BackgroundThe link between elevated serum uric acid (SUA) levels and cardiovascular disease (CVD)–related mortality in the elderly population remains inconclusive. Nutritional status influences both SUA and CVD outcomes. Therefore, we investigated whether SUA‐predicted mortality and the effect‐modifying roles of malnourishment in older people.Methods and ResultsA longitudinal Taiwanese cohort including 127 771 adults 65 years and older participating in the Taipei City Elderly Health Examination Program from 2001 to 2010 were stratified by 1‐mg/dL increment of SUA. Low SUA (<4 mg/dL) strata was categorized by malnourishment status defined as Geriatric Nutritional Risk Index <98, serum albumin <38 g/L, or body mass index <22 kg/m2. Study outcomes were all‐cause and CVD‐related mortality. Cox models were used to estimate hazard ratios (HRs) of mortality, after adjusting for 20 demographic and comorbid covariates. Over a median follow‐up of 5.8 years, there were 16 439 all‐cause and 3877 CVD‐related deaths. Compared with the reference SUA strata of 4 to <5 mg/dL, all‐cause mortality was significantly higher at SUA <4 mg/dL (HR, 1.16; 95% confidence interval, 1.07–1.25) and ≥8 mg/dL (HR, 1.13; confidence interval, 1.06–1.21), with progressively elevated risks at both extremes. Similarly, increasingly higher CVD‐related mortality was found at the SUA level <4 mg/dL (HR, 1.19; confidence interval, 1.00–1.40) and ≥7 mg/dL (HR, 1.17; confidence interval, 1.04–1.32). Remarkably, among the low SUA (<4 mg/dL) strata, only malnourished participants had greater all‐cause and CVD‐related mortality. This modifying effect of malnourishment remained consistent across subgroups.Conclusions SUA ≥8 or <4 mg/dL independently predicts higher all‐cause and CVD‐related mortality in the elderly, particularly in those with malnourishment.

It has recently been shown that in proteins the atomic mean-square displacement (or B-factor) can be related to the number of the neighboring atoms (or protein contact number), and that this relationship allows one to compute the B-factor profiles directly from protein contact number. This method, referred to as the protein contact model, is appealing, since it requires neither trajectory integration nor matrix diagonalization. As a result, the protein contact model can be applied to very large proteins and can be implemented as a high-throughput computational tool to compute atomic fluctuations in proteins. Here, we show that this relationship can be further refined to that between the atomic mean-square displacement and the weighted protein contact-number, the weight being the square of the reciprocal distance between the contacting pair. In addition, we show that this relationship can be utilized to compute the cross-correlation of atomic motion (the B-factor is essentially the auto-correlation of atomic motion). For a nonhomologous dataset comprising 972 high-resolution X-ray protein structures (resolution <2.0 A and sequence identity <25%), the mean correlation coefficient between the X-ray and computed B-factors based on the weighted protein contact-number model is 0.61, which is better than those of the original contact-number model (0.51) and other methods. We also show that the computed correlation maps based on the weighted contact-number model are globally similar to those computed through normal model analysis for some selected cases. Our results underscore the relationship between protein dynamics and protein packing. We believe that our method will be useful in the study of the protein structure-dynamics relationship.

The incidence of distal SINE seemed to be high; however, there were also low rates of death and complications after TEVAR for aortic dissection using stainless steel-based stent grafts. Complicated distal SINE can successfully be resolved by distal endograft implantation. Excessive oversizing of the distal stent graft, as measured by the true lumen area, may be a significant factor causing delayed distal SINE. Precise size selection is crucial for the distal end of the stent, especially for high taper ratio dissection pathology in which the implantation sequence of a distal small-sized stent graft first might be considered to prevent future distal SINE.

Background-Substantial infective endocarditis (IE)-related morbidity and mortality may occur even after successful treatment. However, no previous study has explored long-term hard end points (ie, stroke, myocardial infarction, heart failure, cardiovascular death) in addition to all-cause mortality in IE survivors. Methods and Results-A nationwide population-based cohort study was conducted among IE survivors identified with the use of the Taiwan National Health Insurance Research Database during 2000 to 2009. IE survivors were defined as those who survived after discharge from first hospitalization with a diagnosis of IE. A total of 10 116 IE survivors were identified. IE survivors were matched to control subjects without IE at a 1:1 ratio through the use of propensity scores. The primary outcomes were stroke, myocardial infarction, readmission for heart failure, and sudden cardiac death or ventricular arrhythmia. The secondary outcomes were repeat IE and all-cause mortality. Compared with the matched cohort, IE survivors had higher risks of ischemic stroke (adjusted hazard ratio [aHR], 1.59; 95% confidence interval [CI], 1.40-1.80), hemorrhagic stroke (aHR, 2.37; 95% CI, 1.90-2.96), myocardial infarction (aHR, 1.44; 95% CI, 1.17-1.79), readmission for heart failure (aHR, 2.24; 95% CI, 2.05-2.43), sudden death or ventricular arrhythmia (aHR, 1.69; 95% CI, 1.44-1.98), and all-cause death (aHR, 2.27; 95% CI, 2.14-2.40). Risk factors for repeat IE were older age, male sex, drug abuse, and valvular replacement after an initial episode of IE. Conclusion-Despite treatment, the risk of long-term major adverse cardiac events was substantially increased in IE survivors. (Circulation. 2014;130:1684-1691.)Key Words: endocarditis ◼ epidemiology ◼ heart failure ◼ mortality ◼ myocardial infarction ◼ stroke © 2014 American Heart Association, Inc.Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIRCULATIONAHA.114.012717Continuing medical education (CME) credit is available for this article. Go to http://cme.ahajournals.org to take the quiz. addition, a recent nationwide population-based study of patients with IE in Sweden found that the increased risk of long-term mortality persists for up to 5 years. 12 Although the long-term mortality of patients with IE has been studied previously, hard end points other than mortality have not been considered by exploring the risk of major adverse cardiac events (MACEs), including stroke, myocardial infarction, heart failure, cardiovascular death, and all-cause death, in these patients.To reduce the effects of potential confounders stemming from inadequate control for comorbidities and underpowered sample sizes, we used Taiwan's National Health Insurance (NHI) Research Database (NHIRD) to conduct a propensity score-matching study. Our goal was to evaluate long-term adverse cardiac outcomes and mortality in a large, representative group of patients with IE compared with a matched cohort using this nationwide database. Methods Data SourceData were extracted from the NHIRD...