Rotura miocárdica de ventrículo izquierdo secundaria a infarto agudo de miocardio / Myocardial rupture of left ventricle secondary to myocardial infarction

RESUMEN Fundamento: la rotura miocárdica es una complicación rara del infarto agudo de miocardio con una incidencia global de alrededor del 6,2 %. Objetivo: caracterizar los fallecidos por infarto agudo de miocardio con la rotura de pared de ventrículo izquierdo. Métodos: se realizó un estudio retrospectivo, descriptivo y observacional, en el cual se analizaron los fallecidos con diagnóstico de causa directa de muerte: taponamiento cardíaco por hemopericardio, rotura de miocardio e infarto agudo de miocardio. Resultados: de 877 infartos agudos de miocardio diagnosticados entre 2010 a 2018, 16 de ellos presentaron rotura de pared miocárdica de los cuales 68,8 % eran del masculino. El hábito de fumar fue el factor de riesgo predominante. Solo en un 35,7 % se realizó el diagnóstico clínico correcto de IAM y en ninguno de los casos fue planteado el diagnóstico de rotura de miocardio o taponamiento cardíaco por hemopericardio. La región anatómica del corazón donde con mayor frecuencia se localizaron las roturas de miocardio fue en la pared posterior. Conclusiones: la rotura de la pared de miocardio es una complicación del infarto poco frecuente pero catastrófica con una mortalidad elevada, sin embargo, esta puede reducirse si el cuadro clínico es sospechado, y se realiza un diagnóstico precoz con instauración de medidas de apoyo para mantener la estabilidad hemodinámica.

ABSTRACT Background: myocardial rupture is a rare complication of acute myocardial infarction with an overall incidence of around 6.2 %. Objective: to characterize the deaths due to acute myocardial infarction with the rupture of the left ventricle wall. Methods: a retrospective, descriptive and observational study was carried out in which the deceased were analyzed with a diagnosis of direct cause of death: cardiac tamponade due to hemopericardium, myocardial rupture and acute myocardial infarction. Results: of 877 acute myocardial infarcts diagnosed between 2010 and 2018, 16 of them had myocardial wall rupture of which 68.8% were male. The habit of smoking was the predominant risk factor. Only in 35.7 % the correct clinical diagnosis of AMI was made and in none of the cases was the diagnosis of myocardial rupture or cardiac tamponade due to hemopericardium. The anatomical region of the heart where myocardial ruptures were most frequently located was in the posterior wall. Conclusions: rupture of the myocardial wall is a rare but catastrophic complication of infarction with a high mortality, however, this can be reduced if the clinical picture is suspected, and an early diagnosis is made with the introduction of support measures to maintain hemodynamic stability.

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.

The diagnosis and treatment of acute myocardial infarction complicated with left ventricular wall rupture:a report of three cases / 天津医药

Objective To investigate the diagnosis and treatment in patients with acute myocardial infarction (AMI) and complicated left ventricular wall rupture (LVWR). Methods A retrospective analysis was made on the clinical features, diagnosis and successful treatment in three AMI patients with LVWR from December 2015 to April 2016. Results Three cases were included in this study. Case 1, the mesh like cardiac rupture after AMI was diagnosed by ultrasonic Doppler. Emergency revascularization was performed due to the combined cardiac shock, and the infarct related artery was opened. The vasoactive drugs were used after revascularization to reduce ventricular pressure load and volume load in the haemodynamic monitoring, and anticoagulation, antiplatelet agents were less used or discontinued to promote local thrombus healing of ventricular rupture. Case 2 was a recurrent myocardial infarction patient. LVWR was diagnosed by ultrasonic Doppler one day after emergency operation. The ruptured ventricular wall was encapsulated by thrombus. The drug therapy was effective in hemodynamic monitoring. LVWR was further confirmed by cardiac CT after clinical stabilization. Case 3 was diagnosed LVWR by ultrasonic Doppler four days after AMI. Because the ruptured ventricular wall was limited by incompletely organized thrombus, and the haemodynamic condition was stable, selective surgical repair of rupture after coronary angiography was performed. Conclusion The effective drug therapy combined with percutaneous coronary intervention and surgical repair can reduce the risk of death in patients with LVWR after AMI.

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.

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.

Lung cysts following pulmonary artery operations: Diagnostic and therapeutic implications.

We describe the case of a child suffering from congenital cyanotic heart disease — double outlet right ventricle (DORV) with transposition of great vessels (TOGV). She underwent a left Blalock-Tausig (BT) shunt at one month of age followed by a Glen procedure with left pulmonary artery augmentation at six months. Following the second procedure she developed extensive cyst formation in the upper lobe of the left lung and pneumothorax. She was managed by intercostal drainage of the pneumothorax. The cysts were observed and on a CT scan X-rays taken at one month and six months no cysts were seen. This case illustrates the occurrence of pneumatoceles after pulmonary artery manipulation, their proclivity for causing pneumothoraces and involution on follow-up. Cysts noted in such a setting should be monitored carefully and followed up to resolution.

Effects of aging on ventricular remodeling and cardiac rupture after acute myocardial infarction in mice / 中华老年医学杂志

Objective To explore the effects of aging on ventricular remodeling and cardiac rupture after acute myocardial infarction in mice. Methods　Male C57BL/6 mice of 3 months and 12 months old were randomly divided into sham operation group and myocardial infarction(MI)group.Following acute myocardial infarction(AMI)modeling induced by open-chest surgery,the events of cardiac rupture were monitored and the echocardiography and hemodynamics were performed on the 7th day after surgery.Zymography,immunohistochemical method and pathological staining were used to measure the activity of matrix metalloproteinases(MMPs),the content of collagen and the degree of inflammatory cell infiltration on the 3rd and 7th days after surgery,respectively. Results　The incidence of cardiac rupture was higher in elderly group than that in young group(38.0% vs.16.0%,X2=6.139,P＜0.05).Compared with young group,significant infarct expansion,left ventricular (LV)remodeling and hemodynamic deterioration were showed in elderly group on the 7th day after surgery(t=5.754,P＜0.05).The degree of inflammatory cell infiltration and the expression of MMP-9 were significantly increased in elderly group on the 3rd day following AMI modeling(P＜0.05),and the collagen content and the expression of type Ⅲ collagen were significantly increased (P＜0.05)compared with young group. Conclusions　Aging is a risk factor for post-infarct cardiac rupture in the mice model.The mechanisms which are responsible for this age-related difference of cardiac rupture are related to increasing degree of inflammatory cell infiltration, overexpression of MMP-9 and type Ⅲ collagen and aggravated early LV remodeling.

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.