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Hypertension is the most common modifiable risk factor for cardiovascular disease (CVD)1 and is a leading cause of death globally.2 Hypertension and CVD share common antecedent risk factors which include physical inactivity, obesity and excess alcohol intake.3 Though these established risk factors explain a large proportion of hypertension risk, its pathogenesis is still not fully established as it appears that other additional lifestyle and genetic factors may be involved. There is therefore a need to identify and evaluate putative risk factors that may increase our knowledge of hypertension development, may have causal or predictive relevance, and which will help develop preventive and management strategies.
There is a wealth of evidence suggesting that inflammatory processes play a key role in the pathogenesis of coronary heart disease (CHD), which is the major manifestation of CVD.4 5 It is reported that the process of atherosclerosis is characterised by a chronic, low-grade inflammatory process.6 Indeed, both ‘upstream’ (proinflammatory cytokines such as interleukin-1 (IL-1), IL-6, IL-18, tumour necrosis factor-α (TNF-α)) and ‘downstream’ biomarkers (eg, C reactive protein (CRP) and fibrinogen) (table 1) have consistently been demonstrated to be associated with CHD risk in several epidemiological studies (table 2). Many ‘upstream’ markers regulate the hepatic synthesis of ‘downstream’ markers such as CRP and fibrinogen; however, IL-6 plays a central role in regulating the downstream inflammatory responsible for initiation and progression of the atherosclerotic process. Given the close link between hypertension and CVD and the established relationship between inflammation and CVD, it is plausible that inflammation would be linked to the risk of hypertension.
Based on the rationale that systematic inflammation may play a role in the development of hypertension and given the inconsistent evidence in the existing literature, …
Contributors Both authors have contributed essentially.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
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