Decreased plasma nesfatin-1 levels in patients with acute myocardial infarction

Nesfatin-1 is a novel anorexigenic hormone which has close relationship with diabetes, obese, anorexia nervosa, psychiatric disorders and neurogenic diseases. The aim of our study was to evaluate levels of plasma nesfatin-1 among patients presenting with coronary artery disease and the correlation between nesfatin-1 levels and other clinical parameters. Fasting plasma levels of nesfatin-1 were tested in 48 acute myocardial infarction (AMI) patients, 74 stable angina pectoris (SAP) patients and 34 control subjects. All of them were examined by coronary angiography. The severity of coronary atherosclerosis was assessed using the Gensini score. Plasma nesfatin-1 levels were significantly lower in AMI group than SAP group or control group (0.91 ± 0.08 ng/mL vs. 0.98 ± 0.19 ng/mL and 1.09 ± 0.39 ng/mL, respectively, P < 0.05). In AMI patients, plasma nesfatin-1 levels were negatively correlated with high-sensitivity C-reactive protein, neutrophil% or Gensini scores. Such information implies that lower nesfatin-1 concentration may play a very important role in the development of AMI.     

Procalcitonin as a prognostic marker in patients with acute myocardial infarction

Background: Procalcitonin is involved in the inflammatory response and is associated with adverse prognosis in certain conditions.

Aims: To investigate the association between procalcitonin and major adverse cardiac events (MACE), left ventricular (LV) function and remodelling following acute myocardial infarction (AMI).

Methods: Plasma procalcitonin was measured in 977 patients with AMI. Subjects were followed for MACE (median 671 days). A subgroup underwent echocardiography at discharge and follow-up LV function and volume assessment.

Results: Procalcitonin was associated with MACE on uni- and multivariable analysis. Kaplan–Meier assessment revealed an adverse outcome in subjects with procalcitonin above the median. Procalcitonin was related to markers of LV dysfunction and remodelling.

Conclusion: Procalcitonin is associated with MACE, LV dysfunction and remodelling post-AMI.     

Plasma intermedin levels in patients with acute myocardial infarction

It has been shown that adrenomedullin (ADM) may function as a cardiovascular-regulatory peptide in humans. Intermedin (IMD) is a newly discovered peptide related to ADM and has a greater range of biological effects on the cardiovascular in animal experiments. The purpose of the study was to investigate the pathophysiological role of IMD in patients with acute myocardial infarction (AMI). The present study included twenty patients with acute ST-segment elevation myocardial infarction (STEMI), thirty-three with stable coronary heart disease (SCHD), and eighteen healthy controls. Plasma levels of IMD, malonaldehyde (MDA), and superoxide dismutase (SOD) and cardiac biomarkers were determined at one, two, four and seven days following AMI. Plasma IMD levels were significantly increased on day 1 in AMI patients when compared with SCHD subjects (P = 0.014), and reached a peak of 181.88 ± 9.47 pg/ml at 96 h. Plasma IMD concentrations were correlated with MDA and SOD. Furthermore, patients with severe lesions in their coronary arteries tended to have higher plasma IMD levels (P < 0.05) in AMI patients. A significant increase in plasma IMD following AMI may be associated with oxidative stress, and could be used as a marker to reflect the severity of the coronary stenosis.     

Thrombolysis with tissue plasminogen activator in patients with acute myocardial infarction

Thrombolytic agents are being employed clinically in increasing numbers of patients in the attempt to eliminate occlusive coronary thrombi in patients with evolving myocardial infarction. When administered by the intracoronary route, streptokinase lyses is successful in coronary thrombi in more than two-thirds of patients, but when administered intravenously is successful in only one-third. Since streptokinase is a nonselective plasminogen activator, it induces fibrinogenolysis when administered selectively or systematically with an attendant marked reduction in plasma fibrinogen levels and significant bleeding complications. In contrast, the action of tissue plasminogen activator (t-Pa) is relatively selective for fibrinolysis (as opposed to fibrinogenolysis). It induces coronary thrombolysis in at least 60% of patients when administered either into a coronary ostium or a peripheral vein without producing substantial reductions in circulating fibrinogen. Bleeding complications are modest and usually related to high administered doses and concomitant heparinization, and occur primarily at sites of vascular access. Thus, t-Pa appears to be a promising agent for thrombolytic treatment of patients with evolving acute myocardial infarction.     

Use of a commercially available reagent for the selective detection of homocysteine in plasma

A procedure for the detection of homocysteine (Hcy) in blood plasma is described. A commercially available chromogen is added to the plasma sample. The plasma solution turns from yellow to blue upon heating for 4 min when a detectable threshold level of Hcy is present. Chromatographic separations and immunogenic materials are not needed. The protocol takes approximately 30 min.     

急性心肌梗死患者肠道菌群多样性分析

目的 初步探究急性心肌梗死患者肠道菌群的多样性。方法 选择2015年6月至2016年3月于大连大学附属中山医院住院治疗的急性心肌梗死患者作为观察组,年龄51~70岁。选择同期经冠脉造影排除冠心病的住院患者为对照组,年龄51~70岁。排除近1个月内发生感染、炎性肠病及应用抗生素的患者。所有患者按性别与年龄分为A、B、C、D组。直接从患者粪便标本中提取细菌总DNA,PCR扩增后进行梯度凝胶电泳（DGGE）分析。结果 DGGE分析显示急性心梗患者肠道菌群丰度均较对照组下降。A组中观察组与对照组患者电泳条带数为(33.71±4.39) vs (38.71±2.56),t=－2.058,P=0.040;C组患者为(31.14±2.67) vs (35.29±3.55),t=－2.005,P=0.045;差异均具有统计学意义。B与D组中心梗患者肠道菌群丰度亦有下降趋势,但与对照组比差异无统计学意义。UPGAM法聚类分析显示除D组外,各组中观察组与对照组患者肠道菌群呈现分离现象;急性心梗患者肠道菌群有较高相似性,与非冠心病患者肠道菌群差异明显。结论 急性心梗与非冠心病患者肠道菌群存在差异,急性心梗患者肠道菌群多样性较低。肠道菌群改变可能与急性心肌梗死存在一定相关性。     

Severe hypoxemia in a patient with acute myocardial infarction

A case report of a patient with acute myocardial infarction and severe hypoxemia due to acute right to left interatrial shunt (RLIAS) is presented. Diagnostic and therapeutic procedures are discussed.     

Detection of lactate dehydrogenase B4 in human hemolysate of patients deficient in lactate dehydrogenase B subunit activity using enzyme immunoassay

We developed a sensitive enzyme immunoassay system specific for human lactate dehydrogenase (LDH)- B₄ with antiacetylated LDH-B₄ Fab-horse-radish peroxidase conjugate. The enzyme immunoassay system was not interfered with by up to 0.3 mg/tube of hemoglobin. Thus, we measured LDH-B₄ concentrations in the hemolysate of seven heterozygous individuals deficient in LDH-B subunit activity and eight normal individuals. We could not find a significant difference between the LDH-B₄ concentrations in heterozygous and those in normal individuals. These results demonstrate that heterozygous individuals deficient in LDH-B subunit activity produce enzymatically inactive B subunits.This work was supported in part by grants in aid for Scientific Research from the Ministry of Education, Japan (59570998), and from the Clinical Pathology Research Foundation of Japan.     

Ten year mortality in patients with suspected acute myocardial infarction.

OBJECTIVE--To describe the 10 year mortality in patients with suspected acute myocardial infarction. DESIGN--Follow up of all patients below 76 years of age admitted with acute chest pain to 16 coronary care units participating in the Danish verapamil infarction trial in 1979-81. SUBJECTS--Of the 5993 patients included, 2586 had definite infarction, 402 had probable infarction, and 3005 did not have infarction. MAIN OUTCOME MEASURES--Death and cause of death. Standardised mortality ratio (observed mortality/expected mortality in background population). RESULTS--The estimated 10 year mortalities were 58.8%, 55.5%, and 42.8% in patients with definite, probable, and no infarction, respectively (P < 0.0001). Stratified Cox''s analysis identified a hazard ratio for mortality of 1.25 (95% confidence interval 1.08 to 1.44) for probable infarction compared with no infarction and of 1.15 (1.00 to 1.32) for definite compared with probable infarction. The standardised mortality ratio in the first year was 7.1 (6.5 to 7.8) for definite infarction, 5.0 (3.6 to 6.3) for probable infarction, and 4.7 (4.2 to 5.2) for no infarction. From the second year and onwards the annual standardised mortality ratio in the three groups did not differ significantly. Cardiac causes of deaths were recorded in 89%, 84%, and 71% of the deaths in patients with definite, probable, and no infarction, respectively. CONCLUSIONS--The 10 year mortality of patients with and without infarction is significantly higher than in the background population. Most deaths are caused by coronary heart disease, and these patients should consequently be further evaluated at the time of discharge and followed up closely.     

ICAM-1 in acute myocardial infarction: a potential therapeutic target

Current treatments for AMI centre on prompt restoration of epicardial coronary blood flow. Despite improvements, AMI is still associated with significant morbidity and mortality. Novel approaches are therefore keenly sought. Intercellular adhesion molecule-1 (ICAM-1, CD54) is a member of the immunoglobulin superfamily. It is implicated in neutrophil and monocyte-endothelial cell adhesion, processes contributing to myocardial neutrophil infiltration and microvascular coronary slow flow, both viewed as important to the pathophysiologic responses in AMI. ICAM-1 would therefore appear an important potential therapeutic target in this context, and is the subject of this review.     

Systemic inflammation and reperfusion injury in patients with acute myocardial infarction

Despite early recanalization of an occluded infarct artery, tissue reperfusion remains impaired in more than one-third of the acute myocardial infarction (AMI) patients owing to a process of reperfusion injury. The role of systemic inflammation in triggering this phenomenon is unknown. Proinflammatory factors (hs-CRP, TNF-alpha ) and anti-inflammatory mediators (IL-1 receptor antagonist, IL-10) were measured in 65 patients during the acute phase of a myocardial infarction as well as in 11 healthy control subjects. Myocardial reperfusion injury was defined as the presence of persistent ST-segment elevation despite successful coronary intervention (> or = 50 of the initial value) and was observed in 28 patients. Systemic proinflammatory mediators (particularly hs-CRP and leukocytes) were higher in AMI patients compared to control subjects. Within the group of AMI patients, only serum TNF-alpha differed significantly between patients with versus without reperfusion injury: a median value of 25 versus 13 pg/mL was observed, respectively. Logistic regression analysis identified a high level of TNF-alpha as the most important independent determinant of reperfusion injury (P = .001), beyond total ischemic time (P = .01) and extent of jeopardized myocardium (P = .08). There was no correlation between the TNF-alpha level and the total ischemic time (P = .8) or the extent of jeopardized myocardium (P = .6). Systemic inflammation, in particular high levels of TNF-alpha , is strongly associated with the occurrence of reperfusion injury after successful recanalization. Our findings suggest that TNF-alpha is involved in the triggering and/or amplification of local inflammatory responses related to ischemia-reperfusion injury.     

Interpretation of elevated plasma visfatin concentrations in patients with ST-elevation myocardial infarction

Visfatin is a cytokine that is expressed in many tissues, including the heart, and has been proposed to play a role in plaque destabilization leading to acute myocardial injury. The present study evaluates plasma levels of visfatin in acute ST-elevation myocardial infarction (STEMI) patients and examines the temporal changes in visfatin levels from the acute period to the subacute period to determine a correlation with the degree of myocardial ischemia. We evaluated 54 patients with STEMI. Circulating levels of visfatin and brain natriuretic peptide (BNP) were measured by ELISA. In addition, local expression of visfatin and BNP were detected by quantitative real-time polymerase chain reaction and immunohistochemical (IHC) analysis of left ventricular myocytes in a mouse model of myocardial infarction (MI). Plasma levels of visfatin were significantly increased in patients with STEMI on admission, relative to controls (effort angina patients and individuals without coronary artery disease). The visfatin levels reached a peak 24 h after percutaneous coronary intervention (PCI) and then decreased toward the control range during the first week after PCI. The basal plasma visfatin levels were found to correlate with peak troponin-I, peak creatine kinase-MB, total white blood cell count, and BNP levels. Trend analyses confirmed that visfatin levels correlated with the number of diseased coronary arteries. Further, in MI mice, mRNA levels of visfatin and BNP were found to be higher than in sham-treated mice. IHC analysis showed that visfatin and BNP immunoreactivity was diffusely observable in left ventricular myocytes of the MI mice. This study indicates that plasma visfatin levels are significantly higher in STEMI patients and that these higher visfatin levels correlate with elevated levels of cardiac enzymes, suggesting that increased plasma visfatin may be closely related to the degree of myocardial damage.     

Evaluation of left ventricular twist in acute myocardial infarction patients using speckle tracking imaging

The aim of this study is to evaluate the differences of left ventricular (LV) twist and untwisting rate in patients with acute myocardial infarction (AMI) as compared with healthy subjects by means of Speckle Tracking Imaging (STI). 45 AMI patients (AMI group) and 48 healthy subjects (NOR group) were studied. Two-dimensional STI was performed in all patients. Peak apical rotation, peak basal rotation, peak LV twist, peak basal untwisting rate, peak apical untwisting rate, peak LV untwisting rate, time to peak LV twist, and untwisting rate were measured. In comparison with the NOR group, peak LV rotational parameters were found to be decreased in the AMI group (P < 0.01). A strong correlation was found between the peak LV twist and LV ejection fraction in the overall study population (P < 0.001). The LV twist is strongly related to LV systolic function, and the impairment of LV function observed in patients with AMI is associated with a decrease of LV twist and untwist rate. The STI appears to accurately evaluate LV function.     

主动脉内球囊反搏术在急性心肌梗死患者中的临床应用

目的:探讨主动脉内球囊反搏术(IABP)在急性心肌梗死(AMI)患者中的临床应用.方法:收集从2008年1月至2008年12月因急性心肌梗死急诊入住我院CCU并行IABP及经皮冠状动脉介入治疗(PCI)病例32例,回顾性分析患者的临床特征、冠脉造影及介入治疗情况,观察使用IABP前后患者心率血压变化,IABP相关并发症,住院期间死亡率.结果:急性心肌梗死患者入院后及时在IABP支持下成功完成急诊PCI手术,患者应用IABP治疗后心率血压均得到明显改善.IABP相关并发症发生率仅9例,严重并发症0例,无术中死亡,住院期间死亡3例,其中合并心源性休克死亡2例.结论:主动脉内球囊反搏术在急性心肌梗死患者中的应用安全、有效,显著降低了急性心肌梗死患者的住院期间死亡率.     

早期足量应用美托洛尔对急性心肌梗死疗效及安全性的研究

目的:研究早期足量应用美托洛尔对急性心肌梗死的疗效及安全性.方法:将40例AMI患者随机分为治疗组和对照组.治疗组静脉缓慢注射美托洛尔15mg后予关托洛尔150-200mg/d口服;对照组按常规剂量给予美托洛尔25-50mg/d口服.其它治疗相同,两组治疗4周.比较两组治疗后QTcd、心律失常发生的种类、心肌耗氧指数、梗死后心绞痛、梗死延展的发生率和心功能的变化.结果:治疗组QTcd、室性心律失常发生率、心肌耗氧指数、梗死后心绞痛和梗死延展的发生率均低于对照组(P<0.05).心功能两组无显著性差异.结论,AMI患者早期足量使用美托洛尔可以从多方面获益,安全性高.     

Indicators of quality of care for patients with acute myocardial infarction

Background

There is a wide practice gap between optimal and actual care for patients with acute myocardial infarction in hospitals around the world. We undertook this initiative to develop an updated set of evidence-based indicators to measure and improve the quality of care for this patient population.

Methods

A 12-member expert panel was convened in 2007 to develop an updated set of quality indicators for acute myocardial infarction. The panel identified a list of potential indicators after reviewing the scientific literature, clinical practice guidelines and other published quality indicators. To develop the new list of indicators, the panel rated each potential indicator on 4 dimensions (reliability, validity, feasibility and usefulness in improving patient outcomes) and discussed the top-ranked quality indicators at a consensus meeting.

Results

Consensus was reached on 38 quality indicators: 17 that would be measurable using chart-abstracted data and 21 that would be measurable using administrative data. Of the 17 chart-review indicators, 13 address pharmacologic and nonpharmacologic care delivered to patients in hospital. In-hospital mortality was recommended as a key outcome indicator. Three system indicators were recommended to measure the collaborative responsiveness of the health care system from the call for help to intervention. It was recommended that hospitals strive for a minimum target benchmark of 90% or greater on process-of-care indicators.

Interpretation

Implementation of strategies by clinicians and hospitals to meet target benchmarks on these quality indicators could save the lives of many individuals with acute myocardial infarction.There is a large practice gap between optimal and actual patterns of care for patients with acute myocardial infarction in hospitals around the world.¹ Acute myocardial infarction is a highly treatable condition for which many advances in treatment have occurred over the past several decades. However, the uptake of many of these advances and their incorporation into routine clinical practice has often lagged behind their development and publication in clinical journals by many years.^2–4 To reduce this gap and improve quality of care, many jurisdictions are using indicators of the quality of care for patients with acute myocardial infarction. These quality indicators are intended to measure adherence to selected key clinical practice guidelines in routine clinical care and serve as a foundation for efforts to improve quality.⁵ They define the minimum standard of care that might be expected for all “ideal” patients who meet certain criteria and have no contraindications for a given health care intervention.National organizations in Canada, the United States, the United Kingdom and other OECD (the Organisation for Economic Co-operation and Development) countries have all developed indicators to measure and improve the quality of care for patients with acute myocardial infarction both within and across countries, regions and hospitals.^6–9 In 2003, the Canadian Cardiovascular Outcomes Research Team (a Canadian Institutes of Health Research Interdisciplinary Health Research Team) worked in association with the Canadian Cardiovascular Society to develop and publish the first set of quality indicators for myocardial infarction in Canada.⁶ The Canadian Cardiovascular Outcomes Research Team comprises more than 30 leading outcome researchers who work together on projects to measure and improve cardiac care. From the outset, we recognized that the indicators would need to be modified over time to reflect changes in practice guidelines and clinical evidence. In 2007, a Canadian expert panel was convened by the Canadian Cardiovascular Outcomes Research Team to develop and recommend a set of quality indicators that took into account the best indicators developed elsewhere and that also included some unique indicators that were felt to be of particular relevance and use to Canadian clinicians and hospitals.