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Interaction between dyslipidaemia, oxidative stress and inflammatory response in patients with angiographically proven coronary artery disease

INTRODUCTION: Coronary artery disease (CAD) is emerging as the biggest killer of the 21st century. A number of theories have been postulated to explain the aetiology of atherosclerosis. The present study attempts to elucidate the interaction, if any, between inflammation, oxidative stress and dyslip...

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Detalles Bibliográficos
Autores principales: Tayal, D, Goswami, B, Chaudhary, M, Mallika, V, Tyagi, S
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Clinics Cardive Publishing 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3721930/
https://www.ncbi.nlm.nih.gov/pubmed/22331247
http://dx.doi.org/10.5830/CVJA-2010-092
Descripción
Sumario:INTRODUCTION: Coronary artery disease (CAD) is emerging as the biggest killer of the 21st century. A number of theories have been postulated to explain the aetiology of atherosclerosis. The present study attempts to elucidate the interaction, if any, between inflammation, oxidative stress and dyslipidaemia in CAD. METHODS: A total of 753 patients undergoing angiography were evaluated and 476 were included in the study. The parameters studied included complete lipid profile, and apolipoprotein B, ferritin and nitric oxide (NO) levels. Statistical analysis was carried out to determine the interrelationship between these parameters and the best predictor of CAD risk. Cut-off points were determined from the receiver operating characteristics curves, and the specificity, sensitivity, positive predictive value, negative predictive value, odds ratio and confidence intervals were calculated. RESULTS: The levels of the parameters studied increased with the stenotic state and a positive correlation was observed between ferritin, NO and apolipoprotein B. NO emerged as the most reliable predictor of CAD, with an area under the curve of 0.992 and sensitivity and specificity of 97 and 98%, respectively. CONCLUSION: Environmental and genetic risk factors for CAD interact in a highly complex manner to initiate the atherosclerotic process. These risk factors should be considered mutually inclusive, not exclusive when devising pharmacological interventions, as multi-factorial risk management is the cornerstone of CAD management