Ventricular septal rupture caused by myocardial bridge,solved by interventional closure device

Myocardial bridging is a common coronary anomaly, which is generally described as a benign phenomenon. However, a growing number of studies consider this anomaly a relevant pathophysiological phenomenon with serious pathological consequences. Here we report on the case of an 88-year-old woman suffering from myocardial infarction and ventricular septal rupture, lacking any recognizable coronary disease except for a myocardial bridge causing the systolic compression of the left anterior descending coronary artery. A wide range of diagnostic procedures, including coronarography, echocardiography, and magnetic resonance imaging were used. The septal rupture was finally closed by using a percutaneous closure device. This event indicates that myocardial bridges – at least in some cases – may have notable clinical relevance.Some epicardial coronary arteries may have an intramyocardial segment referred to as a myocardial bridge (MB). This condition is generally described as a benign vascular anomaly. However, in some cases it has been reported to cause acute coronary syndrome, malignant ventricular arrhythmia, and sudden cardiac death (1). Research based on coronary angiography, a gold standard for diagnosing myocardial bridging, reports that this anomaly occurs in 1.5%-16% of members of Caucasian population (2). On the other hand, pathologists find myocardial bridging in up to 80% of all examined hearts (1). The relevance of the limitation of myocardial perfusion by compression of the anomalous vessel during the systole is often brought into question. At the same time, some studies report relevant asynergy in the contraction of the bridge during the diastolic blood flow (1). It has been well established that the proximal segment of the MB is more prone to atherosclerosis, while the tunneled coronary segment is spared (1). Plaques within the distal segment also seem to be less frequent (3). This is likely to be related to the higher proximal and lower distal intracoronary pressure-oscillation, which also implies shear stress (4). The tunneled segment is described as being prone to vasospasm (1).     

Microvascular transplantation after acute myocardial infarction

The primary objective of this study was to evaluate epicardial transplantation of an intact microvascular network for treatment of myocardial ischemia in a murine model of acute myocardial infarction. We describe transplantation of an intact microvascular network constructed from isolated microvascular segments stabilized in a 3-dimensional matrix to the epicardial surface after acute myocardial infarction. This microvascular graft was implanted as a patch on the epicardium of mice after left coronary artery ligation. After 14 and 28 days of implantation, left ventricular (LV) function was assessed and grafts evaluated via histology and cytochemistry. Inosculation of microvessels within the graft with host coronary microcirculation occurred as early as 7 days after initial tissue grafting. Morphologic evaluation of the grafts revealed arterioles, venules, capillaries, and erythrocytes within vascular lumina. Control grafts of collagen alone remained avascular. LV infarct size was smaller, and LV function improved in treated animals. Engraftment of whole microvascular units can be achieved to support cell-assisted vascular remodeling. Microvascular grafts may provide therapeutic benefit as a primary treatment or serve as a microvascular platform for cardiac repair and regeneration.     

Ventricular premature beats and mortality after myocardial infarction.

To assess the role of ventricular premature beats in influencing mortality of coronary patients, 1739 men with prior myocardial infarction were monitored for ectopic activity for one hour at a standard base-line examination, and followed for mortality for periods up to four years (average, 24.4 months). Analyses of survival taking into account other important prognostic variables establish that the presence of complex premature beats (R on T, runs of 2 or more, multiform or bigeminal premature beats) in the monitoring hour is associated with a risk of sudden coronary death three times that of the men free of complex ventricular premature beats. The corresponding risk of death from any cause is twice that of men without such complex beats in the hour. These arrhythmias make an independent contribution to increased risk of death that persists over the length of this observation period.     

Papillary muscle rupture as a first event in acute myocardial infarction

Cardiogenic shock caused by papillary muscle rupture in acute myocardial infarction is potentially reversible by surgical treatment. A case of inferior myocardial infarction in a 56-year-old previously healthy man is reported, in which the first event was papillary muscle rupture. The patient was in shock and had a mitral insufficiency murmur. The diagnosis was made by echocardiography and ventriculography. A St. Jude valve was implanted, and the patient was discharged in good health. It is suggested that routine echocardiography be carried out on patients with sudden cardiogenic shock, when a mitral murmur is present.     

自身免疫反应参与大鼠急性心肌梗死后心肌损伤的实验研究

目的：探讨急性心肌梗死(AMI)后自身免疫在心肌损伤和心室重塑中的作用。方法： 在体结扎Wistar大鼠冠状动脉左前降支(LAD)，建立AMI大鼠模型和假手术对照。6周后将其脾细胞(100×106-150×106)过继转输给同源近交大鼠；4周后血流动力学监测心功能改变，ELISA检测大鼠血清抗肌球蛋白重链(MHC)抗体，组织学检查心肌病理改变，免疫组化分析浸润心肌T细胞表型。 结果：AMI大鼠(n=12)心肌非梗死区可见异常炎症反应，所有过继转输大鼠(AMI-T)(n=10)发生器官特异性心肌炎症反应，免疫组化染色显示心肌出现CD4+T细胞浸润，假性手术转输组(sham-T)(n=10)均为阴性；AMI大鼠和AMI-T大鼠血清中检出抗MHC抗体(8/22)，sham-T组均为阴性(阳性率36.4% vs 0.0%)，(P＜0.05)；与sham-T组比较，AMI-T组发生左心室收缩功能受损(+dp/dtmax:1 323±55 kPa/s vs 1 418±82 kPa/s,P＜0.05)。 结论：自身免疫反应参与AMI后心肌损伤，可能是AMI后心室重塑的新机制。     

Papillary muscle rupture after myocardial infarction during left ventricular assist device support

We report a rare case of papillary muscle rupture due to myocardial infarction during left ventricular assist device support. A 69-year-old woman with cardiogenic shock due to acute myocardial infarction requiring venoarterial extracorporeal membrane oxygenation support was transferred for further surgical intervention. Six days after the event, extracorporeal membrane oxygenation was decannulated, and an extracorporeal left ventricular assist device was implanted. On postoperative day 11, she suffered from sudden onset hypoxia due to pulmonary edema. Transesophageal echocardiography showed new onset severe mitral regurgitation. No further surgical intervention was performed according to the family’s wishes, and she passed away on the 22nd postoperative day. Autopsy findings revealed papillary muscle rupture. Although the left ventricle is unloaded by the left ventricular assist device, papillary muscle rupture should be recognized as a possible complication after myocardial infarction.     

Changes in protease inhibitors after acute myocardial infarction.

Plasma levels of fibrinogen, alpha1-antitrypsin, alpha2-macroglobulin, antithrombin III, and C1 inactivator were measured serially for 10 days in 11 patients after acute myocardial infarction. Both fibrinogen and alpha1-antitrypsin rose markedly to reach peak levels 5-7 days after infarction while C1 inactivator levels rose slowly with the highest observed mean level on the 10th postinfarction day. Neither antithrombin III nor alpha2-macroglobulin changed significantly after myocardial infarction. No relationship between C1 inactivator levels and either fibrinogen or alpha1-antitrypsin was found in a study of 30 patients with a variety of disorders while fibrinogen and alpha1-antitrypsin levels were significantly correlated.     

Hospital discharge one week after acute myocardial infarction.

Sixty-seven consecutive patients who had suffered an acute myocardial infarction but no serious complications during the first to fourth hospital days were considered for a trial of hospital discharge at one week. Thirty-three of the 67 patients were discharged at one week, the remainder having a mean hospital stay of 11 +/- 2 days. The incidence of late complications and recurrent infarctions, as well as mortality and functional status, were determined in all patients six months after discharge. No serious complications occurred in either subgroup within three weeks after discharge. There were no deaths in either subgroup and no difference in functional status at six months. Patients without serious complications during the four days after an acute myocardial infarction can be spared the economic costs and psychologic stress of prolonged hospitalization.     

缺血预处理制备急性心肌梗死动物模型

目的探讨犬急性心肌梗死动物模型的制备方法,提高模型制备的成功率。方法健康杂种犬20只,分为为直接结扎冠状动脉左前降支组和缺血预处理后结扎组,制备犬急性心肌梗死模型。结果直接结扎组死亡率为40%(4/10),2只死于术中室颤,2只死于术后心衰。缺血预处理组死亡率为10%(1/10),死于气胸。心脏超声检查显示2组犬术后心功能明显下降,心室腔扩大,其中以直接结扎组更为明显。结论心律失常、心功能衰竭和气胸是围术期死亡的主要原因。缺血预处理后结扎冠状动脉可降低室性心律失常和术后心衰的发生,从而提高构建犬心肌梗死模型的安全性。     

Type A behavior and survival after acute myocardial infarction

To ascertain the influence of personality factors on the course of coronary artery disease, we measured Type A behavior in 516 patients within two weeks after an acute myocardial infarction, using the Jenkins Activity Survey questionnaire. Over a follow-up period of one to three years, there was no relation between the Type A score and total mortality, cardiac mortality, time to death for nonsurvivors, left ventricular ejection fraction, or duration of the stay in the coronary care unit. These negative findings were not changed by restricting the analyses to men below 61 years of age or by comparing extreme score categories. The contributions of behavioral, demographic, and cardiac physiologic factors to postinfarction mortality were also evaluated by multivariate survivorship analyses. The physiologic factors were the only ones that contributed a significant and independent mortality risk; the Type A score did not enter the survivorship model (relative risk, 0.8; 95 per cent confidence interval, 0.5 to 1.5). Thus, we found no relation between Type A behavior and the long-term outcome of acute myocardial infarction.     

Surviving acute myocardial infarction: survivin expression in viable cardiomyocytes after infarction

BACKGROUND: Apoptosis is a key feature in postinfarction remodelling leading to progressive myocyte loss. Both proapoptotic and antiapoptotic factors contribute to the delicate balance between death and survival. The survivin pathway has emerged as essential in the control of apoptosis, although its role in heart disease is unknown.AIM: To evaluate survivin expression after acute myocardial infarction (AMI). METHODS: Survivin expression was assessed immunohistochemically in the peri-infarct and remote viable myocardium in 17 consecutive patients who died 1-30 weeks after AMI and in four control hearts. RESULTS: Survivin was expressed by myocytes in the peri-infarct area in eight patients and in the remote region in 13 patients. The rate of survivin expression after AMI was significantly higher in the remote versus peri-infarct regions and compared with control hearts. Its expression was inversely associated with the presence of dilated cardiopathy and of apoptosis, independently from the gross pathology infarct size. CONCLUSIONS: Survivin myocardial expression after AMI may be associated with the survival of at risk myocardium and may be indicative of more favourable remodelling after AMI. These findings identify a potential new target for the treatment of postinfarction remodelling.