MiR-150 improves cardiac fibrosis after myocardial infarction by targeting c-Myb / 实用医学杂志

Objective To evaluate the role and mechanism of miR-150 in cardiac fibrosis after MI.Methods A rat model of MI was established by up-regulating miR-150 through overexpressing miR-150 lentivirus.Real-time PCR and Western blot were applied in detecting the expression of collagen 1 α 1 and α-SMA protein in infarction area border.Masson coloration was applied in measuring fibrosis.Cardiac fibroblasts were isolated and cultured.UTR was used to report the carrier and lentivirus.And c-Myb siRNA was used to verify the relationship between c-Myb and microRNA-150.Results In vivo,MiR-150 was down-regulated in myocardium border zone in 14 day and 28 day after infarction (P ＜ 0.001,P ＜ 0.05),and overexpressing miR-150 promoted myocardial fibrosis (P ＜ 0.001),and inhibited the expression of collagen1α 1 and α-SMA (P ＜ 0.01,P ＜ 0.05).In vitro,c-Myb was the direct target gene of miR-150,and inhibited the expression of c-Myb resulting in the down regulation of collagen1α 1 and α-SMA,suggesting that the role of miR-150 was achieved by regulating c-Myb.Conclusions MiR-150 was down-regulated in myocardium border zone,and myocardial fibrosis can be improved by targeting c-Myb.

Mitral Valve Plasty in Postinfarction Partial Rupture of a Posterior Papillary Muscle / 日本心臓血管外科学会雑誌

We report the successful treatment of an 81-year-old woman after a difficult diagnosis of mitral valve regurgitation resulting from partial rupture of the posterior papillary muscle. The patient, with a chief complaint of dyspnea, was admitted to our hospital in October, 2010. Echocardiography revealed severe MR and an oscillating abnormal mass attached to the mitral posterior leaflet was assessed as vegetation. Her general condition worsened and coronary angiography revealed 90% stenosis at #6 and 99% stenosis at #12. Partial papillary muscle rupture of post acute myocardial infarction was ruled out. Urgent surgery was performed. It is found that tissue we had assessed as vegetation was a part of the posterior papillary muscle with no signs of infection. MVP with quadrangular resection (P3), annuloplasty and CABG (LITA-LAD, SVG-OM) was performed. The patient was discharged on the 28th postoperative day. Echocardiography showed no MR for four years after the surgery.

Right Atrial Approach for Surgical Repair of a Posterior Postinfarction Ventricular Septal Defect / 日本心臓血管外科学会雑誌

We performed transatrial repair of postinfarction posterior ventricular septal defect (VSP) in a 69-year-old man who was transferred to our hospital with a diagnosis of posterior acute myocardial infarction and VSP. Coronary angiogram revealed total occlusion of the right coronary artery at #3 and 75% stenosis of the left circumflex artery at #13. UCG revealed the ventricular septal defect on the posterior ventricular septum without LV wall motion abnormality. Surgical repair was planned around 3-4 weeks later because his hemodynamic state was stable without inotropes nor IABP support upon arrival. Under general anesthesia, standard median sternotomy was performed and cardiopulmonary bypass was established with the ascending aorta and bicaval cannulation. Cardiac arrest was achieved with antegrade cold crystalloid cardioplegic solution and an oblique right atrial incision was made. The VSP was visualized via the tricuspid valve. The location of VSP was confirmed with saline injection from the LA vent line. VSP was closed with two patches, consist of a Teflon felt and a bovine pericardial patch, from the left and right ventricle side with six 4-0 polypropylene mattress sutures. Also coronary artery bypass for LCx was performed with a saphenous vein graft. The postoperative course was uneventful. There was no residual ventricular septal shunt and LV function was normal by UCG. Right atrial approach for surgical repair seemed to be useful for posterior VSP.

Contained cardiac rupture: An autopsy case.

Rupture of the myocardium due to myocardial infarction is often fatal but when such patients survive, they present with a pseudoaneurysm where the defect is sealed by the pericardium preventing the complete rupture. This is described as a ‘contained myocardial rupture’. We describe here a case of left ventricular contained myocardial rupture following an acute myocardial infarction.

Postinfarct Ventricular Septal Defect after Coronary Covered Stent Implantation

We report a case of a postinfarction ventricular septal defect caused by an acute recurrent occlusion after the implantation of a covered stent, which was performed as a rescue procedure for the ruptured left anterior descending artery during a percutaneous coronary intervention. Although the emergent implantation of a covered stent for the ruptured coronary arteries such as the left main coronary artery or the origins of the left anterior descending artery can be performed during a percutaneous coronary intervention, and a coronary bypass surgery should be considered in order to decrease the risk of complete occlusion, thus providing a superior long term patency.

The implications of serum enzymes and coagulation activities in postinfarction myocardial / As implicações de enzimas séricas e atividades de coagulação em ruptura cardíaca pós-infarto do miocárdio

OBJECTIVE: Associations between cardiovascular diseases and serum enzymes or coagulation activities have been sufficiently documented in patients with myocardial infarction. However, the alterations of these biomarkers in patients with postinfarction myocardial rupture have rarely been reported. The aim of this study is to present the profiles of the markers in patients with postinfarction myocardial rupture. METHODS: From 2004 to 2008, 19 consecutive patients were referred to this hospital for surgical repair of postinfarction myocardial rupture. Eight (42.1%) patients had free wall rupture, 5 (26.3%) had papillary muscle rupture, 5 (26.3%) had ventricular septal rupture, and 1 (5.3%) had double structure (ventricular septum + free wall) rupture. Thirteen patients survived the operation, and 6 died. Laboratory findings including serum enzymes and coagulation activities were collected and analyzed. RESULTS: The coagulation markers and serum enzymes except for fibrinogen increased significantly after the development of myocardial rupture. Statistical differences in D-dimer, partial thromboplastin time, peak lactate dehydrogenase, peak creatine kinase and creatine kinase fraction MB were found between non-survivors and survivors. Troponin I values were elevated significantly during the early days after the onset or surgical repair of myocardial rupture. Multivariant regression analysis did not show any significant relationship between creatine phosphokinase fraction MB (Y) and D-dimer (X1) or fibrinogen (X2). CONCLUSION: Myocardial rupture leads to extremely high serum enzyme and coagulation activities except for fibrinogen after the onset. The evaluation of these biomarkers may help in making diagnostic and treatment decisions and in judging the clinical prognosis of such patients.

OBJETIVO: As associações entre doenças cardiovasculares e enzimas sorológicas ou atividades de coagulação foram amplamente documentadas em pacientes com infarto do miocárdio. No entanto, as alterações destes biomarcadores em pacientes com ruptura cardíaca após infarto do miocárdio foram raramente relatadas. O objetivo deste estudo é apresentar o perfil dos biomarcadores em pacientes com ruptura cardíaca após infarto do miocárdio. MÉTODOS: De 2004 a 2008, 19 pacientes consecutivos foram referidos a este hospital para correção cirúrgica de ruptura cardíaca após infarto do miocárdio. Oito (42,1%) pacientes tiveram ruptura livre de parede, cinco (26,3%) ruptura de músculo papilar, cinco (26,3%) ruptura do septo interventricular e um (5,3%) ruptura dupla de estruturas, envolvendo tanto septo ventricular como parede livre. Treze pacientes sobreviveram à operação e seis faleceram. Amostras sanguíneas foram coletadas e analisadas para mensuração de enzimas sorológicas e atividade de coagulação. RESULTADOS: Os marcadores de coagulação e enzimas com exceção de fibrinogênio aumentaram significativamente depois do desenvolvimento da ruptura do miocárdio. Diferenças estatísticas foram achadas entre não-sobreviventes e sobreviventes em relação a concentração de dímeros-D, tempo de trombina, pico de lactato desidrogenase, creatinoquinase máximo e fração MB da creatinoquinase. Os valores de troponina I foram elevados significativamente durante os primeiros dias depois do infarto ou do reparo cirúrgico da ruptura do miocárdio. A análise de regressão multivariada não mostrou qualquer relação significativa entre fração MB da creatinoquinase e dímeros-D nem fibrinogênio. CONCLUSÕES: A ruptura do miocárdio induz importante elevação de marcadores enzimáticos e de atividade de coagulação, exceto fibrinogênio. As diferenças nestes biomarcadores entre não-sobreviventes e sobreviventes podem ser de grande ajuda no diagnóstico e nas decisões de tratamento, assim como na avaliação do prognóstico clínico de tais pacientes.

Perfil clínico-cirúrgico de pacientes operados por ruptura do septo interventricular pós-infarto do miocárdio / Clinical and surgical profile of patients operated for postinfarction interventricular septal rupture

OBJETIVOS: Estudar características clínicas, complicações e desfechos intra-hospitalares de pacientes operados por ruptura do septo interventricular pós-infarto. MÉTODOS: Estudo retrospectivo envolvendo 21 pacientes entre janeiro/1996 e junho/2009. Todas as operações foram realizadas na Divisão de Cirurgia Cardiovascular do Complexo Hospitalar HUOC/PROCAPE. RESULTADOS: Idade média dos pacientes foi de 62,81 anos (± 8,21), sendo 61,9 por cento (n=13) do sexo masculino. Ruptura ocorreu, em média, 4,8 dias após o infarto. Foi observado choque cardiogênico em 57,1 por cento (n=12) dos casos, sendo este fator de risco para óbito (100 por cento com choque vs. 22,2 por cento sem choque; P<0,001). Sobreviventes apresentaram média de fração de ejeção maior em comparação aos óbitos (66,29 por cento ± 4,61 por cento versus 42,71 por cento ± 4,79 por cento; P<0,001). Todos pacientes foram classificados em alto risco pelo EuroSCORE, tendo os sobreviventes média de pontuação menor em comparação aos óbitos (6,57 ± 0,53 versus 10,93 ± 2,23; P<0,001). A maioria (76,2 por cento; n=16) dos pacientes teve necessidade de uso de drogas vasoativas e 57,1 por cento (n=12) foram considerados instáveis hemodinamicamente. Necessidade de drogas vasoativas foi fator de risco para óbito (81,3 por cento no grupo com drogas vasoativas versus 20 por cento no grupo sem drogas vasoativas, P=0,025). Instabilidade hemodinâmica também foi fator de risco para óbito (100 por cento no grupo instável versus 22,2 por cento no grupo estável; P<0,001). A taxa de mortalidade intra-hospitalar foi de 66,7 por cento (n=14). CONCLUSÕES: Necessidade de drogas vasoativas, instabilidade hemodinâmica e choque cardiogênico se associaram com maiores taxas de mortalidade. Pacientes que evoluem com desfecho adverso apresentam menor função ventricular e maior pontuação no EuroSCORE. A taxa de mortalidade permanece alta.

OBJECTIVES: To study clinical features, complications and in-hospital outcomes of patients operated for postinfarction ventricular septal rupture. METHODS: A retrospective study involving 21 patients between January/1996 and June/2009. All operations were performed at the Division of Cardiovascular Surgery of Complexo Hospitalar HUOC/PROCAPE. RESULTS: Mean age of patients was 62.81 years (± 8.21), 61.9 percent (n = 13) were male. Rupture occurred on average 4.8 days after infarction. Cardiogenic shock was observed in 57.1 percent (n = 12), being risk factor for death (100 percent with shock vs. 22.2 percent without shock; P<0.001). Survivors had a higher mean ejection fraction compared to deaths (66.29 percent ± 4.61 percent versus 42.71 percent ± 4.79 percent, P <0.001). All were classified as high risk by the EuroSCORE, and the survivors had lower average score compared to deaths (6.57 ± 0.53 versus 10.93 ± 2.23; P <0.001). The majority (76.2 percent, n = 16) of the patients needed to use vasoactive drugs and 57.1 percent (n = 12) considered hemodynamically unstable. Need for vasoactive drugs was a risk factor for death (81.3 percent with vasoactive drugs versus 20 percent without vasoactive drugs, P = 0.025). Hemodynamic instability was also a risk factor for death (100 percent in the unstable group versus 22.2 percent in the stable group; P <0.001). The rate of in-hospital mortality was 66.7 percent (n = 14). CONCLUSIONS: The need for vasoactive drugs, hemodynamic instability and cardiogenic shock were associated with higher rates of mortality. Patients who had adverse outcomes had less ventricular function and higher score in the EuroSCORE. Mortality remains high.

Two Cases of Postinfarction Ventricular Septal Perforation due to Obstruction of the Right Coronary Artery / 日本心臓血管外科学会雑誌

We report 2 cases of postinfarction ventricular septal perforation (VSP) attributable to obstruction of the right coronary artery. Case 1 was a 63-year-old man in whom VSP developed after percutaneous coronary angioplasty for complete obstruction of the right coronary artery. He developed papillary muscle rupture intraoperatively, requiring mitral valve replacement and subsequent treatment for right-side heart failure. He was discharged l7 weeks after surgery. Case 2 was a 77-year-old man. During catheterization following the detection of 99% obstruction of the #2 segment of the right coronary artery, VSP was found and the patient underwent emergency surgery. Postoperative echocardiography and ventriculography did not reveal a residual shunt or mitral regurgitation (MR). However, he suddenly developed acute MR in the 4th postoperative week and died of acute heart failure. VSP attributable to obstruction of the right coronary artery is difficult to repair surgically because of its anatomical location, among other reasons, and mitral valve replacement is sometimes needed if VSP is accompanied by necrosis of the mitral valve papillary muscle. Appropriate care is therefore needed in this case.

Post-Infarction Ventricular Septal Rupture: 10 Years of Experience / 대한흉부외과학회지

BACKGROUND: Postinfarction ventricular septal rupture is associated with mortality as high as 85~90%, if it is treated medically. This report documents our experience with postinfarction ventricular septal rupture that was treated surgically. MATERIAL AND METHOD: We retrospectively reviewed the medical records of 11 patients who were operated on due to postinfarction ventricular septal rupture between August 1996 and August 2006. There were 4 men and 7 women, with a mean age of 70+/-11 years (age range: 50~84 years). The location of the rupture was anterior in 7 cases and posterior in 4 cases. The interval between the onset of acute myocardial infarction and the occurrence of the ventricular septal rupture was 2.0+/-1.3 days (range: 1~5 days). Operation was performed at an average of 2.4+/-2.7 days (range: 0~8 days) after the diagnosis of septal rupture. Preoperative intraaortic balloon pump therapy was performed in 10 patients. RESULT: The infarct exclusion technique was used in all cases. Coronary artery bypass grafting was done in 8 cases, with the mean number of distal anastomosis being 1.0+/-0.8. There was one operative death. In 2 patients, reoperation was performed due to a residual septal defect. The postoperative morbidities were transient atrial fibrillation (n=7), paroxysmal supraventricular tachycardia (n=1), low cardiac output syndrome (n=3), bleeding reoperation (n=2), delayed sternal closure (n=2), acute renal failure (n=2), pneumonia (n=1), intraaortic balloon pump-related thromboembolism (n=1), and transient delirium (n=2). Nine patients have been followed up for a mean of 38+/-40 months except for one follow-up loss. There have been 3 late deaths. At the latest follow-up, all 6 survivors were in a good functional class. CONCLUSION: We demonstrated satisfactory operative and midterm results with our strategy of preoperative intraaortic balloon pump therapy, early repair of septal rupture by infarct exclusion and combined coronary revascularization.

Clinicopathologic characteristics of myocardial infarction with or without cardiac rupture in the gerontal patients / 解放军医学杂志

Objective To investigate different clinicopathologic changes in myocardial infarction with and without cardiac rupture in the gerontal patients. Methods 107 gerontal patients with myocardial infarction (rupture group 22, non-rupture group 85) confirmed by necropsy during Jan. 1980 to Oct. 2003 were analyzed to compare the clinicopathologic findings between patients with cardiac rupture and without rupture. Results The mean age of rupture group was higher than that of non-rupture (79.1?9.1 vs 71.8?10.9 years old, P=0.0059). The number of female patients (50.0% vs 24.6%, P=0.0209) and the the number of patients suffering from myocardial infarction for the first time (57.3% vs 52.3%, P=0.0312) were both greater in the rupture group. Previous angina pectoris was significantly less frequently found in the rupture group compared with non-rupture group (45.5% vs 87.1%, P=0.0000). The mean number of major coronary arteries with over 75% stenosis was significantly lower in the rupture group (1.64 vs 2.28 branches/person, P=0.0068). The percentage of single major coronary arteries with significant stenosis was more often seen in the rupture group (59.1% vs 33.8%, P=0.0325). The site of cardiac rupture was more frequenfly located in anterior wall near the apex. Conclusion The results suggested that cardiac rupture occurred more often in older and female patients, in first myocardial infarction episode, with infrequent previous angina pectoris, and frequently involving a severe single coronary artery disease compared with those patients without cardiac rupture. The common location of rupture was anterior wall near the apex.

Early Result of Surgical Revascularization for Acute Myocardial Infarction

BACKGROUND AND OBJECTIVES: There are relatively few studies that have evaluated the optimal timing, risk of mortality, and outcome for patients with coronary artery bypass graft surgery (CABG) performed in the setting of acute myocardial infarction (AMI). MATERIALS AND METHODS: We reviewed our 18 patients who underwent CABG within 14 days after AMI, between June 1994 and June 1997. Thirteen of the patients were male and 5 were female. Their ages ranged from 41 to 77 years (mean age, 60.6+/-10.4 years), and the amount of time betweenAMIandCABGrangedfrom4hoursto14days (meantime,7.0+/-4.7days).Therewere11 anteroseptal infarctions and 7 inferior wall infarctions. Eleven patients had transmural infarctions and 7 had subendocardial infarctions. Indications of operations were postinfarction angina, cardiogenic shock and intractable ventricular arrhythmia. Six patients required preoperative intra-aortic balloon pump (IABP) support, and 3 additional patients required IABP to be separated from cardiopulmonary bypass. An average of 3.4+/-0.5 vessels per patient were bypassed. RESULTS: The early mortality rate for these 18 patients was 5.6% and late mortality rate was 5.9%, and 2-year actuarial survival rates were 89.5%. Univariate analysis of mortality showed that an ejection fraction less than 30% was associated with risk factor (p value=0.016 ). Age, sex, time to CABG, emergency operations, locations of infarctions were not significant. CONCLUSION: Although our studies have weak points in that there was only a small number of patients and the lack of long-term results, we could conclude that early myocardial revascularization is relatively safe after AMI for those individuals with an ejection fraction greater than 30%.

Early Surgical Revascularization for Acute Myocardial Infarction / 대한흉부외과학회지

To assess the early results, risk factors and optimal timing for coronary artery bypass graft surgery(CABG) after an acute myocardial infarction(AMI), we reviewed our 19 patients who underwent CABG within 30 days after AMI, between June 1994 and October 1996. This study excluded 1 patient whose diagnosis was AMI with ventricular septal rupture. 14 of the patients were male and 5 were female. Their ages ranged from 41 to 77 years(mean age, 60.6+/-10.4 years), and the amount of time between AMI and CABG ranged from 8 hours to 24 days(mean time, 10.6+/-6.4 days). There were 11 anteroseptal infarctions and 8 inferior wall infarctions. 11 patients had transmural infarctions and 8 had subendocardial infarctions. Indications of operations were primary revascularization and postinfarction angina. Three patients required preoperative intra-aortic balloon pump(IABP) support, and 4 additional patients required IABP to be separated from cardiopulmonary bypass. An average of 3.6+/-0.6 vessels per patient were bypassed. The early mortality rate for these 19 patients was 5.3% and late mortality rate was 5.5%, 1-year and 2-year actuarial survival rates were 89.5%. Univariate analysis of mortality showed that an ejection fraction less than 30% and intraopretative IABP supports were associated with risk factors(p value=0.018 and 0.015 respectively). Age, sex, time to CABG, emergency operations, types and locations of infarctions were not significant. Although our studies have weak points in that there was only a small number of patients and the lack of long-term results, we could conclude that early myocardial revascularization is relatively safe after AMI for those individuals with an ejection fraction greater than 30%.

The Change of Expression of Troponin T and I Isoforms in the Failing Myocardium of Rat after Myocardial Infarction

BACKGROUND: Contractile dysfunction of rat myocardium in postinfarction remodeling is characterized by decreased response of myofilament both to calcium(Ca++) and adrenergic stimuli. This study tested the hypothesis that above alterations may be linked to molecular switches among the isoforms of troponin T and troponin I, the major regulators of myocardial responsiveness. METHODS: Using Sprague-Dawley rat as a model, myocardiums of fetal heart, 1 day postnatal heart, normal adult heart(n=4), and non-infarcted area of postinfarction heart(n=4, 3 months after left coronary artery ligation, mean LVEDP=21.4mmHg) were studied. For the detection on molecular switches, western blotting and semiquantitative RT-PCR were employed. RESULTS: Immunoblotting of rat myocardium showed normal developmental isoform switch of troponin protein. There was distinct isoform patterns specific for postinfarction rat heart. The postinfarction myocardium developed a marked increase in the fetal isoform and marked decrease in the adult isoform of troponin T, resulting in the reversed ratio of fetal/adult cardiac troponin T isoform(normal adult rat=0.60+/-0.1 vs postinfarction rat=1.79+/-0.15, p<0.01). Also, the postinfarction heart showed approximately 20% decrease in the amount of adult troponin I isoform. In RT-PCR experiments, the postinfarction hearts were characterized by increased amplification of fetal troponin R isoform cDNA(fetal troponin R/GAPDH ; normal adult rat=0.22, postinfarction rat=0.84). However, there was no siginificant difference in the amplification of troponin I cDNA between normal and postinfarction heart. CONCLUSION: These experimental findings indicate that there are molecular switches operative among the regulatory protein troponin T and I in the rat myocardium with development of postianfarction heart failure.

Clinical and Coronary Angiographic Findings in Patients with Postinfarction Angina

To determine the incidence, clinical characteristics and coronary angiographic findings of postinfarction angina, clinical course and coronary angiogram were studied in 45 patients with acute myocardial infarction. During a mean follow-up period of 12 weeks, 17 patients(37.8%) developed angina. Of 5 patients with postinfarction angina within 1 week of infarction, 2 patients died during hospitalization, whereas all 12 patients with postinfarction angina which occured more than 1 week after acute myocardial infarction were discharge alive. The frequency of stenosis over 90% and multivessel disease by coronary angiography were 51.7% and 64.7% respectively in patients with postinfarction angina, and 25%, 28.5% respectively in patients without postinfarction angina.