Arterial stiffness has been recognized as a marker of cardiovascular disease and associated with long-term worse clinical outcomes in several populations. Age, hypertension, smoking, and dyslipidemia, known as traditional vascular risk factors, as well as diabetes, obesity, and systemic inflammation lead to both atherosclerosis and arterial stiffness. Targeting multiple modifiable risk factors has become the main therapeutic strategy to improve arterial stiffness in patients at high cardiovascular risk. Additionally to life style modifications, long-term ω-3 fatty acids (fish oil) supplementation in diet may improve arterial stiffness in the population with hypertension or metabolic syndrome. Pharmacological treatment such as renin-angiotensin-aldosterone system antagonists, metformin, and 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors were useful in individuals with hypertension and diabetes. In obese population with obstructive sleep apnea, weight reduction, aerobic exercise, and continuous positive airway pressure treatment may also improve arterial stiffness. In the populations with chronic inflammatory disease such as rheumatoid arthritis, a use of antibodies against tumor necrosis factor-alpha could work effectively. Other therapeutic options such as renal sympathetic nerve denervation for patients with resistant hypertension are investigated in many ongoing clinical trials. Therefore our comprehensive review provides knowledge in detail regarding many aspects of pathogenesis, measurement, and management of arterial stiffness in several populations, which would be helpful for physicians to make clinical decision.

CHIEF will be among the largest Eastern Asian armed forces cohort, in which physical status was strictly evaluated to follow up the hospitalization events for severe illness.

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Sunitinib malate, an oral multitargeted tyrosine kinase inhibitor (TKI), has been approved for the treatment of advanced renal cell carcinoma and gastrointestinal stromal tumors. It is supposed that this targeted approach improves antitumor activity with less toxicity than traditional chemotherapy. However, unanticipated cardiotoxicity related to TKIs has been reported. Less well described are the treatment and prognosis of patients with sunitinib-related cardiogenic shock. Here, we report a successfully treated case. In contrast to previous case reports, the shock status did not allow for standard heart failure treatment with angiotensin-converting enzyme inhibitor or beta-blocker. We used intra-aortic balloon counterpulsation, and the patient survived. Twenty-four days after onset, the patient's left ventricular ejection fraction had improved from 20% to 48%. To the best of our knowledge, this is the first case report of severe heart failure after sunitinib treatment in Taiwan. As the clinical application of TKIs expands, cardiologists and oncologists should be alert to the possible adverse cardiovascular effects and be ready to institute prompt treatment.

The clinical outcomes of different limus-based drug-eluting stents (DES) in a real-world setting have not been well defined. The aim of this study was to investigate the clinical outcomes of three different limus-based DES, namely sirolimus-eluting stent (SES), Endeavor zotarolimus-eluting stent (E-ZES) and everolimus-eluting stent (EES), using a national insurance claims database. We identified all patients who received implantation of single SES, E-ZES or EES between January 1, 2007 and December 31, 2009 from the National Health Insurance claims database, Taiwan. Follow-up was through December 31, 2011 for all selected clinical outcomes. The primary end-point was all-cause mortality. Secondary end-points included acute coronary events, heart failure needing hospitalization, and cerebrovascular disease. Cox regression model adjusting for baseline characteristics was used to compare the relative risks of different outcomes among the three different limus-based DES. Totally, 6584 patients were evaluated (n=2142 for SES, n=3445 for E-ZES, and n=997 for EES). After adjusting for baseline characteristics, we found no statistically significant difference in the risk of all-cause mortality in three DES groups (adjusted hazard ratio [HR]: 1.14, 95% confidence interval [CI]: 0.94-1.38, p=0.20 in E-ZES group compared with SES group; adjusted HR: 0.77, 95% CI: 0.54-1.10, p=0.15 in EES group compared with SES group). Similarly, we found no difference in the three stent groups in risks of acute coronary events, heart failure needing hospitalization, and cerebrovascular disease. In conclusion, we observed no difference in all-cause mortality, acute coronary events, heart failure needing hospitalization, and cerebrovascular disease in patients treated with SES, E-ZES, and EES in a real-world population-based setting in Taiwan.

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Modified low-density lipoprotein may moderate the association of baseline hs-CRP with incident cardiac events in the Asian populations To the Editor, Baseline high-sensitivity C-reactive protein (hs-CRP) concentrations have been associated with incident cardiovascular disease in the general population, mainly in Western countries; however the association was controversial in the Asian populations [1,2]. Notably, the association was consistently present in the Asian patients with established cardiovascular disease [3,4]. Ogita et al. [5] further found that chronic kidney disease (CKD) may be a moderator for the association between baseline hs-CRP concentrations and the major adverse cardiovascular events in Japanese patients with stable coronary artery disease and who were implanted with first-generation drug-eluting stents. Similarly, Sung et al. [6] also revealed that baseline high-density lipoprotein cholesterol (HDL-C) concentrations may be a moderator for the association between hs-CRP concentrations and coronary artery calcium score in the Korean general population. Whether CRP is a causal or bystander of cardiovascular disease has been an ongoing debate since 2000. CRP could increase lectinlike oxidized low-density-lipoprotein (LDL) receptor 1 (LOX-1) release from macrophages to uptake LDL-cholesterol (LDL-C), and opsonize LDL-C to become capable of uptake by macrophages in the arterial wall [7]. Additionally, CRP may activate complement along with LOX-1 or by binding to modified LDL [8,9]. Evidence appears to indicate that CRP may contribute to the development of arteriosclerosis in the presence of modified LDL such as oxidized LDL [10]. Therefore, hs-CRP concentrations may be correlated with modified LDL concentrations, which were atherogenic and resulted in cardiovascular events, if HDL-C concentrations were low [11]. As we know, carbamylated LDL, occurring primarily in the presence of CKD, has been reported with an association with endothelial dysfunction. CRP incorporated with carbamylated LDL in CKD may lead to a higher risk of cardiovascular disease as well [12]. To date, the hs-CRP association with cardiovascular disease was not present in about one third of observational studies or clinical trials. In conclusion, modified LDL such as oxidized LDL and carbamylated LDL may be a potential moderator for the association of hs-CRP with cardiovascular disease in the Asian populations.

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