Background: Serum uric acid (UA) has been shown to be an independent predictor of outcome in the general population and in patients with heart failure. There are, however, limited data regarding the prognostic value of UA in the context of acute coronary syndromes (ACS) particularly in medium-term follow up and the available results are contradictory. Materials and methods: Study of consecutive patients admitted with an ACS (with and without ST-segment elevation) at a single-centre coronary care unit. Primary endpoint was all-cause mortality at 1-year follow up. We evaluated if serum UA is an independent predictor of outcome and if it has any added value on top of GRACE risk score for risk prediction. Results: We included 683 patients, mean age 64±13 years, 69% males. In-hospital and 1-year mortality were 4.5 and 7.6% respectively. The best cut-off of UA to predict 1-year mortality was 6.25 mg/dl (sensitivity 59%, specificity 72%) and 30.2% of the patients had an increased UA according to this cut off. Independent predictors of UA were male gender (β= 0.078), body mass index (β=0.163), diuretics before admission (β=0.142), and admission serum creatinine (β=0.403). One-year mortality was significantly higher in patients with increased UA (15.5 vs. 4.2%, p<0.001; log rank, p<0.001). After adjustment, both increased UA as a categorical variable (HR 2.25, 95% CI 1.23-4.13, p=0.008) and as a continuous variable (HR 1.26, 95% CI 1.13-1.41, p<0.001) are independent predictors of mortality. The AUC increases only slightly after inclusion of UA in the model with GRACE risk score (from 0.78 to 0.79, p=0.350). Both models had a good fit; however, model fit worsened after inclusion of UA. Overall, the inclusion of UA in the original was associated with an improvement in both the net reclassification improvement (continuous NRI=44%), and the integrated discrimination improvement (IDI=0.052) suggesting effective reclassification. Conclusions: Serum UA is an independent predictor of all-cause mortality in medium-term after the whole spectrum of ACS and has an added value for risk stratification.
Background: Red Cell Distribution Width (RDW) prognostic value in patients with Acute Coronary Syndrome (ACS) has been well validated whereas that of Platelet Distribution Width (PDW) is less well known. Objectives: Investigate the incremental prognostic value, on top of GRACE risk score, of a new variable resulting from the combination of RDW and PDW. Methods: Consecutive patients with ACS. Complete blood count, with RDW and PDW, was obtained. Primary endpoint was one-year all-cause mortality and Cox regression models were used to measure the influence of RDW and PDW on patients' survival time. A new combination categorical variable (RDW/PDW) was created with both discretized RDW and PDW and logistic regression models were used. Predictive value and discriminative ability of the model with GRACE risk score alone and of the model with inclusion of RDW/PDW was assessed. Results: We included 787 patients. Hospital and one-year mortality rates were 5.1% and 7.8%, respectively. Both continuous RDW and PDW were independent predictors of death. The best cut-off for RDW was 13.9%, and 14.5% for PDW. Inclusion of RDW/PDW in a model with GRACE risk score improved the AUC from 0.81 (95% CI 0.75-0.86) to 0.84 (95% CI 0.79-0.90) (p=0.024) with an improvement in total NRI (56%) and IDI (0.048). Conclusions: Simple markers such as RDW and PDW can be useful in risk stratification of death after ACS. Combining both markers with GRACE risk score improved the predictive value for all-cause mortality and reduced the estimated risk of those who did not die.
Background: Chronic exposure to industrial noise is known to affect biological systems, namely, by inducing fibrosis in the absence of inflammatory cells. In rat hearts exposed to this environmental hazard, we have previously found myocardial and perivascular fibrosis. The acoustic spectrum of industrial environments is particularly rich in high-intensity infrasound (b20 Hz), whose effects on the heart are unknown. We evaluated the morphological changes induced by IFS in rat coronaries in the presence and absence of dexamethasone. Methods: Adult Wistar rats were divided into three groups: group A (GA)-IFS (b20 Hz, 120 dB)-exposed rats for 28 days treated with dexamethasone; group B (GB)-IFS-exposed rats; group C (GC)-age-matched controls. The midventricle was prepared for observation with an optical microscope using 100× magnification. Thirty-one arterial vessels were selected (GA 8, GB 10, GC 13). The vessel caliber, thickness of the wall, and perivascular dimensions were quantified using image J software. Mann-Whitney and Kruskal-Wallis tests were used to compare the groups for lumen-to-vessel wall (L/W) and vessel wall-to-perivascular tissue (W/P) ratios. Results: IFS-exposed rats exhibited a prominent perivascular tissue. The median L/W and median W/P ratios were 0.54 and 0.48, 0.66 and 0.49, and 0.71 and 0.68, respectively, in GA, GB, and GC. The W/P ratio was significantly higher in GC compared with IFS-exposed animals (P=.001). The difference was significant between GC and GB (P=.008) but not between GC and GA. Conclusion: IFS induces coronary perivascular fibrosis that differs under treatment with corticosteroid.
Background: Noise is an important environmental risk factor. Industrial environments are rich in high-intensity infrasound (hi-IFS), which we have found to induce myocardial and coronary perivascular fibrosis in rats. The effects of exposure to IFS on the ventricles have been studied, but not on the atria. We hypothesized that rats exposed to hi-IFS develop atrial remodeling involving fibrosis and connexin 43, which we sought to evaluate. Material and methods: Seventy-two Wistar rats, half exposed to hi-IFS (120 dB, < 20 Hz) during a maximum period of 12 weeks and half age-matched controls, were studied. Atrial fibrosis was analyzed by Chromotropeaniline blue staining. The immunohistochemical evaluation of Cx43 was performed using the polyclonal antibody connexin-43 m diluted 1:1000 at 4°C overnight. Digitized images were obtained with an optical microscope using 400× magnifications. The measurements were performed using image J software. A two-way ANOVA model was used to compare the groups. Results: The mean values of the ratio "atrial fibrosis / cardiomyocytes" increased to a maximum of 0.1095 ± 0,04 and 0.5408 ± 0,01, and of the ratio "CX43 / cardiomyocytes" decreased to 0.0834 ± 0,03 and 0.0966 ± 0,03, respectively in IFS-exposed rats and controls. IFS-exposed rats exhibited a significantly higher ratio of fibrosis (p < .001) and lower ratio of Cx43 (p = .009). Conclusion: High-intensity infrasound exposure leads to an increase in atrial interstitial fibrosis and a decrease in connexin 43 in rat hearts. This finding reinforces the need for further experimental and clinical studies concerning the effects of exposure to infrasound.
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