Mural thrombus in an ectatic right coronary artery caused acute myocardial infarction at downstream coronary artery

A 72-year-old woman was admitted to our institution because of sudden chest pain. Emergency coronary angiography revealed thrombotic occlusion of the distal right coronary artery. A large cylindrical thrombus was retrieved from her distal right coronary artery using a thrombus aspiration catheter. IVUS showed minimal atherosclerosis and moderate ectatic change at the proximal right coronary artery. A reconstructed IVUS image also showed that a mural thrombus with abrupt ending was still retained at the ectatic segment. Based on this evidence, coronary ectasia was thought to be the primary cause for the thrombus formation and acute myocardial infarction in this case.     

High wall shear stress proximal to myocardial bridging and atherosclerosis: intracoronary ultrasound and pressure measurements.

BACKGROUND--Studies have shown that myocardial bridging may prevent coronary atherosclerosis and that the segment proximal to the bridge is often sclerosed. The underlying mechanism is still unknown. METHODS--Intracoronary ultrasound and pressure measurements were performed in a patient with myocardial bridging in the left anterior descending coronary artery. A 3.5 F, 20 MHz probe was used to measure the change in cross sectional area of the lumen during the cardiac cycle. Intracoronary pressure was measured with a Double tip, end mounted pressure transducer system, the catheter having two pressure sensors located at the end of the catheter 3 cm apart. Intracoronary pressure was recorded as the catheter was slowly advanced and pulled back through the left anterior descending coronary artery. RESULTS--Systolic compression of the bridge segment was clearly visualised on ultrasonography and an eccentric plaque with calcium deposit was found in the segment proximal to the bridge. The pressure in the segment proximal to the bridge (160/26 mm Hg) was higher than that of the proximal normal segment (126/68 mm Hg). The pressure distal to the bridge was 68/30 mm Hg. A highly characteristic "sucking effect" was found in the bridge segment. The pressure in the bridge segment was 102/-40 mm Hg. CONCLUSION--The pressure in the segment proximal to the myocardial bridging was higher than aortic pressure. Disturbance of blood flow and high wall stress proximal to myocardial bridging was a main contributor to the development of atherosclerosis in the segment proximal to the bridge.     

Acute myocardial infarction after a negative dobutamine stress echocardiogram.

Acute myocardial infarction is a rare complication of dobutamine stress echocardiography (DSE). We described angiographic findings of a patient who developed acute inferior ST segment elevation myocardial infarction 2h after a normal dobutamine stress echocardiogram. The patient failed thrombolysis and underwent coronary angiography, which showed 60% stenosis of proximal right coronary artery with a complex ulcerated lesion and intracoronary thrombus. These findings suggest that myocardial infarction following DSE does not necessarily occur in patients with severe obstructive coronary artery disease. High shear stress may result in destabilization of a complex plaque with subsequent thrombotic occlusion, despite the absence of a flow-limiting lesion at the time of DSE.     

A case of acute myocardial infarction due to coronary embolism from left atrial thrombus with atrial fibrillation

A 55-year-old man, who has been on follow-up observation with chronic atrial fibrillation, came in with a sudden onset of chest pain on July 31, 1986. He was diagnosed as having acute myocardial infarction indicated by abnormal ECG, elevated serum enzyme and characteristic signs of echocardiography. Emergency coronary angiography was performed 2 hours after the onset of chest pain, and it was reported as showing total obstruction of the distal left anterior descending artery. Percutaneous transluminal coronary recanalization using 1,200,000 units of urokinase was unsuccessful. The repeated angiography performed 40 days later, showed normal coronary arteriogram, but left ventriculogram revealed akinesis of the apical segment. Furthermore, left atrium opacified in the levophase of pulmonary arteriogram indicated left atrial thrombus. The cause of the myocardial infarction was considered to be coronary embolism from the left atrial thrombus with atrial fibrillation. It must be the first report documented by coronary angiography, of coronary thrombo-embolism due to chronic atrial fibrillation without any underlying disease.     

The combined use of stent retriever and neuro‐aspiration as successful bail‐out reperfusion strategy in a patient with embolic myocardial infarction

Embolic myocardial infarction account for ≈3% of all ST‐segment myocardial infarction and represents a challenge often left no‐reperfused because current thrombectomy technologies are inefficient to grab thrombus wedged into distal coronary arteries. We present the case of a 34‐year‐old man who presented with anterior STEMI and a proximal left anterior descending coronary artery ulcerated plaque with a great thrombus burden, which led to distal embolization. Failure of several attempts of manual and rheolytic thrombectomy, led us to use the “Solumbra technique”, the combined use of stent retriever and Penumbra catheter was successful in restoring patency and flow.     

Very late stent thrombosis caused by rupture of lipid-laden neointima in a self-expanding coronary stent

A 60-year-old man was admitted to our hospital due to acute ST-segment elevation myocardial infarction. He had a history of self-expanding stent implantation in the proximal left anterior descending artery due to stable angina pectoris 7 years earlier. Emergent coronary angiography on admission showed occlusion in the distal portion of the previously stented segment, in which observation by optical coherence tomography revealed the existence of a remarkable proliferation of lipid-laden neointimal tissues with rupture and thrombus. This suggests that very late stent thrombosis in a self-expanding stent may occur through the process of atheromatous formation.     

Exercise-induced plaque rupture producing myocardial infarction

A 37-year-old man with unstable angina was subjected to coronary angiography. The right coronary artery showed a minor proximal stenosis, but there were no obstructive lesions in the left coronary artery. He developed a small inferior infarction. He was asymptomatic until re-admission 1 month later, 1 hour after a normal exercise test, with anterior myocardial infarction. Acute coronary angiography showed sub-total occlusion of the left anterior descending artery. The occlusion was partially relieved after intracoronary injection of nitroglycerin. Intracoronary infusion of streptokinase had no further effect. Balloon angioplasty was then successfully performed. It is suggested that stress-induced plaque rupture with intimal hemorrhage and secondary spasm resulted in sub-total occlusion of the left anterior descending artery producing the second myocardial infarction.     

冠状动脉造影检出心肌桥的方法探讨

目的探讨提高心肌桥冠状动脉造影检出率的方法.方法研究对象为t999年9月至2000年12月复旦大学附属中山医院所有接受冠状动脉造影的731名病人.方法(1)左冠状动脉造影用右前斜位、右前斜+头位、右前斜+足位、左前斜+足位、左前斜+头位,必要时加用后前+头位.右冠状动脉造影用左前斜、右前斜位;(2)至少二位有经验者同时观察;(3)对LAD近段固定性狭窄者植入支架后再造影观察;(4)对可疑者冠状动脉内注射硝酸甘油后再造影.结果731例病人中检出心肌桥67例,检出率为9.17%,显著高于文献报道的冠状动脉造影对心肌桥的检出率.心肌桥均位于前降支.有16例病人(23.9%)在壁冠状动脉近段有固定性的狭窄,植入支架后复行造影显示了原先不明确的心肌桥.有28例可疑者(41.8%)冠状动脉内注射硝酸甘油200μg后明确显示心肌桥.结论冠状动脉造影中采用多个投照体位,有经验者观察,对LAD近段固定性狭窄病变植入支架后常规复行造影和对可疑者冠状动脉内注射硝酸甘油后再造影观察,可以增加对心肌桥的检出率.     

Acute coronary syndrome due to coronary thrombus formed by severe coronary spasm: a case report

A 47-year-old man was admitted to our hospital complaining of chest pain at rest in the early morning. Electrocardiography showed ST segment elevation in leads II, III and aVF. Emergency coronary angiography revealed total occlusion of the right coronary artery at the proximal portion. Intracoronary administration of isosorbide dinitrate successfully recanalized the right coronary artery. However, there was a thrombus image at the culprit lesion. Intracoronary administration of urokinase caused the residual thrombus to disappear completely. Follow-up coronary angiography at 1 week and 3 months revealed no organic stenotic lesion. Intravascular ultrasound showed only a little plaque without signs of ruptured plaque in the right coronary artery. Provocation coronary angiography revealed remarkable spasm causing total occlusion at the proximal portion of the right coronary artery. This case suggests that only severe coronary spasm without plaque rupture could form a thrombus causing acute coronary syndrome.     

Case of angina pectoris at rest and during effort due to coronary spasm and myocardial bridging

We present a case of a 71-year-old male who had chest symptoms at rest and during effort. He had felt chest oppression during effort for 1 year, and his chest symptoms had recently worsened. One month before admission he felt chest squeezing at rest in the early morning. He presented at our institution to evaluate his chest symptoms. Electrocardiography and echocardiography failed to show any specific changes. Because of the possibility that his chest symptoms were due to myocardial ischemia, he was admitted to our institution for coronary angiography (CAG). An initial CAG showed mild atherosclerotic changes in the proximal segment of the left anterior descending coronary artery (LAD) and mid-segment of the left circumflex coronary artery. Subsequent spasm provocation testing using acetylcholine revealed a bilateral coronary vasospasm, which was relieved after the intracoronary infusion of nitroglycerin. Finally, a CAG showed myocardial bridging (MB) of the mid-distal segments of the LAD. Fractional flow reserve using the intravenous administration of adenosine triphosphate was positive at 0.77, which jumped up to 0.90 through the myocardial bridging segments when the pressure wire was pulled back. Thus, coronary vasospasm and MB might have contributed to his chest symptoms at rest and during effort. Interventional cardiologists should consider the presence of MB as a potential cause of myocardial ischemia.     

肌桥所致心肌缺血机制与治疗

目的研究冠状动脉心肌桥患者心肌缺血机制和治疗措施。方法回顾性分析390例左前降支冠状动脉心肌桥患者的临床特点。根据心脏收缩期桥段血管受压的轻重程度分为两组：A组235例,收缩期压迫〈50％;B组135例,收缩期压迫≥50％。对比两组患者心血管危险因素以及冠状动脉粥样硬化的发生率。结果390例左前降支冠状动脉肌桥近段血管动脉粥样硬化发生率为45．70％,远段血管动脉粥样硬化发生率为2．25％,两者差异有统计学意义（P〈0．05）。两组患者年龄、性别、高血压、高脂血症、家族史、吸烟史方面比较均无统计学意义（P〉0．05）。B组与A组相比,心肌桥近段血管动脉粥样硬化发生率明显增加,差异有统计学意义（P〈0．05）。结论①肌桥患者心肌缺血的主要机制是肌桥收缩时的挤压和肌桥近端动脉粥样硬化。②对靶血管进行再血管化是治疗心肌桥患者较为合理而有效的方法。     

Coronary atherosclerosis within a myocardial bridge, not a benign condition

In patients with myocardial bridging, the area within the bridge usually remains free from atherosclerotic disease. The case of a 47 year old man is described who had the rare combination of myocardial bridging with an atherosclerotic plaque within the area of bridging, which was detected with intravascular ultrasound but not with coronary angiography. The clinical history of the patient demonstrates that this is not a benign condition. In symptomatic patients the bridged segment should be screened for the presence of plaque with intracoronary ultrasound.

Keywords: myocardial bridging;  intravascular ultrasound;  atherosclerotic plaque     

冠状动脉造影检查对心肌桥的诊断价值

目的 探讨冠状动脉造影检查对心肌桥诊断的应用,研究心肌桥和冠状动脉粥样硬化的相关性.方法 收集1523例患者冠状动脉造影检查资料,分析心肌桥检出率,观察心肌桥的发生位置、壁冠状动脉收缩期狭窄程度、心肌桥血管合并粥样斑块的位置、斑块处管腔狭窄程度.结果 全部1523例患者中,201例患者检查结果正常,1225例患者检出粥样斑块,231例患者检出心肌桥.心肌桥检出率为15.2％,共检出心肌桥235处.心肌桥位置：右冠状动脉1处,左主干1处,旋支1处,对角支3处,左前降支229处,以左前降支中段多见,壁冠状动脉收缩期轻度狭窄为主.纯心肌桥97例.134例患者心肌桥血管合并粥样斑块144处,斑块位置：心肌桥近端111处,心肌桥段19处,心肌桥远端14处.心肌桥近端血管粥样硬化较心肌桥段、心肌桥远端发生率高,但粥样斑块的形成与壁冠状动脉收缩期的狭窄程度无显著相关（P＞0.05）.结论 心肌桥多见于左前降支中段血管,壁冠状动脉收缩期多为轻度狭窄,血管合并粥样硬化,多见于心肌桥前端,但粥样斑块的形成与壁冠状动脉收缩期狭窄程度无明显相关性.冠状动脉造影检查对心肌桥及心肌桥合并粥样硬化的诊断有重要价值.     

Stent malapposition,as a potential mechanism of very late stent thrombosis after bare-metal stent implantation: A case report

A 90-year-old man was admitted to our hospital with acute ST-segment elevation myocardial infarction. He had a history of post-infarction angina pectoris 79 months ago and had a bare-metal stent (BMS) implanted in the proximal left anterior descending artery at our hospital. Emergent coronary angiography demonstrated thrombotic occlusion in the previously stented segment. After catheter thrombectomy, antegrade flow was restored, but 90% stenosis with haziness persisted in the proximal and distal portions of the previously stented segment. Intravascular ultrasound imaging showed interstrut cavities or stent malapposition at the proximal and distal sites of stented segment. In close proximity to the sites, residual thrombi were also observed. Optical coherence tomography (OCT) demonstrated neither lipid-laden neointimal tissue nor rupture but clearly demonstrated residual thrombus adjacent to the malapposed region in addition to the stent malapposition. PCI with balloon was successfully performed and stent apposition was confirmed by OCT. Stent malapposition is an unusual mechanism of very late stent thrombosis after BMS implantation. OCT can clearly reveal the etiology of stent thrombosis.     

心肌桥对冠状动脉粥样硬化的作用

目的:探讨心肌桥与冠状动脉粥样硬化病变之间的关系。方法:回顾性分析冠脉造影术中检出的心肌桥患者92例的冠脉病变与临床资料。结果:1500例冠脉造影患者检出心肌桥92例,检出率6.1%;心肌桥近段冠状动脉粥样硬化病变发生率71.7%,远段冠状动脉粥样硬化病变发生率10.9%,两者差异有显著性（P<0.01）。结论:心肌桥可能导致冠状动脉心肌桥近段冠脉粥样硬化病变。     

Coronary spasm-induced acute myocardial infarction associated with intracoronary thrombosis]

A 63-year-old man was admitted with an acute anteroseptal myocardial infarction. Coronary angiography performed 3 hours after the onset of chest pain revealed 99% stenosis of the proximal left anterior descending coronary artery (LAD) with delayed filling and intraluminal thrombus distal to the stenosis. After the intracoronary injection of isosorbide dinitrate, the delayed filling disappeared and a subsequent intracoronary urokinase partially dissolved the thrombus. Repeat coronary angiography in the chronic phase disclosed 75% stenosis of the LAD and disappearance of the thrombus. Intracoronary acetylcholine provoked a coronary spasm at the stenotic site of the LAD, concomitantly with chest pain and ST-segment elevation in the anterior leads. The present case demonstrated that coronary spasm plays an important role in thrombus formation and acute myocardial infarction. To date, the concept has been postulated that a dynamic interaction between atherosclerosis, platelet aggregation and spasm may work to cause coronary thrombosis and subsequently lead to acute myocardial infarction. Our report shed light on the importance of coronary spasm in the pathogenesis of myocardial infarction.     

Combination of aneurysm and myocardial bridging at the same site of a coronary artery in a patient with obstructive hypertrophic cardiomyopathy.

This case report describes the rare finding of myocardial bridging and a coronary aneurysm in the same coronary artery segment of a 57-year-old patient with obstructive hypertrophic cardiomyopathy. At the site of the aneurysm in the proximal LAD, the myocardial bridging resulted in an almost normal vessel diameter during systole with an aneurysmatic expansion of the vessel during diastole. This accidental finding does not necessarily require special therapy, since the underlying coronary aneurysm is small, with a low risk of thrombus formation or rupture, but it is big enough to prevent a coronary obstruction due to the myocardial bridging.     

Coronary ectasia resulting in thrombotic coronary occlusion after warfarin interruption: a case report

A 68-year-old man taking aspirin and warfarin for ectatic right coronary artery complained of chest pain and was admitted to our hospital with acute myocardial infarction. He had discontinued taking warfarin due to nail bleeding for a month. Coronary angiography revealed total occlusion at segment 3 of the ectatic right coronary artery with massive thrombus. Because of unsuccessful reperfusion by an aspiration device, a 5F straight catheter was inserted into the ectatic right coronary artery to aspirate the massive thrombus, and Thrombolysis in Myocardial Infarction grade 3 flow reperfusion was obtained. Intravascular ultrasonography showed "moyamoya" vessels in the ectatic right coronary artery, suggesting an abnormal coronary flow pattern, but there was no evidence of unstable plaque. Warfarization should be considered to treat ectatic coronary artery.     

Size of coronary artery in a myocardial bridge compared with adjacent nontunneled left anterior descending coronary artery

Patients with myocardial bridging (MB) may experience myocardial ischemia. Coronary stenting was reported to serve as an effective interventional approach to improve symptoms in selected patients with MB, but is related to high risk of coronary perforation. The aim of this study is to investigate vessel area in the myocardial bridge segment in comparison to that of adjacent segments proximal and distal to MB using intravascular ultrasound. A total of 81 myocardial bridge segments, characterized by a half-moon-shaped echolucent zone surrounding the intramural artery, were found in 78 patients using intravascular ultrasound. The cross-sectional area within the external elastic membrane and minimum and maximum diameters in the myocardial bridge segment and adjacent reference vessel segments were measured. Diastolic cross-sectional area within the external elastic membrane in the myocardial bridge segment was significantly smaller than that in adjacent segments both proximal and distal to MB (5.48+/-2.59 vs 9.40+/-3.48 and 7.22+/-2.87 mm2, respectively, both p<0.001). Maximum vessel diameter in the myocardial bridge segment during diastole was also smaller than that in the segment distal to MB (2.74+/-0.61 vs 3.12+/-0.59 mm, p<0.001). In conclusion, our study showed that vessel area in the myocardial bridge segment was smaller than that in adjacent segments proximal and distal to MB.     

Coronary fistulas can develop collateral vessels: angiographic follow-up of an embolized giant right coronary artery-superior vena cava fistula in a patient with variant angina

A 54-year-old man was transferred to our emergency department because of acute inferior myocardial infarction. However, ST-segment elevation resolved after intravenous nitrate administration on admission and coronary angiography revealed a nonobstructive atherosclerotic plaque at the mid-portion of the circumflex artery and a giant tortuous fistula from the right sinus of Valsalva to the superior vena cava. The patient was diagnosed with variant angina and coronary arteriovenous fistula after vasodilator treatment and maximal treadmill stress test. After effective medical treatment of variant angina and successful percutaneous coil embolization of the fistula, the patient had not experienced any angina episodes for 1 year. However, control coronary angiography revealed partial persistence of fistula flow because of new collateral vessels, bridging distal and proximal parts of the occluded segment. We present the first coexistence of coronary to superior vena cava fistula and variant angina in the literature. This report also shows the ability of coronary fistulas to develop collateral vessels, like coronary arteries.