Objective-One potential mechanism through which obesity exerts adverse effects on the vascular system is by increasing aortic stiffness, a change known to be predictive of increased cardiovascular mortality. The aim of this study was to investigate the pathophysiology that links obesity to aortic stiffening. Approach and Results-Obese (ob/ob) mice were used to examine physical, morphological, and molecular changes in the aorta in response to obesity. ob/ob mice had increased aortic pulse wave velocity and tissue rigidity. ob/ob aorta exhibited decreases of lysyl oxidase (LOX) activity and cross-linked elastin, and increases of elastin fragmentation and elastolytic activity. The aortas of ob/ob mice were surrounded by a significant amount of proinflammatory and pro-oxidative perivascular adipose tissue. In vitro studies revealed that the conditioned medium from differentiated adipocytes or the perivascular adipose tissue of ob/ob mice attenuated LOX activity. Furthermore, inhibition of LOX in wild-type lean mice caused elastin fragmentation and induced a significant increase in pulse wave velocity. Finally, we found that obese humans had stiffer arteries and lower serum LOX levels than do normal-weight humans. Conclusion-Our results demonstrated that obesity resulted in aortic stiffening in both humans and mice, and established a causal relationship between LOX downregulation and aortic stiffening in obesity.
BackgroundThe American Heart Association Get With the Guidelines (GWTG) program has improved care quality of acute myocardial infarction (AMI) with important implications for other countries in the world. This study evaluated the incidence and care of AMI in Taiwan and assessed the compliance of GWTG in Taiwan.Methods and ResultsWe used the Taiwan National Health Insurance Research Database (1999–2008) to identify hospitalized patients ≥18 years of age presenting with AMI. The temporal trends of annual incidence and care quality of AMI were evaluated. The age‐adjusted incidence of AMI (/100 000 person‐years) increased from 28.0 in 1999 to 44.4 in 2008 (P<0.001). The use of guideline‐based medications for AMI was evaluated. The use of dual antiplatelet therapy (DAPT) increased from 65% in 2004 to 83.9% in 2008 (P<0.001). Angiotensin‐converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) was used in 72.6% in 2004 and 71.7% in 2008 (P=NS) and β‐blocker was used in 60% in 2004 and 59.7% in 2008 (P=NS). Statin use increased from 32.1% to 50.1% from 2004 to 2008 (P<0.001). The in‐hospital mortality decreased from 15.9% in 1999 to 12.3% in 2008 (P<0.0001). Multivariable analysis showed that DAPT, ACE inhibitor/ARB, β‐blocker, and statin use during hospitalization were all associated with reduced in‐hospital mortality in our AMI patients.ConclusionsAMI incidence was increasing, but the guideline‐based medications for AMI were underutilized in Taiwan. Quality improvement programs, such as GWTG, should be promoted to improve AMI care and outcomes in Taiwan.
In real-world AMI Taiwanese patients, ticagrelor seemed to offer better anti-ischemic protection than clopidogrel, without an increase in the rate of major bleeding. A large-scale randomized trial is needed to assess the efficacy and safety of ticagrelor in East Asian AMI patients.
Increased PSI was associated with increased procollagen type I carboxyterminal propeptide and diastolic dysfunction in hypertension. Postsystolic shortening was associated with delayed diastolic lengthening which contributed to diastolic dysfunction in hypertension.
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