Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Más filtros

Bases de datos
Tipo de estudio
Tipo del documento
País de afiliación
Intervalo de año de publicación
1.
Am J Cardiol ; 101(2): 199-202, 2008 Jan 15.
Artículo en Inglés | MEDLINE | ID: mdl-18178406

RESUMEN

The present study was undertaken to assess the effect of statins on collagen type I degradation and C-reactive protein in patients with coronary artery disease and atrial fibrillation. One hundred six patients with coronary artery disease and atrial fibrillation were studied: 40 (36 men, mean age 72 +/- 8 years) treated with a statin and 66 (48 men, mean age 74 +/- 9 years) not treated with a statin. Serum concentrations of carboxy-terminal telopeptide of collagen type I, an index of collagen type I degradation, and high-sensitivity C-reactive protein were measured in all patients. Carboxy-terminal telopeptide of collagen type I levels were significantly higher (p <0.001) in statin-treated patients (0.64 ng/ml, 95% confidence interval [CI] 0.57 to 0.71) compared with nonstatin-treated patients (0.38 ng/ml, 95% CI 0.31 to 0.44). These changes were independent of cholesterol levels (before or after therapy). Statin-treated patients had significantly lower (p <0.001) C-reactive protein levels (0.25 mg/dl, 95% CI 0.23 to 0.28) compared to statin nonusers (1.1 mg/dl, 95% CI 0.92 to 1.25). In conclusion, this study suggests that therapy with statins in patients with coronary artery disease and atrial fibrillation is associated with an increase in collagen degradation and an attenuation of inflammation, independently of cholesterol lowering.


Asunto(s)
Fibrilación Atrial/tratamiento farmacológico , Proteína C-Reactiva/metabolismo , Colágeno Tipo I/sangre , Enfermedad de la Arteria Coronaria/tratamiento farmacológico , Inhibidores de Hidroximetilglutaril-CoA Reductasas/uso terapéutico , Anciano , Fibrilación Atrial/sangre , Fibrilación Atrial/complicaciones , Enfermedad de la Arteria Coronaria/sangre , Enfermedad de la Arteria Coronaria/complicaciones , Femenino , Humanos , Inhibidores de Hidroximetilglutaril-CoA Reductasas/administración & dosificación , Masculino , Resultado del Tratamiento
2.
Int J Cardiol ; 170(2): 173-81, 2013 Dec 10.
Artículo en Inglés | MEDLINE | ID: mdl-24215985

RESUMEN

BACKGROUND: Lipid core expansion is partly responsible for the conversion of a stable atherosclerotic lesion to a rupture-prone plaque. Intraplaque hemorrhage contributes to the accumulation of cholesterol within unstable plaques. In the present study, we investigated, using a rabbit model of atherosclerosis, the extent to which diet-induced increases in cholesterol content of erythrocyte membranes (CEM) contribute to lipid core expansion and the modulatory effect of rosuvastatin use. METHODS AND RESULTS: Rabbits fed with atherogenic diet (0.75% cholesterol) for 5 months exhibited advanced atherosclerotic lesions (mean plaque area, 0.39 ± 0.03 mm(2)), and lipid core size was associated with the concentration-time integral (CTI) of CEM levels (r=0.567, P=0.004) independent of other established predictors of lipid core size. Further experiments were performed by feeding rabbits atherogenic diet (1% cholesterol) for 3 months, followed by either normal diet or normal diet plus rosuvastatin for the next 3 months. Although no differences were observed in total plaque area between both groups, administration of rosuvastatin was associated with significantly smaller lipid cores, fewer macrophages within the lipid core, less microvessels as well as with lower CTI of CEM levels compared to normal diet alone. Moreover, intraplaque erythrocyte membranes covered a smaller lipid core area in rabbits under rosuvastatin plus normal diet as opposed to rabbits under diet alone. CONCLUSIONS: Increased CEM levels, induced by high-cholesterol diet, are associated with lipid core growth. Ingestion of a potent HMG-CoA reductase inhibitor (rosuvastatin) may decrease CEM levels, and this effect may contribute to regression of the lipid core.


Asunto(s)
Aterosclerosis/tratamiento farmacológico , Colesterol/metabolismo , Membrana Eritrocítica/efectos de los fármacos , Fluorobencenos/farmacología , Placa Aterosclerótica/tratamiento farmacológico , Pirimidinas/farmacología , Sulfonamidas/farmacología , Animales , Aterosclerosis/metabolismo , Aterosclerosis/patología , Dieta Aterogénica , Modelos Animales de Enfermedad , Membrana Eritrocítica/metabolismo , Membrana Eritrocítica/patología , Inhibidores de Hidroximetilglutaril-CoA Reductasas/farmacología , Masculino , Placa Aterosclerótica/metabolismo , Placa Aterosclerótica/patología , Conejos , Rosuvastatina Cálcica
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA