the early 1920s.The current gold standard for diagnosing     

Acute myocardial infarction: myocardial salvage assessment

Primary coronary revascularization by means of percutaneous coronary intervention(PCI)is a highly effective treatment of acute myocardial infarction re-establishing coronary perfusion and stopping the ongoing necrosis in the dependent myocardium.Single-photon emission computed tomography(SPECT)is the most widely used modality assessing myocardial salvage as the difference between the acute perfusion defect before intervention and the remaining scar size measured in a second scan several days after the event.SPECT allows quantification of area at risk(AAR)and final infarct size(FIS)by tracer injection prior to revascularization and after 1 month,respectively.SPECT provides the most validated measure of myocardial salvage and has been utilized in multiple randomizedclinical trials.However,SPECT is logistically challenging,expensive,and includes radiation exposure.More recently,a large number of studies have suggested that cardiac magnetic resonance(CMR)can determine salvage in a single examination by combining measures of myocardial oedema in the AAR exposed to ischaemia reperfusion with FIS quantification by late gadolinium enhancement.     

Evaluation of Myocardial Viability after Myocardial Infarction with Intravenous Real-time Myocardial Contrast Echocardiography

The myocardial viability after myocardial infarction was evaluated by intravenous myocardial contrast echocardiography. Intravenous real-time myocardial contrast echocardiography was performed on 18 patients with myocardial infarction before coronary revascularization. Follow-up echocardiography was performed 3 months after coronary revascularization. Segmental wall motion was assessed using 18-segment LV model and classified as normal, hypokinesis, akinesis and dyskinesis. Viable myocardium was defined by evident improvement of segmental wall motion 3 months after coronary revascularization. Myocardial perfusion was assessed by visual interpretation and divided into 3 conditions： homogeneous opacification; partial or reduced opaciflcation or subendocardial contrast defect; contrast defect. The former two conditions were used as the standard to define the viable myocardium. The results showed that 109 abnormal wall motion segments were detected among 18 patients with myocardial infarction, including 47 segments of hypokinesis, 56 segments of akinesis and 6 segments of dyskinesis. The wall motion of 2 segments with hypokinesis before coronary revascularization which showed homogeneous opacification, 14 of 24 segments with hypokinese and 20 of 24 segments with akinese before coronary revascularization which showed partial or reduced opaciflcation or subendocardial contrast defect was improved 3 months after coronary revascularization. In our study, the sensitivity and specificity of evaluation of myocardial viability after myocardial infarction by intravenous real-time myocardial contrast echocardiography were 94.7% and 78.9%, respectively. It was concluded that intravenous real-time myocardial contrast echocardiography could accurately evaluate myocardial viability after myocardial infarction.     

心肌声学造影对急性心梗PCI术后心肌灌注的评价

目的:通过心肌声学造影(MCE)对急性心梗经皮冠状动脉支架术(PCI)后心肌灌注的情况进行判断,了解其对左心功能及左室重构的影响.方法:采用病例对照的研究方法,根据PCI术后1周的MCE检查,将急性心梗患者分为灌注正常组、灌注稀疏组和灌注缺失组,并随访检查3个月、6个月的左室射血分数(LVEF)及左室舒张末内径(LVDd)的变化情况,比较组内及组间不同时段LVEF与LVDd的变化.结果:PCI术后3个月灌注稀疏组LVEF恢复到正常;灌注缺损组PCI术后LVEF的平均水平随时间变化而逐渐降低;灌注缺损组患者的LVEF低于灌注稀疏组和灌注正常组(P<0.05);术后6个月灌注缺损组LVDd平均水平高于灌注正常组和灌注稀疏组(P<0.05),灌注缺损组随时间的变化左室内径逐渐增大(P<0.05).结论:急性心梗患者PCI术后心肌微循环较差时,其左室射血分数降低,左室内径增大;MCE有利于对急性心梗患者PCI术后左心功能及左室重构评估.     

水飞蓟素通过抑制心肌细胞凋亡减轻心肌梗死

目的：观察水飞蓟素对心肌梗死小鼠的血流动力学、梗死面积及梗死边缘区凋亡蛋白表达情况。方法：将60只小鼠随机分为心肌梗死组、假手术组、心肌梗死+水飞蓟素组和心肌梗死溶剂组。建模成功4周后检测小鼠血流动力学变化,进行心脏超声检查,评价梗死面积、细胞凋亡指数以及凋亡蛋白Bcl-2、Bax、Cleaved-Caspase3的表达。结果：与心肌梗死组小鼠相比,水飞蓟素可显著减轻心肌梗死,改善心梗小鼠心功能,降低心肌细胞凋亡指数,增强Bcl-2蛋白表达和减弱Bax和Cleaved-Caspase3蛋白表达。结论：水飞蓟素能够减轻心肌梗死,改善心梗小鼠心室收缩功能,保护心肌,减少心肌细胞的凋亡,其机制与升高Bcl-2蛋白、降低Bax和Cleaved-Caspase3蛋白表达水平有关。     

超声心肌造影技术对心肌梗塞患者心肌微循环的定量评价

目的：探讨超声心肌造影技术在心肌梗塞(简称心梗)患者心肌微循环灌注改变中的应用价值。方法：对30例急性心梗患者进行超声心动图及心肌造影检查,观察患者梗塞区域(AMI组,同时以患者非梗塞区域为自身对照组)心肌微循环灌注并以CPS造影软件进行分析。结果：心肌梗塞患者梗塞区域心肌微循环灌注开始时间(AT)、达峰时间(APT)较同一切面内的非梗塞区域明显延长（P<0.05）,梗塞区域造影剂灌注的峰值强度(PI)及灌注速度(β)均明显低于同一切面内的非梗塞区域（P<0.05）。结论：超声心肌造影技术可以定量评价心梗患者心肌微循环灌注,具有重要的临床应用价值。     

“肾阳虚证”下心肌梗死模型与单纯心肌梗死模型大鼠心肌形态学、心肌酶学及血液流变学的比较

目的：建立大鼠“肾阳虚证”下心肌梗死模型,探讨其与单纯心肌梗死模型大鼠在心肌形态学、心肌酶学及血液流变学方面的差异,为评价治疗胸痹心痛中药的药效学提供理论依据。方法：60只Wistar大鼠随机分为空白对照组、肾阳虚模型组、心肌梗死假手术组、单纯心肌梗死模型组及“肾阳虚证”下心肌梗死模型组,每组12只。在大鼠 “肾阳虚”情况下复制急性心肌梗死模型,测定各组大鼠心肌梗死面积 (MIS),血清天门冬氨酸氨基转化酶（AST）、肌酸磷酸激酶（CK）及乳酸脱氢酶（LDH）活性,同时测定血小板黏附率（PAR）、血小板聚集率（PAG）、红细胞沉降率（ESR）、红细胞压积（HCT）、体外血栓长度、血栓干重与湿重以及血栓弹力图等参数。结果： 大鼠“肾阳虚证”下心肌梗死模型与单纯心肌梗死模型在MIS,血清AST、CK及LDH活性,PAR、PAG、ESR及HCT增加程度差异无统计学意义（P>0.05）;肾阳虚模型组、单纯心肌梗死模型组及“肾阳虚证”下心肌梗死模型组大鼠体外血栓干重及长度均明显增加（P<0.05或P<0.01）,“肾阳虚证”下心肌梗死模型组的增加程度大于单纯心肌梗死模型组及肾阳虚模型组,但三者之间差异无统计学意义（P>0.05）;尽管“肾阳虚证”下心肌梗死模型组大鼠血栓弹力图r、k值的缩短程度及ma值的增大程度高于单纯心肌梗死模型组,但2组之间差异无统计学意义（P>0.05）。结论：大鼠“肾阳虚证”下心肌梗死模型与单纯心肌梗死模型心肌梗死面积、血清心肌酶学、红细胞压积、血沉、血小板功能、体外血栓重量及血栓弹力图等指标均无明显差异。     

Relation of myocardial bridge to myocardial infarction: a meta-analysis

Background Small case series have suggested an association of coronary myocardial bridge （MB） with myocardial infarction （MI）.However,the relationship between MB and major adverse cardiac events （MACE） remains largely unknown.The aim of this study was to assess the relationship between MB and MACE involving MI.Methods We performed a systematic search of MEDLINE,PreMEDLINE,and all EMB Reviews as well as a reference list of relevant articles according to the SPICO （Study design,Patient,Intervention,Control-intervention,and Outcome） criteria using the following keywords：myocardial bridging,myocardial bridge,intramural coronary artery,mural coronary artery,tunneled coronary artery,coronary artery overbridging,etc.Bibliographies of the retrieved publications were additionally hand searched.Studies were included for the meta-analysis if they satisfied the following criteria：（1） they evaluate the association of MB with cardiovascular endpoint event; （2） they included individuals with MB and those without MB; 3） they excluded individuals with obstructive coronary artery disease （CAD）.Studies were reviewed by a predetermined protocol including quality assessment.Dates were pooled using a random effect model.Results Seven observational studies that followed 5 486 patients eligible for the enrolled criteria were included from 7 136 initially identified articles.The prevalence of MB was 24.8％ （1 363/5 486）.During 0.5-7.0 years of follow-up of this cohort of population,crude outcome rates were 8.0％ in the MB group and 7.7％ in the non-MB group.The odds ratio of overall MACE and MI were 1.34 （95％ confidence interval （CI）：0.57-3.17,P=0.51,n=7 studies） and 2.75 （95％ CI：1.08-7.02,P ＜0.03,n=5 studies） respectively for subjects of MB compared to non-MB.Conclusion Relationship between MB and MI appears to be a real one,although the study did not reveal a connection of MB to MACE,suggesting whether the necessity of antiplatelet therapy needs to be further studied in a larger cohort of patients with MB prospectively.     

Factors affecting thrombolysis in myocardial infarction myocardial perfusion frame count: insights of myocardial tissue-level reperfusion from a novel index for assessing myocardial perfusion

Background  Myocardial tissue-level perfusion failure is associated with adverse outcomes following ST-elevation myocardial infarction (STEMI) despite successful epicardial recanalization. We have developed a new quantitative index—thrombolysis in myocardial infarction (TIMI) myocardial perfusion frame count (TMPFC)—for assessing myocardial tissue level perfusion. However, factors affecting this novel index of myocardial perfusion are currently unknown.

Methods  A total of 255 consecutive STEMI patients undergoing primary angioplasty were enrolled. Myocardial tissue level perfusion was assessed by TMPFC, which measures the filling and clearance of contrast in the myocardium using cine-angiographic frame counting. We differentiate three groups with two cut off values for TMPFC: a TMPFC of 90 frames was the upper boundary of the 95% confidence interval (CI) for the TMPFC observed in normal arteries, and a TMPFC of 130 was the 75th percentile of TMPFC.

Results  STEMI patients with TMPFC >130 frames (68 patients, 26.7%) had higher clinical and angiographic risk factor profiles as well as a higher 30-day MACE rate compared with those with TMPFC ≤90 frames and those with TMPFC >90 and ≤130 frames. Multivariable analysis identified that the independent predictors of TMPFC >130 frames were age ≥75 years (OR 2.08, 95% CI 1.21 to 3.58, P=0.007), diabetes (OR 1.37, 95% CI 1.01 to 1.86, P=0.042), Killip class ≥2 (OR 1.52, 95% CI 1.05 to 2.21, P=0.027), and prolonged pain-to-balloon time (OR 1.73, 95% CI 1.07 to 2.79, P=0.013). TMPFC >130 frames was identified as the strongest independent predictor of 30-day major adverse cardiac event (MACE) (OR 2.77, 95% CI 1.21 to 6.31, P=0.008), along with age ≥75 years (OR 2.19, 95% CI 1.11 to 4.33, P=0.016), female gender (OR 1.67, 95% CI 1.03 to 2.70, P=0.038), and Killip class ≥2 (OR 1.83, 95% CI 1.07 to 3.14, P=0.021).

Conclusions  STEMI patients with poor myocardial perfusion assessed by TMPFC had higher risk factor profiles. Advanced age, diabetes, higher Killip class, and longer ischemia time were independent predictors of impaired TMPFC after primary percutaneous coronary intervention. These results emphasize that particular attention should be paid on myocardial microvascular reperfusion in STEMI patients with these risk factors.