促红细胞生成素对急性心肌梗死家兔心室重构的影响

目的：探讨促红细胞生成素（EPO）对急性心肌梗死（AMI）家兔心室重构的影响。方法：开胸冠状动脉结扎法制备家兔AMI模型,随机分为假手术组、AMI对照组和EPO组,每组各10只。腹腔注射EPO5000U/kg,3次/周,24h后采血测心肌酶,4周后处死动物,获取心肌组织测定心室重量、心肌胶原含量及组织标本固定做病理分析。结果：与AMI组相比,EPO组的心肌酶水平、左心室重量（LVW）和右心室重量（RVW）、心肌胶原含量显著降低（P〈0.05）,心肌特殊染色可见左心室非梗死区AMI组变性的心肌细胞周围、血管周围胶原成分增生明显,而在EPO组胶原沉积比AMI对照组明显减轻。结论：EPO对AMI家兔有明显的心脏保护作用,抑制心室重构。     

卡维地洛对家兔急性心肌梗死左室重构的作用

目的评价第三代β-受体阻滞剂卡维地洛对家兔急性心肌梗塞(AMI)后的左室重构的防治作用,以及对梗死区损伤心肌细胞的修复.方法采用家兔制备心肌梗死模型,20只AMI术后成活的雄性家兔随机分为AMI对照组、卡维地洛(CVD)组,另设假手术组.灌胃给药4周后处死动物.用电子精确天平称量左室、右室的重量,用羟脯氨酸方法测定心肌组织的胶原的含量及采集标本进行病理分析.结果梗死后左心室、右心室重量均比假手术组增加,差异显著.梗死区胶原含量显著增加,非梗死区胶原含量增加明显.经卡维地洛治疗后,左心室、右心室重量均下降,但未能恢复至正常水平.梗死区胶原含量亦略有下降,但差异不显著.非梗死区胶原含量下降明显,差异显著.病理分析结果显示卡维地洛组心肌细胞损伤程度减轻.结论卡维地洛能有效防治家兔AMI后的左室重构及减轻心肌细胞损伤程度.     

螺内酯对心肌梗死大鼠心室重塑保护作用的研究

目的:观察醛固酮受体拮抗剂螺内酯对大鼠心肌梗死后心室重塑参数、非梗死区心肌醛固酮及胶原含量的影响,探讨螺内酯对心室重塑保护作用的机制。方法:24只术后存活的雌性Wistar急性心肌梗死(AMI)大鼠随机分为对照组、螺内酯组,另设假手术组。每组12只。螺内酯组给予螺内酯(40mg.kg-1.d-1),对照组及假手术组给予等量自来水。28 d后行病理分析,非梗死区醛固酮及胶原含量的测定。结果:对照组与假手术组相比,左心室截面直径、球形指数、左心室实际重量和左心室相对重量都显著增加(P<0.05,P<0.01),室间隔厚度差异不明显(P>0.05)。左心室非梗死区醛固酮、胶原容积密度分数(CVF)及Ⅰ、Ⅲ型胶原含量均显著增加(P<0.05,P<0.01),螺内酯组与对照组相比,各指标均显著下降(P均<0.05)。结论:AMI大鼠28 d后即发生了心室重塑;螺内酯能通过减少非梗死区醛固酮的含量及胶原的沉积而改善心室重塑。     

卡维地洛对兔心肌梗死后转化生长因子β1表达和心室重构的影响

目的探讨卡维地洛对兔心肌梗死后转化生长因子β1（TGF-β1）的表达和心室重构的影响。方法采用结扎冠状动脉左室支建立心肌梗死（MI）模型（假手术组开胸后在相应部位挂线不结扎）。术后24h将存活兔分为3组：假手术组、MI组、MI＋卡维地洛组。各组饲养4周后行血流动力学检查;测量体质量,左、右心室重量;采用苦味酸-酸性品红（VG）染色检测非梗死区的胶原容积分数（CVF）;采用免疫组化检测TGF-β1的表达情况。结果MI组与假手术组比较,左心室重量/体质量值（RVW/BW）、右心室重量/体质量（LVW/BW）、左室舒张末压（LV-EDP）、非梗死区CVF均显著升高（P〈0.05或P〈0.01）,TGF-β1的表达显著增强（P〈0.01）;MI＋卡维地洛组与MI组比较,RVW/BW、LVEDP、CVF均显著降低（P〈0.05或P〈0.01）,TGF-β1表达明显减弱（P〈0.05）。结论TGF-β1可能与心肌梗死后心室重构有关;卡维地洛能缓解心肌梗死后非梗死区的重构,其机制可能与减低TGF-β1的表达有关。     

安体舒通、培哚普利及其合用对大鼠心肌梗死后心室重构和心肌间质胶原的影响

目的 观察醛固酮受体拮抗剂-安体舒通、血管紧张素转换酶抑制剂-培哚普利对大鼠急性心肌梗死(AMI)后左心室重构和胶原增生的影响,探索醛固酮受体拮抗剂和血管紧张素转换酶抑制剂降低AMI后病死率的机制.方法 结扎大鼠左前降支建立急性心肌梗死模型,将48只雌性Sprague-Dawley(SD)AMI大鼠随机分为:AMI对照组(n=11)、安体舒通组(n=10,20mg/kg/d)、培哚普利组(n=10,10mg/kg/d)及其联合用药组(n=9,安体舒通20mg/kg/d 培哚普利10mg/kg/d),另设假手术组(n=8).术后4周进行血流动力学测定、病理分析和非梗死区Ⅰ、Ⅲ型胶原含量的测定.结果 AMI对照组与假手术组相比,左心室舒张末压(LvEDp)、容积、重量和非梗死区Ⅰ、Ⅲ型胶原含量均显著增加;左心室球形指数、左心室内压最大上升和下降速率(±dp/dt/LVSP)均显著降低.安体舒通组与AMI对照组相比,以上各指标多数无显著差异,仅左心室非梗死区Ⅰ、Ⅲ型胶原含量显著减少.培哚普利组和联合用药组与AMI组相比,LVEDP、左心室实际重量显著降低;左心室容积仅联合用药组有显著降低;而两组的 dp/dt/LVSP显著增加;联合用药组的-dp/dt/LVSP显著增加.安体舒通、培哚普利和联合用药3组与AMI组相比,左心室非梗死区Ⅰ型和Ⅲ型胶原含量显著减少;且3组之间对胶原沉积的防治作用无显著性差异.结论 单纯应用安体舒通能有效抑制AMI左心室非梗死区Ⅰ、Ⅲ型胶原的增生,提示安体舒通可能有改善左心室重构的潜在作用.培哚普利与安体舒通两药合用可更有效防治AMI后左心室重构,改善左心室舒张功能,其降低AMI后病死率和防治左心室重构的原因之一与减轻胶原沉积有关.     

辛伐他汀对大鼠急性心肌梗死后Ⅰ型胶原合成及TNF-α表达的影响

目的:观察辛伐他汀对大鼠急性心肌梗死(AMI)后肿瘤坏死因子(TNF)- a表达及Ⅰ型胶原合成的影 响。方法:Wistar大鼠随机分3组:辛伐他汀治疗组(AMI S组)、梗死对照组(AMI- C组)和假手术组(SH组)。前2 组大鼠结扎左冠状动脉前降支(LAD)制成AMI模型,AMI S组给辛伐他汀40mg/kg灌胃治疗,余2组给予生理盐 水灌胃。4周后,RT- PCR法检测左心室非梗死心肌TNF αmRNA表达,Westernblot法测定左心室非梗死区心肌 TNF -α蛋白表达,免疫组化法测定左心室非梗死区心肌I型胶原合成量。结果:AMI C和AMI S组大鼠4周后心脏 质量、左心室心肌I型胶原合成量、TNF -α蛋白及mRNA表达较SH组都明显升高(P<0.05),AMI S组心脏质量、I 型胶原合成量、TNF -α蛋白及mRNA表达均较AMI C组显著降低(P<0.05),但仍高于SH组(P<0.05)。结论:辛 伐他汀减少大鼠心肌梗死4周后I型胶原合成量,可能与其抑制心肌TNF -α表达有关。     

卡维地洛对兔心肌梗死后胞外基质重构及基质金属蛋白酶的影响

目的:探讨第三代β受体阻滞剂卡维地洛对兔心肌梗死(MI)后胞外基质重构的作用及机制. 方法:将36只新西兰大耳白兔随机分为MI组、MI 卡维地洛组、假手术组,每组12只. 采用结扎冠状动脉左室支建立MI模型,另以开胸后在相应部位挂线不结扎为假手术组. 4 wk后行血流动力学检查; 测量体质量(BW)、左、右心室质量(LVW,RVW); 苦味酸-酸性品红染色检测非梗死区的胶原容积分数(CVF); 免疫组化检测基质金属蛋白酶2(MMP-2)、基质金属蛋白酶9(MMP-9)的表达,酶谱法测定二者的活性. 结果: MI后4 wk存活动物为MI组8只,MI 卡维地洛组9只,假手术组10只. MI组RVW, LVW/BW, 左室舒张末压(LVEDP)、非梗死区CVF均显著升高,MMP-2, MMP-9的表达及其活性亦明显升高(P均＜0.01);MI 卡维地洛组与MI组比较,RVW/BW, LVEDP, CVF显著降低(P＜0.05～0.01). MMP-2, MMP-9表达及活性显著减弱(P＜0.05～0.01). 结论:卡维地洛缓解了MI后心肌细胞外基质的重构,其机制可能与对MMPs的表达和活性调节有关.     

辛伐他汀对大鼠心肌梗死后血清TNF-α水平及心室肌间质胶原的影响

目的观察辛伐他汀对心肌梗死后大鼠血流动力学及心室肌Ⅰ、Ⅲ型胶原含量变化和血清肿瘤坏死因子-α（TNF-α）水平的影响。方法通过结扎冠状动脉前降支诱导大鼠急性心肌梗死（AMI）模型,模型建立后24h存活的30只大鼠随机分为AMI组（A组）和辛伐他汀组（S组）,每组15只;另设假手术组（C组）（n=10）,手术方法同模型组,但不结扎冠状动脉。建模后24h灌胃给药,A组及C组予生理盐水灌胃,S组予辛伐他汀20mg·kg-1·d-1灌胃,至术后8周。术后8周测定血流动力学参数〔心率、左室收缩压（LVSP）、左室舒张末压（LVEDP）、左室内压上升与下降速率（±dp/dt）及校正的速率（±dp/dt/LVSP）〕和血清TNF-α水平（ELLSA法）;取心脏标本测定左室相对质量〔左室质量（LVW）/体质量（BW）〕;心肌梗死面积及非梗死区Ⅰ、Ⅲ型胶原含量。结果与A组比较,S组心肌梗死面积、左心室截面直径、面积和左心室容积差异均无统计学意义（P均〉0.05）;LVW、LVW/BW和LVEDP均显著降低（P〈0.01或P〈0.05）,±dp/dt/LVSP绝对值升高（P〈0.05或P〈0.01）。与A组相比,S组左心室非梗死区Ⅰ型和Ⅲ型胶原含量和血清TNF-α水平显著减少（P均〈0.05）。左心室非梗死区Ⅰ型、Ⅲ型胶原含量和血清TNF-α水平均呈显著正相关（r分别为0.56和0.71,P均〈0.01）。结论辛伐他汀能有效抑制AMI左心室非梗死区Ⅰ、Ⅲ型胶原的产生以及缓解大鼠AMI后心室重构、改善心功能,这种作用可能与抑制体内TNF-α的水平有关。     

普伐他汀与阿托伐他汀对大鼠心梗后胞外基质重构及基质金属蛋白酶的影响

目的探讨他汀类药物对大鼠心肌梗死(MI)后胞外基质重构的作用机制,以及普伐他汀与阿托伐他汀对基质金属蛋白酶-2(MMP-2)和心室重构的影响。方法将雄性大鼠50只随机分为MI组、MI 普伐他汀组、MI 阿托伐他汀组和伪手术组。结扎冠状动脉前降支建立心肌梗死(MI)模型,在相应部位挂线不结扎作为伪手术组。8周后血流动力学检查,测量体质量(BW)、左、右心室质量(LVW,RVW);苦味酸-酸性品红染色检测非梗死区的胶原容积分数(CVF),ELISA法检测血清基质金属蛋白酶2(MMP-2)水平。结果MI组RVW/BW,LVW/BW,左室舒张末压(LVEDP)、非梗死区CVF均显著升高,MMP-2的水平亦明显升高(P均<0.05);与MI组比较,MI 他汀组的RVW/BW,LVW/BW,LVEDP,CVF显著降低,血清MMP-2水平显著减弱(P均<0.05)。两用药组间上述指标差异均无显著性(P>0.05)。结论他汀类药物缓解了MI后心肌细胞外基质的重构,其机制可能与基质金属蛋白酶(MMPs)的表达和活性调节有关。而普伐他汀与阿托伐他汀两组药物在心肌重构中差异无显著性。     

缬沙坦与依那普利对心肌梗死后心肌胶原重构的影响

目的研究选择性血管紧张素Ⅱ受体1拮抗剂(AR1B)、血管紧张素转化酶抑制剂(ACEI)对心肌梗死(MI)后心肌胶原重构的影响。方法新西兰大白兔心梗后随机分组用Valsartan治疗(V组)、Enalapril治疗(E组)或不治疗(C组),并设假手术组(S组)。治疗10周后测量血流动力学参数、胶原含量。结果MI后10周C组梗死区和非梗死区胶原含量明显高于S组。V,E组中上述指标显著下降,但仍高于S组。非梗死区胶原含量与左室舒张末压呈明显正相关。结论①在家兔心梗后早期应用Valsartan,Enalapril能改善血流动力学、抑制心肌纤维化;②非梗死区胶原沉积是降低心功能的主要因素之一。非梗死区胶原含量与左室舒张末压有明显相关性。     

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     

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.     

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.     

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。     

“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.     

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。     

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.