Key result
Low-grade inflammation has a bidirectional pathophysiological relationship with arterial hypertension, and biomarkers like hs-CRP show predictive value for hypertension incidence and clinical outcomes.
This review summarizes the pathophysiological links between low-grade inflammation and arterial hypertension, emphasizing the predictive value of inflammatory biomarkers in hypertensive patients.
Supports hs-CRP for hypertension risk stratification; leaves open whether targeting inflammation improves outcomes.
Over the last years, ample data have demonstrated the pivotal role of low-grade inflammation in the pathophysiology of atherosclerosis and cardiovascular disease. It is well established that inflammatory activation, serving either as a substrate, in the chronic phase of atherosclerotic disease, or as a trigger, in the acute phase, increases cardiovascular events. Considering hypertension, the inflammatory process is implicated in its pathophysiology through a bidirectional relationship since arterial hypertension may enhance inflammation and vice versa. Inflammatory biomarkers such as highsensitivity C-reactive protein, have shown predictive value for both the incidence of hypertension and the clinical outcomes in hypertensive patients. In the present review, data on the association between arterial hypertension and low-grade inflammation will be reported and potential pathophysiological pathways and clinical implications underlying this association will be discussed.
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Pietri et al. (2015) conducted a review in Arterial hypertension and low-grade inflammation. Low-grade inflammation was evaluated. Low-grade inflammation has a bidirectional pathophysiological relationship with arterial hypertension, and biomarkers like hs-CRP show predictive value for hypertension incidence and clinical outcomes.
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