No abstract

BackgroundCompared with whites, black Americans suffer from a disproportionate burden of cardiovascular disease (CVD). We hypothesized that racial differences in the prevalence of CVD could be attributed, in part, to impaired vascular function in blacks after adjustment for differences in risk factor burden.Methods and ResultsWe assessed vascular function in 385 black and 470 white subjects (mean age, 48±11 years; 45% male). Using digital pulse amplitude tonometry (EndoPAT) we estimated the reactive hyperemia index (RHI), a measure of microvascular endothelial function, and peripheral augmentation index (PAT‐AIx). Central augmentation index (C‐AIx) and pulse‐wave velocity (PWV) were measured as indices of wave reflections and arterial stiffness, respectively, using applanation tonometry (Sphygmocor). Compared with whites, blacks had lower RHI (2.1±0.6 versus 2.3±0.6, P<0.001), greater arterial wave reflections assessed as both PAT‐AIx (20.4±21.5 versus 17.0±22.4, P=0.01) and CAIx (20.8±12.3 versus 17.5±13.3, P=0.001), and greater arterial stiffness, measured as PWV (7.4±1.6 versus 7.1±1.6 m/s, P=0.001). After adjustment for traditional CVD risk factors, black race remained a significant predictor of lower RHI and higher PAT‐AIx and CAIx (all P<0.001) in all subjects and of higher PWV in men (P=0.01). Furthermore, these associations persisted in a subgroup analysis of “healthy” individuals free of CVD risk factors.ConclusionBlack race is associated with impaired microvascular vasodilatory function, and greater large arterial wave reflections and stiffness. Because impairment in these vascular indices may be associated with worse long‐term outcomes, they may represent underlying mechanisms for the increased CVD risk in blacks.

Objective-To investigate the efficacy of cholecalciferol (vitamin D 3 ) in raising serum ]D) levels and reducing parathyroid hormone (PTH) levels in patients with chronic kidney disease (CKD).Methods-In this double-blind, randomized controlled pilot study, participants with CKD stage 3 and 4 (estimated glomerular filtration rate, 15-59 mL/min/1.73 m 2 ), vitamin D insufficiency (serum 25[OH]D <30 ng/mL), and serum intact PTH levels >70 pg/mL were randomly assigned to receive either 50 000 IU of cholecalciferol or placebo once weekly for 12 weeks. Primary outcomes (25[OH] D and PTH levels) were measured at baseline, week 6, and week 12. Secondary outcomes (1,25-dihydroxvitamin D and bone turnover markers) were measured at baseline and week 12. Because of skewed data distribution, statistical analyses were performed on a logarithmic scale. The difference between the group means was exponentiated to provide the geometric mean ratio. A linear mixed model using an unstructured variance-covariance matrix was used to examine change in the primary and secondary outcomes over time.Results-Geometric mean serum 25(OH)D concentrations of the study groups were similar at baseline (P = .77). At week 6, a significant difference between the treatment and placebo groups was detected (P = .001); this difference was maintained at week 12 (P = .002). Among cholecalciferoltreated participants, serum 25(OH)D concentration increased on average from 17.3 ng/mL (95% confidence interval [CI],.2) at baseline to 49.4 ng/mL (95% CI, 33.9-72.0) at week 12. Astreated analysis indicated a trend toward lower PTH levels among cholecalciferol-treated participants (P = .07). Conclusion-Weekly cholecalciferol supplementation appears to be an effective treatment to correct vitamin D status in patients with CKD.

BackgroundExtremes of wall shear stress (WSS) have been associated with plaque progression and transformation, which has raised interest in the clinical assessment of WSS. We hypothesized that calculated coronary WSS is predicted only partially by luminal geometry and that WSS is related to plaque composition.Methods and ResultsTwenty‐seven patients with coronary artery disease underwent virtual histology intravascular ultrasound and Doppler velocity measurement for computational fluid dynamics modeling for WSS calculation in each virtual histology intravascular ultrasound segment (N=3581 segments). We assessed the association of WSS with plaque burden and distribution and with plaque composition. WSS remained relatively constant across the lower 3 quartiles of plaque burden (P=0.08) but increased in the highest quartile of plaque burden (P<0.001). Segments distal to lesions or within bifurcations were more likely to have low WSS (P<0.001). However, the majority of segments distal to lesions (80%) and within bifurcations (89%) did not exhibit low WSS. After adjustment for plaque burden, there was a negative association between WSS and percent necrotic core and calcium. For every 10 dynes/cm2 increase in WSS, percent necrotic core decreased by 17% (P=0.01), and percent dense calcium decreased by 17% (P<0.001). There was no significant association between WSS and percent of fibrous or fibrofatty plaque components (P=NS).ConclusionsIn patients with coronary artery disease: (1) Luminal geometry predicts calculated WSS only partially, which suggests that detailed computational techniques must be used to calculate WSS. (2) Low WSS is associated with plaque necrotic core and calcium, independent of plaque burden, which suggests a link between WSS and coronary plaque phenotype. (J Am Heart Assoc. 2012;1:e002543 doi: 10.1161/JAHA.112.002543.)

No abstract

Despite the higher STS PROM in TMVR patients, there was no difference in 1-year mortality between the TMVR and SMVR groups. Echocardiographic findings after TMVR were similar to SMVR at 30 days. There was a statistically significant difference in mitral gradient at 1 year, though this is likely not clinically important. TMVR may be an alternative to SMVR in patients with previous mitral bioprosthetic valves.

A total of 214 patients with acute PE were treated by SPE. The mean age was 56.0 ± 14.5 years, and 92 (43.6%) patients were female. Of those, 176 (82.2%) PEs were submassive and 38 (17.8%) were massive. Fifteen (7.0%) patients underwent concomitant cardiac procedures, with 10 (4.7%) having simultaneous valvular interventions and 5 (2.4%) undergoing concomitant bypass grafting. Cardiopulmonary bypass (CPB) was used for all cases. Cardioplegic arrest was used for 80 (37.4%) patients. The median CPB and aortic cross clamp times were 71.5 (interquartile range [IQR], 47.0-109.5) and 46.0 (IQR, 26.0-74.5), respectively. Notably, only 25 (11.7%) patients died in the hospital. Mortality was highest among the 28 patients who experienced preoperative cardiac arrest (9, 32.1%) CONCLUSIONS: These data represent the first multicenter experience with SPE for acute pulmonary emboli. Surgical pulmonary embolectomy for acute massive and submassive PE is safe and can be performed with acceptable in-hospital outcomes; the procedure should be included in the multimodality treatment of life-threatening pulmonary emboli.

Summary Objective Redox status and inflammation are important in the pathophysiology of numerous chronic diseases. Epidemiological studies have linked vitamin D status to a number of chronic diseases. We aimed to examine the relationships between serum 25-hydroxyvitamin D (25(OH)D) and circulating thiol/disulfide redox status and biomarkers of inflammation. Design This was a cross-sectional study of N=693 adults (449 females, 244 males) in an apparently healthy, working cohort in Atlanta, GA. Plasma glutathione (GSH), cysteine (Cys), and their associated disulfides were determined with high performance liquid chromatography, and their redox potentials (Eh GSSG and Eh CySS) were calculated using the Nernst equation. Serum inflammatory markers included interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α, assayed on a multiplex platform; and C-reactive protein (CRP), assayed commercially. Relationships were assessed with multiple linear regression analyses. Results Serum 25(OH)D was positively associated with plasma GSH (β ± SE: 0.002 ± 0.0004) and negatively associated with plasma Eh GSSG (β ± SE: −0.06 ± 0.01) and Cys (β ± SE: −0.01 ± 0.003) (P<0.001 for all); statistical significance remained after adjusting for age, gender, and race, percent body fat, and traditional cardiovascular risk factors (P=0.01-0.02). The inverse relationship between serum 25(OH)D and CRP was confounded by percent body fat, and full adjustment for covariates attenuated serum 25(OH)D relationships with other inflammatory markers to non-statistical significance. Conclusions Serum 25(OH)D concentrations were independently associated with major plasma thiol/disulfide redox systems, suggesting that vitamin D status may be involved in redox-mediated pathophysiology.