Table 2.

Proposed pathogenetic mechanisms of H. pylori and MetS-induced inflammation on arterial hypertension.

Mechanism	Comment	References
Upregulation of inflammatory mediators	MetS-related inflammatory mediators damage directly or indirectly the vascular walls and trigger atherosclerosis	[93,94,95,96,97]
Cag A	H. pylori virulence factor connected with: (1) greater inflammatory response, (2) atherosclerosis, and (3) coronary artery disease.	[100,101,102]
VacA	H. pylori virulence factor connected with: (1) gastric inflammation and carcinogenesis, (2) chemotactic activation of bone marrow-derived mast cells and stimulation and damage to the blood–brain barrier, (3) promotion of intracellular H. pylori survival, and (4) brain access of activated monocytes (the Trojan horse theory)	[45,49]
Cross reactivity of H. pylori	Autoimmune response triggering by H. pylori cross-reactivity → vascular endothelial damage → MetS-related ischemic disorders	[108,109,110]
Atrophic gastritis	Vitamin B12 and folic acid deficiency induced by H. pylori and/or MetS → hyperhomocysteinemia resulting in: (1) vascular endothelial cells damage and (2) MetS-related atherosclerosis—arterial hypertension	[111,112,113,114,115,116]
Diastolic blood pressure	Higher concentrations of H. pylori/MetS-related fibrinogen → inhibition of endothelial nitric oxide and nitric oxide synthase → vasoconstriction and augmented peripheral vascular tension but not cardiac output → isolated diastolic blood pressure	[117,118]

CagA, Cytotoxin-associated gene A; H. pylori, Helicobacter pylori; MetS, metabolic syndrome; VacA, vacuolating cytotoxin A.