Síndrome de Wellens: o infarto agudo do miocárdio iminente / Wellens Syndrome: impending acute myocardial infarction

A síndrome de Wellens foi descrita em 1982 por Zwaan, Bär e Wellens. No eletrocardiograma, observam-se alterações morfológicas da onda T nas derivações precordiais, sugerindo estenose proximal grave da artéria coronária descendente anterior que representa iminente risco de infarto agudo do miocárdio e/ou morte súbita, com discreta ou nenhuma alteração da troponina sérica. Seu reconhecimento antecipado e a abordagem com reperfusão miocárdica precoce evitam desfechos desfavoráveis. A intervenção coronária percutânea e a revascularização miocárdica cirúrgica são as estratégias mais utilizadas para tratamento. Os autores descrevem dois casos de síndrome de Wellens tipos A e B tratados por diferentes estratégias de reperfusão.

Wellens syndrome was described by Zwaan, Bär and Wellens, in 1982. On the electrocardiogram, T wave morphological alterations are observed in precordial leads, suggesting severe proximal stenosis of the left anterior descending coronary artery and an imminent risk of acute myocardial infarction and/or sudden death, with slight or no alteration in serum troponin. Its early recognition and management with early myocardial reperfusion avoid unfavorable outcomes. Percutaneous coronary intervention and surgical myocardial revascularization are the most used strategies for treatment. The authors describe two cases of types A and B Wellens syndrome treated with different reperfusion strategies.

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.

Telemedicine network Program for reperfusion of Myocardial infarction / Programa en red para la reperfusión del infarto con telemedicina

background: Early management of myocardial infarction in the area of public health requires the integration of specific programs for the coordination of healthcare services. Objective: The aim of this study was to evaluate the impact on delay times and reperfusion rate of a comprehensive program for the reperfusion of myocardial infarction in a hospital network of the Southern Greater Buenos Aires. Methods: The network consists of six low-mid-complexity hospitals and a third-level referral center with 24-hour cath-lab. Stage 1 of the program (2009-2010) evaluated the existing barriers to reperfusion; Stage 2 (2011-2013) implemented the progressive incorpora-tion of improvements and Stage 3 assessed the program (2013-2014) complemented with fellows in each hospital. Program impact was evaluated by the proportion of patients reperfused and time to its implementation. results: A total of 432 patients referred from the network were hospitalized with diagnosis of ST-segment elevation myocardial infarction. Mean age was 56±9 years and 83.3% were men. The proportion of reperfused patients progressively increased: S1 60.7%, S2 69% and S3 78%, p for trend=0.01. Time to reperfusion decreased significantly between S1 and S3, from 120 minutes (IQR 55-240) to 90 minutes (IQR 35-150), p=0.04, with a median reduction of 30 minutes in the door-to-balloon and door-to-needle times. Conclusions: The application of a program for myocardial reperfusion based on the diagnosis of barriers was associated with 28.5% increase in reperfusion, and a significant reduction in the implementation times. This public network model built on algorithms adapted to local barriers may contribute to improve the care of myocardial infarction in our country.

Infarto agudo do miocárdio em jovem com síndrome de Turner / Acute myocardial infarction in a young with Turner?s syndrome

A Síndrome de Turner (ST) é uma doença genéticacaracterizada pela monossomia completa ou parcial docromossomo X e possui uma grande variabilidade fenotípica,podendo se manifestar na forma clássica oucom poucos sinais dismórficos que possam chamaratenção ao diagnóstico. Mulheres com Síndrome deTurner têm um risco cardiovascular duas vezes maiorque a população geral e apresentam maior prevalênciade hipertensão arterial sistêmica, dislipidemia, aumentoda resistência insulínica e deficiência estrogênica,além de doenças cardíacas congênitas, principalmenteacometendo grandes vasos, podendo estar presenteem até 50% das mulheres com ST. Devido a essas complicaçõescardiovasculares, o reconhecimento de possíveismanifestações cardíacas agudas em pacientescom anomalias genéticas torna-se imprescindível parao sucesso terapêutico. O objetivo do presente artigo édescrever um caso de infarto agudo do miocárdio emuma paciente jovem com Síndrome de Turner.

Turner?s syndrome is a genetic disease related eitherto a homogeneous complete or a partial XO monosomyand has a fenotipic variability, presenting suchin a classic syndrome or with few dysmorfic signs thatcan draw attention to diagnosis. Womem with Turner?ssyndrome have a cardiovascular risk twice higher thangeneral population and presents more prevalence inhypertension, dyslipidemia, insulin resistence and estrogendeficiency, besides cardiac congenital cardiacdiseases, mainly affecting big vassels, in approximately50% of these patients. Due to these cardiovascularcomplications, recognition of possible acute cardiacmanifestations in patients with genetic abnormalities isnecessary to therapeutic success. The goal of this articleis to present a case report of a young woman with AMIand Turner syndrome.

Risk Factors of No-Reflow Phenomenon after Primary Percutaneous Coronary Intervention with Stent Implantation

BACKGROUND AND OBJECTIVES: No-reflow is an important phenomenon for limiting the prognosis of patients following primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). Coronary stenting is the current standard procedure for primary PCI in AMI. However, stenting is suspected to cause more microembolization, and no-reflow phenomenon. This study was performed to elucidate the risk factors for the no-reflow phenomenon following primary PCI with stenting, in patients with AMI. SUBJCETS AND METHODS: The clinical, angiographic and procedure related parameters were reviewed in patients with AMI that had undergone primary PCI, with stent implantation, within 12 h of the onset of chest pain, at Seoul National University Hospital, Yonsei University Hospital Cardiovascular Center and Chungbuk National University Hospital (n=183). RESULTS: 29 patients (16%) showed no-reflow phenomenon (final TIMI flow grade less than 3). Conventional risk factors for coronary artery disease were not significant risk factors for the no-reflow phenomenon. In a univariate analysis, a high initial CK-MB level (>50 IU) (8.45% vs. 21.9%, p=0.04), low left ventricular ejection fraction (LV EF) (30 sec) (31% vs. 15%, p=0.04) were significant risk factors of the no-reflow phenomenon. A low LV EF and long pre-dilatation balloon inflation time were significant risk factors in a multivariate analysis. CONCLUSION: LV dysfunction at presentation and a long pre-dilatation balloon inflation time were independent risk factors for the no-reflow phenomenon following primary PCI with stenting for AMI. Preventive measures against the no-reflow phenomenon should be considered in patients with these risk factors.

Risk Factors of No-Reflow Phenomenon after Primary Percutaneous Coronary Intervention with Stent Implantation

BACKGROUND AND OBJECTIVES: No-reflow is an important phenomenon for limiting the prognosis of patients following primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). Coronary stenting is the current standard procedure for primary PCI in AMI. However, stenting is suspected to cause more microembolization, and no-reflow phenomenon. This study was performed to elucidate the risk factors for the no-reflow phenomenon following primary PCI with stenting, in patients with AMI. SUBJCETS AND METHODS: The clinical, angiographic and procedure related parameters were reviewed in patients with AMI that had undergone primary PCI, with stent implantation, within 12 h of the onset of chest pain, at Seoul National University Hospital, Yonsei University Hospital Cardiovascular Center and Chungbuk National University Hospital (n=183). RESULTS: 29 patients (16%) showed no-reflow phenomenon (final TIMI flow grade less than 3). Conventional risk factors for coronary artery disease were not significant risk factors for the no-reflow phenomenon. In a univariate analysis, a high initial CK-MB level (>50 IU) (8.45% vs. 21.9%, p=0.04), low left ventricular ejection fraction (LV EF) (30 sec) (31% vs. 15%, p=0.04) were significant risk factors of the no-reflow phenomenon. A low LV EF and long pre-dilatation balloon inflation time were significant risk factors in a multivariate analysis. CONCLUSION: LV dysfunction at presentation and a long pre-dilatation balloon inflation time were independent risk factors for the no-reflow phenomenon following primary PCI with stenting for AMI. Preventive measures against the no-reflow phenomenon should be considered in patients with these risk factors.

Therapeutical effects of salvianolic acid B on myocardial infarction in dogs / 中成药

AIM: To study the therapeutical effects of salvianolic acid B (Sal B) on myocardial infarction(MI) in dogs. METHODS : The models of myocardial infarction were produced by ligation of the left anterior descending (LAD) coronary artery in the anaesthetized dogs. The extent of myocardial ischemia was detected by epicardial-electrocardiogram and the extent of infarction was determhled by N-BT staining method. The parameter of lactate dehydrogenase was determined in the serums of dogs. RESULTS : It was indicated that the adminstration of Sal B(1、3 and 10mg/kg) by the way of intravenous injection reduced the extent of myocardial infarction (N-ST) ( P