Relationships Between Biomarkers and Left Ventricular Filling Pressures at Rest and During Exercise in Patients After Myocardial Infarction

BackgroundIncreased pulmonary capillary wedge pressure (PCWP) is an independent prognostic predictor after myocardial infarction (MI), but PCWP is difficult to assess noninvasively in subjects with preserved ejection fraction (EF). We hypothesized that biomarkers would provide information regarding PCWP at rest and during exercise in subjects with preserved EF after MI.Methods and ResultsSeventy-four subjects with EF >45% and recent MI underwent right heart catheterization at rest and during a symptom-limited semisupine cycle exercise test with simultaneous echocardiography. Plasma samples were collected at rest for assessment of midregional pro–A-type natriuretic peptide (MR-proANP), N-terminal pro–B-type natriuretic peptide (NT-proBNP), galectin-3 (Gal-3), copeptin, and midregional pro-adrenomedullin (MR-proADM). Plasma levels of MR-proANP and PCWP were associated at rest (r = 0.33; P = .002) and peak exercise (r = 0.35; P = .002) as well as with changes in PCWP (r = 0.26; P = .03). Plasma levels of NT-proBNP and PCWP were weakly associated at rest (r = 0.23; P = .03) and peak exercise (r = 0.28; P = .02) but not with changes in PCWP (r = 0.20; P = .09). In a multivariable analysis, plasma levels of MR-proANP remained associated with rest and exercise PCWP (P < .01), whereas NT-proBNP did not. Plasma levels of Gal-3, copeptin, and MR-proADM were not associated with PCWP at rest or peak exercise.ConclusionsIn subjects recovering from an acute MI with preserved EF, plasma levels of natriuretic peptides, particularly MR-proANP, are associated with filling pressures at rest and during exercise.     

Melatonin attenuates postmyocardial infarction injury via increasing Tom70 expression

Mitochondrial dysfunction leads to reactive oxygen species (ROS) overload, exacerbating injury in myocardial infarction (MI). As a receptor for translocases in the outer mitochondrial membrane (Tom) complex, Tom70 has an unknown function in MI, including melatonin‐induced protection against MI injury. We delivered specific small interfering RNAs against Tom70 or lentivirus vectors carrying Tom70a sequences into the left ventricles of mice or to cultured neonatal murine ventricular myocytes (NMVMs). At 48 h post‐transfection, the left anterior descending coronary arteries of mice were permanently ligated, while the NMVMs underwent continuous hypoxia. At 24 h after ischemia/hypoxia, oxidative stress was assessed by dihydroethidium and lucigenin‐enhanced luminescence, mitochondrial damage by transmission electron microscopy and ATP content, and cell apoptosis by terminal deoxynucleotidyl transferase dUTP nick‐end labeling and caspase‐3 assay. At 4 weeks after ischemia, cardiac function and fibrosis were evaluated in mice by echocardiography and Masson's trichrome staining, respectively. Ischemic/hypoxic insult reduced Tom70 expression in cardiomyocytes. Tom70 downregulation aggravated post‐MI injury, with increased mitochondrial fragmentation and ROS overload. In contrast, Tom70 upregulation alleviated post‐MI injury, with improved mitochondrial integrity and decreased ROS production. PGC‐1α/Tom70 expression in ischemic myocardium was increased with melatonin alone, but not when combined with luzindole. Melatonin attenuated post‐MI injury in control but not in Tom70‐deficient mice. N‐acetylcysteine (NAC) reversed the adverse effects of Tom70 deficiency in mitochondria and cardiomyocytes, but at a much higher concentration than melatonin. Our findings showed that Tom70 is essential for melatonin‐induced protection against post‐MI injury, by breaking the cycle of mitochondrial impairment and ROS generation.     

Acute coronary syndromes with ongoing myocardial ischemia (ACS with OMI) versus acute coronary syndromes without ongoing ischemia (ACS without OMI): The new classification of acute coronary syndromes should replace old classification based on ST segment elevation presence or absence—Expert consensus statement of the Czech Society of Cardiology

The Czech Society of Cardiology is proposing here the new classification of acute coronary syndromes at the time of the first medical contact. The proposal suggests to remove the terms “ST elevation myocardial infarction” and “non-ST elevation acute coronary syndrome” and to replace these terms by “acute coronary syndrome with ongoing myocardial ischemia” and “acute coronary syndrome without ongoing myocardial ischemia”. The proposed new classification better reflects current treatment approaches and will facilitate the decision making at the first medical contact.     

抗血小板聚集治疗在大面积脑梗塞中的应用分析

目的探讨抗血小板聚集对大面积脑梗塞进行治疗的临床效果。方法选取100例大面积脑梗塞患者作为研究对象,并将其随机列入观察组和对照组,各50例。观察组应用抗血小板聚集进行治疗,对照组行常规治疗。对比分析两组的疗效。结果观察组的总有效率、神经功能的缺损积分以及日常生活能力的恢复情况均显著优于对照组(P0.05)。结论应用抗血小板聚集对大面积脑梗塞患者进行治疗,疗效确切,安全性强。     

适合机械性取栓的急性栓塞性脑梗死动物模型的建立与评价

目的:建立并评价适合动脉内机械取栓的急性栓塞性脑梗死动物模型。方法:血流临时阻断凝血酶注入法制作急性栓塞性脑梗死模型,利用颅内动脉取栓装置行机械性取栓。应用数字减影血管造影(DSA)、磁共振弥散成像(DWI)、经颅多普勒及病理检查来评价模型建立的效果,比较模型建立前后表观弥散系数(ADC)、大脑中动脉流速(Vmca)变化情况。结果:DSA显示制模的成功率为83%。栓塞6 h DWI显示梗塞灶,24 h病理检查TTC染色可见梗死区。取栓后颈总动脉再通率为80%,栓塞前后、取栓前后Vmca的比较差异有统计学意义(P<0.05),取栓组与非治疗组6 h Vmca比较差异有统计学意义;取栓组ADC值呈上升趋势,非治疗组ADC值下降,两组24 h的比较差异有统计学意义(P<0.05)。结论:本研究所建立的模型稳定,重复性好,适用于颅内动脉取栓装置的实验研究和疗效评价。     

低分子肝素联合尿激酶治疗急性心肌梗死的临床研究

目的探讨低分子肝素与尿激酶在急性心肌梗死患者中的联合应用价值。方法选择急性心肌梗死患者104例，随机将患者分为研究组和对照组。对照组患者给予常规治疗，研究组患者加用低分子量肝素钠注射液与注射用尿激酶的药物联合治疗方案，比较两组患者的临床治疗情况。结果研究组患者的显著进步率和总有效率较对照组患者均明显提高，分别达到63.46％和92.31％，而无效率则明显减少，仅为7．69％，并且均呈现出统计学差异（P〈0.05）。结论低分子肝素联合尿激酶对急性心肌梗死患者临床治疗效果的改善具有极其重要的临床意义。     

急性心肌梗死后快速延迟整流K~+通道基因表达的变化

目的探讨猪心肌梗死(MI)后梗死边缘区快速延迟整流K+通道KCNH2和KCNE2基因表达水平的改变及意义。方法通过结扎猪左前降支远端1/3～1/2处2h建立急性心肌梗死(AMI)模型,手术后存活猪进入MI组,术后24h取左心室梗死边缘区内层(Endo)、中层(Mid)和外层(Epi)心肌,应用半定量RT-PCR方法检测KCNH2和KCNE2mRNA含量。同时,设立相应的假手术组(SH组),SH组取与MI组对应区域的心肌组织。结果 KCNH2和KCNE2基因的表达在SH组左心室En-do、Mid和Epi心肌间没有差异,与SH组比较,AMI后梗死边缘区3层心肌KCNH2mRNA表达均明显下降(P<0.05),而且3层心肌间的基因表达呈不均一性(P<0.05),KCNE2mRNA表达量差异无统计学意义(P>0.05)。结论 AMI后梗死边缘区3层心肌KCNH2基因表达的不均一性下调,可能在MI后早期室性心律失常的发生中起重要作用。