RESUMEN
New methods of studying the human genome offer novel ways to examine the relationship between biomarkers and common, chronic human diseases. As an example, we will review a large genomics study (Elliott et al, JAMA 2009; 302:37-48) that concluded that C-reactive protein (CRP) is likely not a cause of coronary heart disease, although it is a marker for it.
Asunto(s)
Biomarcadores , Proteína C-Reactiva/análisis , Enfermedades Cardiovasculares/genética , Genoma Humano , Enfermedades Cardiovasculares/patología , Estudio de Asociación del Genoma Completo , Humanos , Factores de RiesgoRESUMEN
As the leading cause of death worldwide and a major cause of disability, cardiovascular disease remains a central focus of basic research, pharmacological treatment, surgical interventions, and long-term care. Inherited, monogenic syndromes have provided insight into pathophysiological mechanisms across the range of cardiovascular diseases. With the advent of post-Human Genome Project resources and technology, there has been a flood of research aimed at genome-wide predisposition markers, pharmacogenetics, and genomic signatures in complex cardiovascular disorders. Genomic research has both further elucidated the impact of genes previously identified in cardiovascular disease development and progression and discovered genomic regions as yet unknown to be associated with cardiovascular outcomes. The promise of personalized medicine lies in combining this genetic information with other biomarkers to tailor preventive and therapeutic strategies to individual patients for effective management, fewer adverse events, and preventive care.