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Background: There have been few studies done regarding young patients with ST-elevation myocardial infarction (STEMI). The purpose of this study was to investigate the clinical characteristics and coronary angiographic features in young patients with STEMI. Methods: We collected data on 849 consecutive patients with STEMI from 1992 to 2006. Baseline clinical characteristics, coronary anatomy, and outcome were compared in young (≤45 yrs) and older patients (>45 yrs). Results: Young patients presented 11.6% of all patients with STEMI. These patients were predominantly male (92.9% vs 80.3%, P < 0.001), more likely to smoke (75.8% vs 47.2%, P < 0.001), obese (48.2% vs 27.9%, P = 0.002), have higher triglyceride levels (176.9 ± 153.8 mg/dL vs 140.7 ± 112.7 mg/dL, P = 0.005), and lower high-density lipoprotein cholesterol (37.1 ± 7.9 mg/dL vs 42.8 ± 14.3 mg/dL, P = 0.005) than older patients. Also, younger patients had a shorter hospital stay (7.1 ± 4.9 d vs 8.5 ± 6.7 d, P = 0.04), less in-hospital morbidity (29.3% vs 39.7%, P = 0.02), and mortality (3.0% vs 12.3%, P = 0.002). Killip class III or IV could predict in-hospital morbidity and mortality in young patients. Both groups had similar rates of repeated percutaneous coronary intervention (PCI; 45.5% vs 41.5%, P = 0.23) and reinfarction (6.1% vs 3.2%, P = 0.32). Mortality rate during follow-up was significantly lower in younger patients (3.0% vs 19.6%, P < 0.001). Conclusion: Cigarette smoking, obesity, and dyslipidemia were the most important modifiable risk factors in young patients with STEMI. These patients had a better outcome than older patients without differences in repeated PCI and reinfarction between them. Only Killip class III or IV could predict in-hospital morbidity and mortality in young patients with STEMI.

In Taiwan, the incidence of non-ST segment elevation acute coronary syndrome (NSTE-ACS) continues to increase in recent years. The purpose of this guideline is to help health care professionals in Taiwan to use adequate tests and treatments for management of NSTE-ACS. For rapid diagnosis, in addition to history and physical examination, 0/3 h rapid diagnosis protocol with high sensitivity cardiac troponin assay is recommended in this guideline. Dual antiplatelet and anticoagulation therapies are important parts in the initial treatment. Risk stratification should be performed to identify high risk patients for early coronary angiography. Through evaluation of the coronary anatomy and other clinical factors, the decision for coronary revascularization, either by percutaneous coronary intervention or coronary artery bypass grafting, should be decided by the heart team. The duration of dual antiplatelet therapy should be given for at least 12 months after discharge. Other secondary preventive medications are also recommended for long term use.

BackgroundLeptin, produced mainly by white adipose tissue, is a hormone that promotes vascular smooth muscle cell (VSMC) migration and proliferation, a process involved in the pathophysiology of atherosclerosis. Leptin expression in human coronary artery smooth cell (HCASMC) is induced by hypoxia. However, our understanding of the process of atherosclerosis in HCASMC is only emerging. Since the mechanisms by which hypoxia regulates leptin in HCASMC are as yet unknown, this study aims to investigate the mechanics of molecular regulation of leptin expression in HCASMC under hypoxia. We subjected cultured HCASMCs to hypoxia for varying periods of time. Through use of different signal pathway inhibitors, we were able to sort out and identify the pathway through which hypoxia-induced leptin expression occurs.ResultsLeptin mRNA and protein levels increased after 2.5% hypoxia for 2-to-4 hours, with earlier expression of angiotensin II (AngII) and reactive oxygen species (ROS). The addition before hypoxia of the c-Jun N-terminal kinase (JNK) pathway inhibitor (SP600125), JNK small interfering RNA (siRNA), AngII receptor blockers (ARBs; losartan), or N-acetyl-L-cysteine (NAC, an ROS scavenger), had the effect of inhibiting JNK phosphorylation and leptin expression. Gel shift assay and luciferase promoter study showed that leptin/activator protein 1 (AP-1) binding and transcriptional activity to the leptin promoter increased after hypoxia, and SP600125, JNK siRNA, losartan, and NAC abolished the binding and transcriptional activity induced by hypoxia. The use of SP600125, JNK siRNA, losartan, and NAC effectively inhibited the binding and transcriptional activity induced by hypoxia. Migration and proliferation, ROS generation, and the presence of leptin in the nuclei of HCASMCs also increased under hypoxia.ConclusionHypoxia in HCASMCs increases leptin expression through the induction of AngII, ROS, and the JNK pathway to enhance atherosclerosis in HCASMCs.Electronic supplementary materialThe online version of this article (doi:10.1186/s12929-014-0109-8) contains supplementary material, which is available to authorized users.

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