BackgroundBenefits of antiplatelet agents in preventing future cardiovascular events have been well established. However, the prescription pattern of antiplatelet usage in patients with acute coronary syndrome (ACS) is rarely investigated. Hence, Taiwan ACute CORonary Syndrome Descriptive Registry (T‐ACCORD Registry) aimed to evaluate medical practices in Taiwan in managing ACS patients.HypothesisThe guidelines of antiplatelet treatment is not properly implanted in the management of ACS patients.MethodsThis prospective observational study was performed between April 2004 and December 2006 in 27 hospitals in Taiwan. A total of 1331 patients with unstable angina or non–ST‐elevation myocardial infarction (NSTEMI) discharged from hospitals was analyzed.ResultsThe patients with older age, lower hemoglobin levels, or previous cardiovascular ischemic diseases were less likely to receive aspirin at discharge, whereas patients with NSTEMI were less likely to receive clopidogrel at discharge. The prescription of dual antiplatelet agents declined rapidly from 61.8% at discharge to 12.6% at 12 months. The most common reason for clopidogrel discontinuation was recorded as physician's judgment. Dual antiplatelet treatment for 9 months or longer was associated with lower 1‐year mortality. Percutaneous coronary intervention (PCI) was the only factor leading to dual antiplatelet therapy for at least 9 months.ConclusionsOur registry showed that underlying medical conditions may affect antiplatelet prescriptions at discharge. During the first year following an ACS episode, the prescription rate of dual antiplatelet therapy declined over time, mainly due to physician's judgment leading to the discontinuation of clopidogrel. Adherence to dual antiplatelet treatment was associated with lower total mortality at 1 year. Copyright © 2010 Wiley Periodicals, Inc.

The patients with multi-vessel CAD had significantly more global and territorial dyssynchrony at early post-stress than at rest. Such quantitative measures of myocardial stunning may assist in the diagnosis of multi-vessel CAD.

Dipyridamole-induced worsening of LVEF, as shown by Tl-201 gated SPECT, is a valuable nonperfusion marker of significant CAD. Although the sensitivity of LVEF worsening in detecting significant CAD is only 35%, the specificity is as high as 93%.

Platelet-derived growth factor (PDGF) is a potent stimulator of growth and motility of smooth muscle cells (SMCs) and fibroblasts. Abnormalities of PDGF/PDGF receptor (PDGFR) are thought to contribute to vascular diseases and malignancy. We previously showed that natural carotenoid lycopene can directly bind to PDGF-BB and affect its related functions in vascular SMCs. In this study we examined lycopene effect on PDGF-AA/-AB-induced signaling and migration in SMCs and fibroblasts. We found that lycopene inhibited PDGF-AA-induced SMC and fibroblast migration in a concentration-dependent manner. Lycopene reduced PDGF-AA signaling, including phosphorylation in PDGFR-alpha and its downstream protein kinases/enzymes. It also inhibited PDGF-AB-induced signaling and cell migration. However, lycopene did not affect PDGF-induced reactive oxygen species production and H2O2-induced PDGFR phosphorylation. The binding analysis revealed that lycopene but not beta-carotene could directly bind to PDGF-AA in vitro and in plasma and this binding competitively inhibited lycopene interaction with PDGF-BB, suggesting that lycopene bound to PDGF-AA/-BB at a homologous/similar region within PDGF. Moreover, the docking and binding analyses predicted that the lycopene-binding region within PDGF was located at loop 2 region. Taken together, we provide here evidence that lycopene interacts with PDGF-AA/-AB and compromises their intracellular signaling, leading to a marked inhibition on PDGF-AA/-AB-induced migration in both SMCs and fibroblasts. We also predicted its binding region within PDGF and proved its anti-vascular injury effect in vivo. The results, together with our previous findings, suggest lycopene special affinity/effect for PDGF family and its possible application in prevention in vascular diseases and malignancy.

Background and objectiveCOPD patients with community-acquired pneumonia (CAP) have worse clinical outcomes, as compared to those without COPD. Cardiovascular disease (CVD) is a common comorbidity for COPD patients. Whether COPD with comorbid CVD will increase the risk of CAP is not well investigated. The incidence and factors associated with CAP in COPD patients with and without CVD were analyzed.MethodsThe medical records of patients with newly diagnosed COPD between 2007 and 2010 were reviewed. The patients’ characteristics, medical history of CVD, occurrence of CAP, and type of medication were recorded. Kaplan–Meier curves were used to assess the differences in cumulative incidence of CAP. Cox’s proportional hazards regression model was used to determine the adjusted hazard ratios with 95% confidence intervals in relation to factors associated with CAP in COPD patients with and without CVD.ResultsAmong 2,440 patients, 475 patients (19.5%) developed CAP during the follow-up period. COPD patients who developed CAP were significantly older, had lower forced expiratory volume in 1 second, frequent severe exacerbation and comorbid CVD, as well as received inhaled corticosteroid (ICS)-containing therapy than those without CAP. The cumulative incidence of CAP was higher in COPD patients with CVD compared to those without CVD. Patients who received ICS-containing therapy had significantly increased risk of developing CAP compared to those who did not.ConclusionFor patients with COPD, comorbid CVD is an independent risk factor for developing CAP. ICS-containing therapy may increase the risk of CAP among COPD patients.