用结扎法建立小型猪心肌缺血再灌注损伤模型

目的用结扎法建立小型猪心肌缺血再灌注损伤模型,为研究干细胞移植对小型猪心肌缺血再灌注损伤后的治疗作用提供基础。方法选用中国小型猪25头,结扎冠状动脉左前降支中远1/3处,90 min后松开。在结扎前后及松开时分别进行冠状动脉造影和描记心电图,4周后处死, 进行心肌TTC染色、HE染色和PTAH染色。结果造模成功率为92％(23/25),结扎法阻断冠状动脉血流及重新开放血流血管再通的成功率均为100％。模型猪心肌经病理显微镜检查有坏死心肌。结论结扎法阻断冠状动脉血流及血管再通的成功率均为100％,此法是建立小型猪心肌缺血再灌注损伤模型的较好方法。     

小型猪急性心肌梗死经皮冠状动脉再通后无复流模型的建立

目的复制小型猪急性心肌梗死冠状动脉再通(AMI-PCI)后无复流(no-reflow)现象,提供更为接近人类心血管组织生物学特性的动物模型。方法小型猪20头,雌雄不限,行左、右冠状动脉造影和左心室造影,并记录有创血流动力学参数,通过球囊闭塞、微血栓注入造成左前降支(LAD)无复流。监测心电图变化。结果(1)制模共有16头小型猪成活,其中14头达到AMI-PCI后无复流动物模型标准[TIMI血流≤2级,校正的TIMI血流记帧法(CTFC)≥36.2帧],制模成功率为70%。(2)小型猪在无复流模型建立成功后较闭塞前心率增快、血压下降、心肌耗氧量(PRI)增加、左心室舒张期末压(LVEDP)升高、肺毛细血管楔压(PCWP)升高,较闭塞前差异均具有统计学意义(P<0.05)。(3)在整个实验中,体表心电图和冠状动脉内心电图的演变均出现类似人类急性心肌梗死缺血再灌注的心电图演变规律。结论通过选择性冠状动脉前降支急性闭塞、再灌注、微血栓注入制备的无复流小型猪模型是无复流研究中一种较理想的实验动物模型。     

重组腺相关病毒介导CD151转染心肌梗死小型猪促进心肌功能性血管形成

目的 观察重组腺相关病毒(rAAV)介导的CD151基因转染促小型猪心肌梗死后心肌血管形成的有效性.方法 结扎小型猪冠状动脉左前降支建立心肌梗死模型,梗死区及梗死周围心肌分别注射rAAV-CD151、rAAV-anti-CD151和rAAV-绿色荧光蛋白(rAAV-GVP).8周后用Western blot分析心肌组织CD151蛋白表达,免疫组化检测心肌微血管密度和小动脉密度,用13N-NH3电子发射计算机断层心脏显影(PET)评价心肌血流灌注.结果 CD151基因转染促进心肌组织局部CD151高表达.rAAV-CD151组心肌微血管密度为(83.8±6.7)个/mm2,明显高于正常对照组的(33.2±4.5)个/mm2和rAAV-GFP组的(41.6±5.6)个/mm2,均P＜0.05;rAAV-CD151组小动脉密度为(16.4±2.5)个/mm2,也明显高于正常对照组的(6.6±2.3)个/mm2和rAAV-GFP组(8.4±1.6)个/mm2,均P＜0.05.rAAV-anti-CD151组心肌微血管密度和小动脉密度明显低于其他各组.13N-NH3 PET心肌血流灌注显像示rAAV-CD151组缺血区心肌血流灌注明显增加,rAAV-anti-CD151组血流灌注减少.结论 CD151基因转染能增加小型猪局部心肌组织的CD151表达,明显增加缺血心肌微血管和小动脉的生成,并显著增加心肌血流灌注.     

壁冠状动脉心肌桥的造影和临床分析

目的:观察、分析壁冠状动脉(冠脉)和心肌桥的临床特点与诊断、治疗方法。方法:观察、分析经冠脉造影确诊的96例109处心肌桥患者的心肌桥分布特点、临床症状、心电图、心肌酶谱、肌钙蛋白T、心脏超声,评价药物或支架治疗心肌桥的疗效。结果:心电图、临床症状、心肌酶谱、肌钙蛋白T和心脏超声对心肌桥的诊断均无特异性。造影发现93.7%的心肌桥发生于冠脉前降支(LAD)。心肌桥患者临床症状与收缩期狭窄程度有关。药物治疗、手术治疗均有一定疗效。结论:冠脉造影发现"收缩期狭窄"为目前确诊心肌桥的主要方法。心肌桥与心绞痛、动脉粥样硬化、心肌梗死的发生有密切关系。药物治疗可选用肾上腺素β受体阻滞剂和Ca2+拮抗剂。     

13N-NH3、18F-FDG PET显像在对心肌存活状况评估中的临床应用

目的探讨^13N-氨水(^13N-NH3)、^18F-脱氧葡萄糖(^18F-FDG)正电子断层显像(PET)心肌血流／代谢显像在陈旧性心肌梗死患者心肌存活状况评估中的临床应用价值。方法陈旧性心肌梗死患者20例，均采用^13N-NH3、^18F-FDG PET心肌灌注／代谢显像预测存活心肌。灌注缺损、代谢填充(血流-代谢不匹配)为心肌存活；灌注、代谢均缺损(血流-代谢匹配)为心肌无存活；同时进行超声心动图检查评价左室壁运动。PTCA 支架术后3—6个月，进行超声心动图检查随访评价左室壁运动的改善情况，其中12例患者在术后进行了^13N-NH3、^18F-FDG PET显像随访。结果PET显像判定为存活的心肌，介入治疗后87．5％的心肌节段运动功能得到改善；而判定为无存活的心肌节段介入治疗后，仅有2．4％的心肌节段运动功能得到改善。12例中，术后^13N-NH3、^18F-FDG PET、结果证实，存活心肌介入治疗后85．7％的心肌节段血流灌注及代谢恢复正常，而治疗前判定为无存活的心肌节段仅有3．3％的心肌节段血流灌注及代谢恢复正常。结论^13N-NH3、^18F-FDG PET显像对于心肌存活的估价及预测和(或)评价冠状动脉血管重建的疗效具有重要的临床应用价值。     

综合影像学评价猪急性心肌梗死模型的实验研究

目的:应用开胸结扎冠状动脉前降支法,探索构建中国小型猪急性心肌梗死(AMI)模型的可行性及有效性。方法:选取中国小型猪52只,应用开胸法结扎冠状动脉左前降支第二对角支开口远端,构建AMI模型。分别于造模前、造模后3 d、28 d,行超声心动图检查。造模后28 d行单电子发射型计算机断层显像(SPECT)检查、正电子发射型计算机断层显像(PET)检查,并行病理检查,评价模型的稳定性、有效性和可靠性。结果:共39只猪成功造模。造模后28 d,左室射血分数(LVEF)明显减低,左室舒张末径(LVEDD)及左室收缩末径(LVESD)明显增大(P<0.05)。SPECT提示静息及药物负荷状态下,心肌灌注缺损面积分别占左心室面积的(31.3±2.5)%和(39.3±3.8)%。PET提示心肌灌注缺损主要集中在左室局限前壁、心尖部和室间隔。结论:应用开胸结扎冠状动脉法建立的AMI模型,效果确切可靠,可为相关研究提供可靠的动物模型。     

心肌肌球蛋白结合蛋白C在急性心肌梗死、心肌缺血再灌注损伤模型猪中的表达及意义

目的 分析心肌肌球蛋白结合蛋白C(cMyBP-C)在急性心肌梗死(AMI)、心肌缺血再灌注损伤模型猪中的表达及意义。方法 本实验时间为2020年6—12月。将9头试验用滇南小耳猪随机分为假手术组(开胸后打开心包,不结扎冠状动脉,n=1)、AMI组〔开胸后打开心包,结扎左前降支(LAD)中远段血管,n=4〕、心肌缺血再灌注损伤组(开胸后打开心包,结扎LAD中远段血管3 h后再开放,n=4)。观察各组滇南小耳猪手术前后心率及心电图表现、术后心脏组织病理切片,检测假手术组、AMI组术前及术后0.5、1.0、2.0、3.0、4.0、6.0、8.0、10.0、12.0、18.0、24.0 h心肌肌钙蛋白Ⅰ(cTnⅠ)、cMyBP-C水平,心肌缺血再灌注损伤组术前及术后0.5、1.0、2.0、3.0、3.5、4.5、5.5、6.5、7.5、9.5、11.5、13.5、15.5、21.5、27.5 h cTnⅠ、cMyBP-C水平。结果 假手术组无死亡发生;AMI组有1头滇南小耳猪死亡;心肌缺血再灌注损伤组有2头滇南小耳猪死亡。假手术组滇南小耳猪术前心率正常,节律规整,无ST段抬高,术后心率较术前增...     

冠状动脉心肌桥临床意义及诊断分析

目的探讨冠状动脉心肌桥的临床意义及诊疗策略。方法回顾16例心肌桥病人的临床和冠状动脉造影资料,分析心肌桥与冠状动脉粥样硬化、心肌缺血的关系。结果心肌桥在冠脉造影中的检出率为2.85%;其中位于左前降支（LAD）15例,左回旋支（LCX）1例,合并冠状动脉粥样硬化症3例。16例病人中,心电图ST-T改变11例,有4例心肌核素显像提示有前壁心肌缺血,有1例患者为陈旧前壁心肌梗塞,心肌桥于收缩期致100%血流阻断。结论冠脉造影是冠状动脉心肌桥的特异性诊断方式。心肌桥绝大部分位于左前降支,心肌桥所致的冠状动脉狭窄,可致心肌缺血,引起心绞痛、心肌梗死甚至猝死。     

非开胸法建立室壁瘤动物模型的实验研究

目的　探讨运用PTCA球囊封堵猪冠状动脉建立急性心肌梗死后室壁瘤的动物模型的实验方法。方法　选用家猪 7只 ,麻醉后经颈总动脉或股动脉置入PTCA球囊至左前降支 (LAD)第一对角支远端 ,对堵血流 15 0分钟。观察 :心电图、心肌酶、心脏二维超声检查及冠状动脉和左心室造影。结果　 7只猪均完成LAD的封堵 ,2只分别在堵闭 12 0分钟和 2 0分钟后因心室纤颤死亡。存活的 5只猪成功建立左室前壁急性心肌梗死模型 ,术后 6周造影复查示左室前壁、心尖部室壁瘤形成 ,4只猪堵闭的LAD远端闭塞。心电图显示急性心肌梗死的典型图形和动态演变过程。cTnI明显升高并呈动态演变。术后 1小时超声检查出现间隔上部及前壁局部运动异常 ,术后 2周即有室壁瘤形成。结论　运用PTCA球囊封堵冠状动脉可成功建立急性心肌梗死后室壁瘤的动物模型 ,与开胸法相比更接近人体的状态 ,具有创伤小、动物成活率高、生存时间长、技术要求不高等优点 ,可为进一步的研究提供较好的实验模型。     

经皮球囊扩张封堵冠状动脉前降支制备巴马香猪急性心肌梗死模型

目的 探讨经皮球囊扩张封堵冠状动脉前降支(LAD)制备巴马香猪急性心肌梗死(AMI)模型的方法及可行性.方法 经右股动脉置入冠状动脉球囊导管至左前降支;预适应3～4次,每次球囊充盈30 s,间隔5～10 min;以3～5 atm扩张球囊封闭LAD远端血流,40 min后撤除球囊.结果 8头巴马香猪中有6头存活,造模成功率为75%.模型梗死面积变异系数为11.7%(33.2±3.9).封堵后心电图呈动态变化,心肌酶学指标(CK、CK-MB、cTnI、Myo、LDH)较术前明显升高,心脏彩超左心室舒张末内径、左心室舒张末容积及左心室收缩末容积均增大,LVEF均下降,部分实验猪出现心室壁瘤,TTC染色、HE染色证实心肌梗死模型建立成功.结论 经皮球囊扩张封堵法制备巴马香猪急性心肌梗死模型成功率高,保持了梗死区冠脉可重复进行造影,为干细胞植入梗死区心肌治疗AMI提供了较好的动物模型.     

大鼠急性心肌梗死模型的建立

目的建立大鼠急性心肌梗死实验模型。方法采用戊巴比妥钠腹腔注射麻醉、直视下经口腔气管插管、开胸行冠脉左前降支结扎法,术后给予呼吸道管理;并进行心电图、心肌酶谱、病理组织学和坏死心肌组织学定量检查来证实。结果 40只模型组大鼠中,死亡6只,模型制备成功率85%。大鼠术后30 min,心电图肢体导联ST段弓背向上抬高,出现病理性Q波;结扎前降支血管后24 h和40 h时间点,模型组肌酸激酶同工酶、血清乳酸脱氢酶、乳酸脱氢酶同工酶较假手术组明显高,差异有统计学意义(P0.05),在60 h时间点血清乳酸脱氢酶、乳酸脱氢酶同工酶亦升高(P0.05);组织切片镜下观察病变区心肌细胞排列紊乱、疏松,细胞核固缩、碎裂;模型组心肌梗死与左心室湿重比值较假手术组明显高,差异有统计学意义(P0.01)。结论该心肌梗死动物模型构建方法简单,创伤轻,成功率高,结果可靠。     

Creatine kinase kinetics and myocardial infarction in different regions of the left ventricle

The interval from the onset of infarction pain to culmination of plasma creatine kinase activity (t-peak) was measured in 68 patients with their first myocardial infarction. There is a major difference in this parameter in patients with infarction in the area of the right coronary artery and that supplied by the left anterior descending coronary artery (LAD). While, in 29 patients with infarction in the right coronary artery area, t-peak was 17.7 +/- 4.7 hours, in 39 subjects with infarction in area supplied by the LAD, t-peak was 13.2 +/- 4.6 hours (p less than 0.001). The type of thrombolytic treatment (intravenous or intracoronary, used no difference, just as the time from onset of pain to start of therapy, infarct size and presence or absence of collaterals. A detailed analysis of creatine kinase culmination in relation to the type of artery recanalization is given. The authors conclude that, besides the known factors, creatine kinase culmination is influenced also by the necrosis site, a fact somewhat modifying the informative value of this parameter. However, explanations of this phenomenon are only hypothetical at the present time.     

Complement and neutrophil activation in the pathogenesis of ischemic myocardial injury

Complement depletion with cobra venom factor (CVF) before coronary artery ligation has been previously shown to reduce subsequent ischemic myocardial tissue injury in the baboon; however, whether complement depletion after the initiation of acute myocardial ischemia affords similar myocardial preservation is not known. Both complement depletion with CVF or the administration of certain nonsteroidal anti-inflammatory drugs, including ibuprofen, are thought to decrease myocardial infarct size by reducing polymorphonuclear leukocytic (PMN) infiltration; nevertheless, complement activation also could alter tissue injury by PMN-independent actions. Thus, the relative effects of CVF administered after coronary artery ligation on the subsequent development of myocardial tissue injury were assessed in a baboon myocardial infarction model. The animals were randomized into three treatment groups (n = 6): either CVF (125 units/kg) or saline was given 30 minutes after coronary artery ligation, and ibuprofen (12.5 mg/kg) was administered 30 minutes and 4 hours after ligation. The extent of ischemic myocardial injury was assessed 24 hours later. Relative to saline-treated baboons, both CVF and ibuprofen reduced PMN infiltration (36 +/- 4 vs. 24 +/- 4 and 24 +/- 4 PMN/mm2, respectively; mean +/- SEM) and histological evidence of transmural myocardial infarction (100% vs. 47% and 53%, respectively) in electrocardiographically designated, expected infarct sites. In both saline- and ibuprofen-treated animals, there was extensive localization of C4, C3, and C5 in all infarct sites; in contrast, there was only C4 localization in the CVF-treated baboons. When expected infarct sites were assessed for creatine kinase content as an indicator of tissue injury, there was significantly less epicardial and endocardial creatine kinase depletion in the CVF-treated animals (31.7 +/- 5.6% and 39.3 +/- 4.8%) than in the saline-treated animals (54.1 +/- 5.4% and 59.0 +/- 4.7%; p = 0.012 and 0.011, respectively). The percent creatine kinase depletion in the ibuprofen-treated animals was intermediate between the two other groups. These results suggest that depletion of complement after coronary ligation has beneficial effects in reducing tissue injury that cannot be explained solely on the basis of reducing PMN infiltration into the ischemic myocardium.     

The efficacy of intermittent coronary sinus occlusion in the absence of coronary artery collaterals

The purpose of this study was to evaluate the efficacy of time-controlled intermittent coronary sinus occlusion (ICSO) in preserving regional and global mechanical function during acute ischemia in an animal preparation without significant arterial collateral vessels. Seventeen (eight control, nine ICSO) swine heart preparations undergoing extracorporeal coronary perfusion in situ were subjected to ligation of the left anterior descending coronary artery (LAD) distal to the first major diagonal branch. Data were obtained before and immediately after coronary artery ligation in both animal groups. ICSO, 15 sec of occlusion alternating with 5 sec of release, was then begun in the treatment group. Additional data were obtained in both control and treatment groups at 15 min intervals for 1 hr starting immediately after coronary artery ligation. Global left ventricular function was assessed by shifts in left ventricular end-diastolic pressure and left ventricular dP/dt with left ventricular systolic pressure maintained at about 100 mm Hg. Regional mechanical function was evaluated with transmurally placed ultrasonic crystals. Pressure was also measured directly in the coronary sinus and LAD distal to the ligature. Regional myocardial blood flow was measured in the ischemic bed using 9 micron diameter radiolabeled microspheres injected before, immediately after, and 60 min after coronary artery ligation in both treated and control animals. LAD mean pressure measured distal to the ligation (less than 16 mm Hg) and ischemic bed myocardial blood flow (less than 0.01 ml/g/min) confirmed the absence of significant arterial-arterial collaterals in this preparation. Mean coronary sinus pressure increased significantly (p less than .001) in treated animals during ICSO (e.g., 11.2 +/- 1.6 to 66.2 +/- 10.0 mm Hg at 15 min after coronary ligation). Mean LAD pressure distal to the coronary ligature also increased during ICSO (14.2 +/- 1.2 to 26.8 +/- 1.6 mm Hg), with a similar but delayed rate of pressure rise. No significant differences in left ventricular end-diastolic pressure or left ventricular dP/dt were noted between control or treated animals after coronary ligation. Ischemic bed systolic wall thickening, present before coronary ligation, was not present after occlusion and was not improved during intermittent coronary sinus occlusion in the treatment group. We conclude that in an animal preparation without significant collateral circulation, intermittent coronary sinus occlusion is incapable of restoring regional or global left ventricular mechanical function during conditions of acute ischemia.     

The effects of propranolol on myocardial perfusion and metabolism during acute regional ischaemia

The unique physical properties of the short-lived inert and freely diffusing isotope ^81mkrypton allow a continuous observation to be made of regional myocardial perfusion. Eighteen dogs were anaesthetised and a reversible snare placed on the left anterior descending coronary artery (LAD). ^81mKrypton was used to study regional myocardial perfusion, and myocardial metabolism was assessed using the epicardial ECG and release of creatine kinase activity (CK). Six dogs did not undergo LAD occlusion (“sham operated”); in six other dogs the LAD was occluded (controls), and another six dogs were given propranolol, 0.5 mg/kg, 20 min after LAD occlusion. All the parameters were measured before and for 5 h after LAD occlusion. When compared to controls, dogs treated with propranolol showed significant improvement (p<0.01) in regional myocardial perfusion; smaller loss of electrically active myocardium for any given degree of early ST-segment elevation; and a delay in the release of CK activity from a local coronary vein. These results suggest that propranolol exerts a beneficial effect following the development of acute myocardial infarction.     

Effect of coronary occlusion site on angiographic and clinical outcome in acute myocardial infarction patients treated with early coronary intervention

In acute myocardial infarction that is treated with thrombolysis, proximal coronary artery occlusion is associated with worse prognosis, irrespective of the infarcted artery. Primary percutaneous coronary intervention (PCI) is currently the treatment of choice for ST-segment elevation acute myocardial infarction. Therefore, we evaluated the prognostic significance of proximal versus distal coronary artery occlusion in patients with acute myocardial infarction that was treated with primary PCI. Between 1994 and 2001, patients with a first acute myocardial infarction that was treated with primary PCI were analyzed. A lesion was considered proximal if it was located proximal to the first diagonal branch in the left anterior descending coronary artery (LAD), the first marginal obtuse branch in the left circumflex coronary artery, and the first right acute marginal branch in the right coronary artery. Lesions distal of these side branches were considered distal. In total, 1,468 patients were analyzed. Left ventricular ejection fraction (LVEF) for proximal LAD lesions was lower than that for distal ones (37 +/- 11% vs 42 +/- 11%, p <0.0001). Adjusted relative risk of 3-year mortality for proximal versus distal LAD was 4.04 (95% confidence interval 1.95 to 8.38). In patients with infarcts related to the right or left circumflex coronary artery, no significant association between lesion location and LVEF or mortality was seen. No difference was seen in adjusted 3-year mortality between distal LAD and non-LAD-related infarcts (p = 0.145). In conclusion, our analysis shows that, even in patients with acute myocardial infarction that is treated with primary PCI, infarcts related to the proximal LAD have the worst 3-year survival and lowest residual LVEF compared with distal LAD or non-LAD-related infarcts.     

The influence of combined intra-aortic balloon counterpulsation and hyperosomotic mannitol on regional myocardial blood flow in ischemic myocardium in the dog.

We investigated the combined effectiveness of intra-aortic balloon counterpulsation and hyperosmotic mannitol (25%) on regional myocardial blood flow during acute coronary insufficiency. Cardiac output and paced heart rate were held constant in chloralose-anesthetized dogs during right heart bypass. Acute coronary insufficiency was produced by ligation of the proximal left anterior descending coronary artery (LAD). Regional myocardial blood flow was measured using radioactive microspheres. Left ventricular end-diastolic pressure, mean aortic pressure, maximum left ventricular dp/dt, and hematocrit were unchanged by combined mannitol infusion and balloon pumping. Studies of combined treatment with balloon pumping and mannitol immediately after the second of two 13-minute consecutive reversible ligations of the LAD demonstrated that (1) collateral coronary blood flow increased 46% (P less than 0.02) in ischemic myocardium compared with mannitol infusion along during the first LAD ligation, and (2) collateral coronary blood flow increased 27% (P less than 0.05) in ischemic myocardium compared with balloon pumping along during the first LAD ligation. Studies in which combined treatment was delayed until 20 minutes after LAD ligation demonstrated that collateral coronary blood flow was elevated by 33% (P les than 0.05) in ischemic myocardium compared to control studies in which balloon pumping alone had no effect. The results suggest that the increase in collateral coronary blood flow was in part a result of an increased transmural pressure gradient produced by balloon diastolic augmentation and the ability of mannitol to reduce coronary vascular resistance in ischemic myocardium.     

Spontandissektion der Koronararterien: Eine seltene kardiologische Diagnose

A 55-year-old woman who was admitted to hospital with acute chest pain as a case of emergency suffered from an acute anteroseptal myocardial infarction. Four weeks later coronary angiography revealed a long dissection of the left anterior descending artery (LAD) as well as a significant stenosis of the left main and the proximal circumflex. Cardiovascular surgery was done subsequently. In addition to myocardial revascularization using coronary artery bypass grafts a readaptation of the dissecting artery walls and a proximal ligation of the LAD before anastomosis were performed. Clinical data, pathogenesis, and indications for medical and surgical treatment of spontaneous artery dissection are presented.     

Effect of carotid sinus nerve stimulation on coronary blood flow in myocardial ischaemia: Role of the collateral vessels

The carotid sinus nerves of dogs were electrically stimulated to reveal reflex effects exerted on the coronary blood flow both in normal and ischaemic states. Myocardia ischaemia was produced by occlusion of the left anterior descending (LAD) coronary artery. In 10 experiments the coronary sinus outflow was measured as an index of the overall coronary flow; in 30 cases the local myocardial blood flow was registered by means of the heat clearance technique. In the overall coronary flow carotid sinus nerve stimulation (CSNS) elicited coronary dilatation. After acute LAD occlusion this effect was slightly potentiated. A similar but significantly greater potentiation was observed in the local reflex vascular dilatation recorded with the aid of the thermal probes immediately after LAD occlusion when the myocardial area explored was supplied exclusively by collateral channels. 24-48 hours and 5-64 days after the coronary ligation the effect of the CSNS on the local blood flow was tested in the developing and the regenerative phases of the myocardial infarction. In both phases an enhanced reflex dilatation was found in the collateral-dependent ischaemic areas as compared to the myocardial areas supplied by the normal vessels. The results suggest that reflexly induced intrinsic redistribution of the myocardial blood flow is one of the mechanisms responsible for the therapeutical effects of the CSNS.     

Coronary occlusion: Cause or consequence of acute myocardial infarction?

A 45-year-old man with unstable angina developed persistent ECG changes of myocardial ischemia during coronary angiography. Occlusion of the left anterior descending branch (LAD) was documented 20 minutes after these changes. Intracoronary nitrate, Ca antagonist, urokinase, removal by percutaneous transluminal coronary angioplasty (PTCA) of atherosclerotic obstructions, and emergency bypass surgery failed to restore myocardial perfusion. Only short periods of reflow were obtained by urokinase and PTCA. The repeated coronary injections demonstrated a progressive disappearance of the left anterior descending artery (LAD) starting from the distal portion and progressing retrogradely up to the origin of the vessel. The patient developed a transmural anterolateral myocardial infarction and 12 months later underwent cardiac transplantation for untractable failure. His heart was examined and the infarct confirmed. Analysis of this case suggests that coronary occlusion in acute myocardial infarction can be an event secondary to increased intramyocardial resistance rather than the cause of reduced coronary blood flow in subepicardial coronary arteries.