Predictors and in-hospital prognosis of recurrent acute myocardial infarction

Objective To investigate the contributing factors and in-hospital prognosis of patients with or without recurrent acute myocardial infarction （AMI）. Methods A total of 1686 consecutive AMI patients admitted to Peking University People＇s Hospital from January 2010 to December 2015 were recruited. Their clinical characteristics were retrospectively compared between patients with or without a recurrent AMI. Then multivariable logistic regression was used to estimate the predictors of recurrent myocardial infarction. Results Recurrent AMI patients were older （69.3 ± 11.5 vs. 64.7 ± 12.8 years, P 〈 0.001） and had a higher prevalence of diabetes mellitus （DM） （52.2% vs. 35.0%, P 〈 0.001） compared with incident AMI patients, they also had worse heart function at admission, more severe coronary disease and lower reperfusion therapy. Age （OR = 1.03, 95% CI： 1.02-1.05; P 〈 0.001）, DM （OR = 1.86, 95% CI： 1.37-2.52; P 〈 0.001） and reperfusion therapy （OR = 0.74; 95% CI： 0.52-0.89; P 〈 0.001） were independent risk factors for recurrent AMI Recurrent AMI patients had a higher in-hospital death rate （12.1% vs. 7.8%, P = 0.039） than incident AMI patients. Conclusions Recurrent AMI patients presented with more severe coronary artery conditions. Age, DM and reperfusion therapy were independent risk factors for recurrent AMI, and recurrent AM1 was related with a high risk of in-hospital death.

Characteristics of elevated cardiac troponin I in patients with acute ischemic stroke

Objective To study prognostic characteristics of cardiac troponin I （cTnI） elevation in acute ischemic stroke. Methods We retrospectively studied patients （n = 248） with acute ischemic stroke, acute ST-segment elevation myocardial infarction, and acute non-ST-elevation myocardial infarction who were treated between January 2013 and October 2015. Baseline demographic data and changes in cTnI levels among these three groups were compared. Patients with acute ischemic stroke were assigned to either the cTnI elevation group （cTnI 〉 0.034 ng/mL） or the no cTnI elevation group （cTnI ≤ 0.034 ng/mL）. Logistic regression analysis was used to identify risk factors associated with elevated serum cTnI in patients with acute ischemic stroke. Moreover, the duration of hospital stay and incidence of major cardiovascular outcomes were compared in patients with acute ischemic stroke, with or without elevated cTnI. Results In this study population of patients with acute ischemic stroke （n = 178）, acute ST-segment elevation myocardial infarction （n = 35）, and acute non-ST-elevation myocardial infarction （n = 35）, patients with acute ischemic stroke with elevated cTnI comprised 18.54% of subjects. Patients with elevated cTnI were older and more likely to have a history of hypertension. In addition, these patients had higher levels of inflammatory markers, reduced renal functions, increased D-dimer levels, higher NIH stroke scores, and lower left ventricular ejection fractions. Logistic regression analysis showed that both percentage of neutrophil and NIH stroke scores were elevated; estimated glomerular filtration rate and left ventricular ejection fraction were decreased in patients with acute ischemic stroke who had elevated cTnI, and they had more frequent major cardiovascular events during hospital stay. Conclusion Elevated cTnI detected in patients with acute ischemic stroke, indicated a greater likelihood of poor short-term prognosis during hospital stay.

Angiotensin-（1-7）： new perspectives in atherosclerosis treatment

Angiotensin （Ang）-（1-7） is recognized as a new bioactive peptide in renin-angiotensin system （RAS）. Ang-（1-7） is a counter-regulatory mediator of Ang-II which appears to be protective against cardiovascular disease. Recent studies have found that Ang-（1-7） played an important role in reducing smooth muscle cell proliferation and migration, improving endothelial function and regulating lipid metabolism, leading to inhibition of atherosclerotic lesions and increase of plaque stability. Although clinical application of Ang-（1-7） is restricted due to its pharmacokinetic properties, identification of stabilized compounds, including more stable analogues and specific delivery compounds, has enabled clinical application of Ang-（1-7）. In this review, we discussed recent findings concerning the biological role of Ang-（1-7） and related mechanism during atherosclerosis development. In addition, we highlighted the perspective to develop therapeutic strategies using Ang-（1-7） to treat atherosclerosis.

Total ischemic time and outcomes for patients with ST-elevation myocardial infarction： does time of admission make a difference？

Objective To investigate whether admission time was associated with the delay of reperfusion therapy and in-hospital death in patients with ST-elevation myocardial infarction （STEMI）. Methods All patients with STEMI who were admitted to the emergency depart- ment and underwent primary percutaneous coronary intervention at Peking University People＇s Hospital between April 2012 and March 2015 were included. We examined differences in clinical characteristics, total ischemic time, and in-hospital death between patients admitted during off-hours and those admitted during regular hours. Multivariate logistic regression was used to estimate the relationship between off-hours admission and clinical outcome. Results The sample comprised 184 and 105 patients with STEMI admitted to hospital during off-hours and regular hours, respectively. Total ischemic and onset-to-door times were significantly shorter in patients admitted during off-hours than among those admitted during regular hours （all P 〈 0.05）. Door-to-balloon （DTB） time, the rate of DTB time 〈 90 min, and in-hospital death were comparable between groups. Multivariate logistic regression showed that age and creatinine level, but not off-hours admission, were associated independently with increased in-hospital death. Conclusions Off-hours admission did not result in delayed reperfusion therapy or increased in-hospital mortality in patients with STEMI. Further efforts should focus on identifying pivotal factors associated with the pre-hospital and in-hospital delay of reperfusion therapy, and implementing quality improvement initiatives for reperfusion programs.

Unusual course of congenital complete heart block in an adult:A case report

BACKGROUND Congenital complete heart block(CCHB)with normal cardiac structure and negativity for anti-Ro/La antibody is rare.Additionally,CCHB is much less frequently diagnosed in adults,and its natural history in adults is less well known.CASE SUMMARY A 23-year-old woman was admitted to our hospital for frequent syncopal episodes.She had bradycardia at the age of 1 year but had never had impaired exercise capacity or a syncopal episode before admission.The possible diagnosis of acquired complete atrioventricular block was carefully ruled out,and then the diagnosis of CCHB was made.According to existing guidelines,permanent pacemaker implantation was recommended,but the patient declined.With regular follow-up for 28 years,the patient had an unusually good outcome without any invasive intervention or medicine.She had an uneventful pregnancy and led a normally active life without any symptoms of low cardiac output or syncopal recurrence.CONCLUSION This case implies that CCHB in adulthood may have good clinical outcomes and does not always require permanent pacemaker implantation.

Clopidogrel induced arthritis and fever

A 67-year-old woman with a history of diabetes mellitus and smoking was admitted to our hospital with chest pain for one month. Her resting electrocardiogram and serial troponin I measurements were normal. As the coronary artery angiography performed in another hospital showed severe lesions in the left anterior descending artery, we planned to perform the intervention on the left anterior descending artery by stent. Before the procedure, clopidogrel （300 mg loading dose） was initiated.

Effect of Endothelial Microparticles Induced by Hypoxia on Migration and Angiogenesis of Human Umbilical Vein Endothelial Cells by Delivering MicroRNA-19b

Background: Microparticles (MPs) are small extracellular plasma membrane particles shed by activated and apoptotic cells, which are involved in the development of atherosclerosis. Our previous study found that microRNA (miR)-19b encapsulated within endothelial MPs (EMPs) may contribute to the upregulation of circulating miR-19b in unstable angina patients. Hypoxia is involved in atherosclerosis as a critical pathological stimulus. However, it still remains unclear whether the increase of miR-19b levels in EMPs is related to hypoxia and if the effect of miR-19b - wrapped within EMPs - stimulates hypoxia on vascular endothelial cells. This study aimed to explore the changes of miR-19b in EMPs induced by hypoxia as well as their effects on endothelial cells.Methods: Human umbilical vein endothelial cells (HUVECs) were culturedin vitro and arranged to harvest EMPs in two parts: the first part consisted of EMPcontrol and EMPhypoxia and the second part included EMPvehicle, EMPNC mimic, and EMPmiR-19b mimic. Cell migration was detected by scratch migration and transwell chamber migration. Angiogenesis was assessed by tube formation assays. Furthermore, we predicted the target gene of miR-19b by bioinformatics analysis, and luciferase assay was used to verify the targeted gene of miR-19b. Data were analyzed by one-way analysis of variance. Student’st-test was used when two groups were compared.Results: Compared with EMPcontrol- and EMPhypoxia-inhibited migration of cells by scratch migration assay (80.77 ± 1.10 vs. 28.37 ± 1.40,P < 0. 001) and transwell chamber migration assay (83.00 ± 3.46 vs. 235.00 ± 16.52,P < 0.01), the number of tube formations was markedly reduced by 70% in the EMPhypoxia group (P < 0.001)in vitro analysis of HUVECs. Meanwhile, a strong inhibition of migration and tube formation of HUVECs in the presence of miR-19b-enriched EMPmiR-19b mimic was observed. This effect might be due to the delivery of miR-19b in EMPs. Transforming growth factor-β2 (TGFβ2) was predicted to be one of the target genes of miR-19b, and we further confirmed thatTGFβ2 was a direct target gene of miR-19b using the luciferase assay. The expression ofTGFβ2 in HUVECs was inhibited by treatment with EMPhypoxia and EMPmiR-19b mimic .Conclusions: MiR-19b in EMPs induced by hypoxia could reduce endothelial cell migration and angiogenesis by downregulating TGFβ2 expression, which may have inhibited the progression of atherosclerosis.

MiR-106b-5p Inhibits Tumor Necrosis Factor-α-induced Apoptosis by Targeting Phosphatase and Tensin Homolog Deleted on Chromosome 10 in Vascular Endothelial Cells

Background： Apoptosis of endothelial cells （ECs） plays a key role in the development of atherosclerosis and there are also evidence indicated that phosphatase and tensin homolog deleted on chromosome 10 （PTEN） is a viable target in therapeutic approaches to prevent vascular ECs apoptosis. Aberrant miR-106b-5p expression has been reported in the plasma of patients with unstable atherosclerotic plaques. However, the role and underlying mechanism of miR-106-5p in the genesis of atherosclerosis have not been addressed. In this study, we explored the anti-apoptotic role of miR-106-5p by regulating PTEN expression in vascular ECs. Methods： Real-time reverse transcription polymerase chain reaction （RT-PCR） was performed to detect the expression levels of miR-106b-5p in human atherosclerotic plaques and normal vascular tissues. Human umbilical vein endothelial cells （HUVEC） were transfected with miR-106b-5p mimic or negative control mimic, and apoptosis was induced by serum starvation and tumor necrosis factor-α （TN F-α） treat. Western blotting and real-time RT-PCR experiments were used to detect PTEN expression levels and TN F-α-induced apoptosis was evaluated by the activation of caspase-3 and cell DNA fragmentation levels in HUVEC. Results： The expression ofmiR-106b-5p was significantly downregulated in plaques than in normal vascular tissues. TNF-α significantly downregulated miR-106b-5p expression levels and upregulated activation of caspase-3 and cell DNA fragmentation levels in HUVEC. Overexpression ofmiR-106b-5p with miR-106b-5p mimic inhibited PTEN expression and TNF-α-induced apoptosis in HUVEC. Luciferase reporter assays confirmed that miR-106b-5p binds to PTEN mRNA 3＇ untranslated region site, Conclusion： MiR-106b-5p could inhibit the expression of PTEN in vascular ECs, which could block TNF-α-induced activation of caspase-3, thus prevent ECs apoptosis in atherosclerosis diseases.