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.

The LA had a slower recovery of tachycardia-induced changes of atrial electrophysiological properties, and this might play a critical role in initiation of AF.

In order to examine the functional differentiation of tumor cells of adenomatoid odontogenic tumor (AOT) as ameloblasts and to determine the participation of the extracellular matrix (ECM) in the formation of its characteristic histologic architecture, tissue samples from five cases of adenomatoid odontogenic tumor were examined by immunohistochemical staining for enamel proteins and ECM molecules. Amelogenin, enamelin, laminin, heparan sulfate proteoglycan, fibronectin, collagen type IV and type V were immunolocalized within the luminal space and along the inner rim of duct-like structures. Eosinophilic hyaline droplets within the whorled or rosette masses of tumor cells showed basically the same staining pattern as the luminal contents. High columnar tumor cells that formed duct-like structures were immunopositive for amelogenin, while the staining intensity decreased with flattening of the cells, which was a result of luminal growth. The findings suggest that the constituent cells of duct-like structures are differentiated once to ameloblasts but fail to mature further due instead to increased production of ECM molecules and due to their retention in the lumina. It is possible to regard these special structures in AOT as stromal pseudocysts.

No abstract