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BACKGROUND AND AIMS: Pharmacological lowering of inflammation has proven effective in reducing recurrent cardiovascular event rates. Aim of the current study is to evaluate lifestyle changes (smoking cessation, weight loss, physical activity level increase, alcohol moderation, and a summary lifestyle improvement score) in relation to change in plasma C-reactive protein (CRP) concentration in patients with established cardiovascular disease. METHODS: In total, 1794 patients from the UCC-SMART cohort with stable cardiovascular disease and CRP levels ≤10 mg/L, who returned for a follow-up study visit after median 9.9 years (IQR 5.4-10.8), were included. The relation between changes in smoking status, weight, physical activity, alcohol consumption, a summary lifestyle improvement score and change in plasma CRP concentration was evaluated with linear regression analyses. RESULTS: Smoking cessation was related to a 0.40 mg/L decline in CRP concentration (ß-coefficient -0.40; 95%CI -0.73,-0.07). Weight loss (per 1SD = 6.4 kg) and increase in physical activity (per 1 SD = 48 MET hours per week) were related to a decrease in CRP concentration (ß-coefficients -0.25; 95%CI -0.33,-0.16 and -0.09; 95%CI -0.17,-0.01 per SD). Change in alcohol consumption was not related to CRP difference. Every point higher in the summary lifestyle improvement score was related to a decrease in CRP concentration of 0.17 mg/L (ß-coefficient -0.17; 95%CI -0.26,-0.07). CONCLUSIONS: Smoking cessation, increase in physical activity, and weight loss are related to a decrease in CRP concentration in patients with stable cardiovascular disease. Patients with the highest summary lifestyle improvement score have the most decrease in CRP concentration. These results may indicate that healthy lifestyle changes contribute to lowering systemic inflammation, potentially leading to a lower cardiovascular risk in patients with established cardiovascular disease.
Assuntos
Doenças Cardiovasculares , Proteína C-Reativa/análise , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/prevenção & controle , Seguimentos , Estilo de Vida Saudável , Humanos , Inflamação , Fatores de RiscoRESUMO
AIMS: The aim is to investigate (multifocal) cardiovascular calcification in patients with established cardiovascular disease (CVD), regarding prevalence, risk factors, and relation with recurrent CVD or vascular interventions. Coronary artery calcification (CAC), thoracic aortic calcification (TAC) (including ascending aorta, aortic arch, descending aorta), mitral annular calcification (MAC), and aortic valve calcification (AVC) are studied. METHODS: The study concerned 568 patients with established CVD enrolled in the ORACLE cohort. All patients underwent computed tomography. Prevalence of site-specific and multifocal calcification was determined. Ordinal regression analyses were performed to quantify associations of risk factors with cardiovascular calcification, and Cox regression analyses to determine the relation between calcium scores and recurrent CVD or vascular interventions. RESULTS: Calcification was multifocal in 76% (N = 380) of patients with calcification. Age (per SD) was associated with calcification at all locations (lowest OR 2.17; 99%CI 1.54-3.11 for ascending aorta calcification). Diabetes mellitus and systolic blood pressure were associated with TAC, whereas male sex was a determinant of CAC. TAC and CAC were related to the combined endpoint CVD or vascular intervention (N = 68). In a model with all calcium scores combined, only CAC was related to the combined outcome (HR 1.39; 95%CI 1.15-1.68). CONCLUSION: Cardiovascular calcification is generally multifocal in patients with established CVD. Differences in associations between risk factors and calcification at various anatomical locations stress the divergence in pathophysiological pathways. CAC is most strongly related to recurrent CVD or vascular interventions independent of traditional risk factors, and independent of heart valve and thoracic aorta calcification.
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OPINION STATEMENT: Heart valve disease is a major health burden, treated by either valve repair or valve replacement, depending on the affected valve. Nearly 300,000 valve replacements are performed worldwide per year. Valve replacement is lifesaving, but not without complications. The in situ tissue-engineered heart valve is a promising alternative to current treatments, but the translation of this novel technology to the clinic still faces several challenges. These challenges originate from the variety encountered in the patient population, the conversion of an implant into a living tissue, the highly mechanical nature of the heart valve, the complex homeostatic tissue that has to be reached at the end stage of the regenerating heart valve, and all the biomaterial properties that can be controlled to obtain this tissue. Many of these challenges are multidimensional and multiscalar, and both the macroscopic properties of the complete heart valve and the microscopic properties of the patient's cells interacting with the materials have to be optimal. Using newly developed in vitro models, or bioreactors, where variables of interest can be controlled tightly and complex mixtures of cell populations similar to those encountered in the regenerating valve can be cultured, it is likely that the challenges can be overcome.