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Atherosclerotic disease is a primary cause of cardiovascular morbidity and mortality. This disease is generally undiagnosed before the onset of symptoms or complications. Experimental and clinical evidence indicate that inflammation is central to the initiation and progression of atherosclerosis.1 Therefore, vascular inflammation may serve as a potential marker of the disease process itself. Although potentially useful in risk stratification, the current systemic markers of inflammation lack sufficient disease specificity to be used satisfactory as screening tools in cardiovascular disease. The inaccuracy of current inflammatory markers may reflect the fact that these markers are neither derived primarily from the vascular wall nor produced primarily by cells involved in the vascular inflammatory process. Furthermore they may signal inflammation in a number of different organs and tissues, which may or may not have direct implications for the vasculature. Because of heterogeneity of the disease phenotype in the population, a single marker may not provide sufficient biological information for an acute assessment of vascular damage, and, therefore, it may be more interesting to look into a cluster of inflammatory markers. Human studies support an association between inflammatory gene polymorphisms and subclinical and clinical cardiovascular disease.2The predictive value of arterial stiffness or 1:elasticity for cardiovascular morbidity and mortality has now been very well established.3 Arterial …

Genetic Variants of Inflammatory Markers and Arterial Stiffness