High Salt Intake and Atherosclerosis Progression—Not Only via Blood Pressure: A Narrative Review

Excessive dietary salt intake remains a critical and underestimated global health concern, strongly associated with increased cardiovascular disease risk. While the relationship between salt and arterial hypertension is well established, accumulating evidence highlights additional, blood pressure-independent mechanisms linking high salt intake with the progression of atherosclerosis. Beyond its hypertensive effects, high dietary salt directly damages the vascular endothelium by disrupting the glycocalyx, reducing nitric oxide synthesis, and increasing endothelial stiffness and inflammation. Excess sodium also impairs glycosaminoglycan buffering capacity and promotes immune cell adhesion, even in normotensive individuals. Furthermore, salt-induced dysbiosis of the gut microbiota alters the metabolic and inflammatory environment, lowering beneficial short-chain fatty acids and increasing pro-atherogenic metabolites such as trimethylamine N-oxide. Recent findings also implicate salt-driven modulation of hematopoiesis via Th17 cytokines, which enhances the production of pro-inflammatory monocytes that accelerate plaque development. These findings support the notion that high salt intake may be an independent and modifiable residual risk factor for atherosclerotic cardiovascular disease. Reducing dietary sodium—particularly from processed foods—should therefore remain a central component of both primary and secondary cardiovascular prevention. Although the optimal range of salt intake remains under discussion, a moderate reduction to below 5 g/day is considered safe and beneficial.