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Jawahar L. Mehta, Reviewer Critique of “Enhanced Plasma Soluble CD40 Ligand Levels in Essential Hypertensive Patients With Blunted Nocturnal Blood Pressure Decrease”, American Journal of Hypertension, Volume 20, Issue 1, January 2007, Page 77, https://doi.org/10.1016/j.amjhyper.2006.07.019
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In this issue to the journal, Desideri et al1 have shown, not unexpectedly, that hypertensive subjects have greater carotid intima–media thickness (IMT) than control normotensive subjects. They also show that hypertensive subjects with blunted nocturnal blood pressure (BP) decrease (nondippers) have higher plasma levels of soluble CD4 ligand (sCD40L) than hypertensive subjects with normal physiologic decline in BP (dippers). Circulating sCD40L levels correlated with carotid IMT in hypertensive subjects and on multivariate analysis were the major determinant of IMT. Circulating sCD40L levels also correlated with plasma 8-iso-PGF1α levels, a marker of lipid peroxidation and urinary albumin excretion. Furthermore, there was a weak, but significant, direct relationship between IMT and nocturnal systolic BP and an inverse correlation between IMT and nocturnal systolic BP decrease. These data are consistent with other studies showing that lack of physiologic BP variability correlates with end-organ damage in experimental animals.2
Inflammatory markers such as C-reactive protein, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and sCD40L, have been shown to be elevated in patients with vascular disease, and may be used as predictors of disease onset and outcome.3 Whether inflammation is a cause of vascular disease or a consequence of vascular injury, remains to be shown.4 The sCD40L levels in plasma have been shown to be elevated in patients with atherothrombotic disease syndromes by many investigators, including the authors of the present study. The source of circulating sCD40L could be vascular endothelial cells, smooth muscle cells, inflammatory cells or platelets, or all of these cell types. The authors appear to suggest that the hemodynamic stress state in hypertension may activate platelets with subsequent shedding of CD40L. They provide correlation between the lipid peroxidation product 8-iso-PGF1α and sCD40L as evidence for their suggestion.
