The study aimed to investigate the correlation between PGR and baPWV. As we predicted, both RbaPWV and LbaPWV were significantly correlated with patients’ PGR levels. Negative correlations between PGR and RbaPWV/LbaPWV were observed in the unadjusted model. Furthermore, this negative correlation persisted even after adjusting for gender, age, and other potential confounding factors.

Smooth curve fitting revealed a nonlinear relationship between PGR and both RbaPWV and LbaPWV. We identified inflection points at 22.5 and 22.3, respectively. Below these inflection points, each unit increase in PGR was associated with a 6.3 cm/s decrease in RbaPWV and a 7.0 cm/s decrease in LbaPWV. Given that PGI primarily originates from gastric chief cells, while PGII is derived from all gastric glands as well as duodenal mucosa [15, 16], a decline in PGR levels occurs in the context of chronic gastric mucosal atrophy.

A study conducted in 2012 investigated the risk of myocardial infarction, stroke, and all-cause mortality, concluding that chronic atrophic gastritis —defined by PGI levels below 70 ng/mL and a PGI/PGII ratio under 3—was not a significant risk factor for cardiovascular disease or mortality [17]. Conversely, a 2021 study contrasted PGI, PGII, and PGR levels between patients with atherosclerotic cardiovascular disease (ASCVD) and a healthy control group. This research indicated that low PGR levels increased risk factor for ASCVD, whereas high PGR levels were inversely correlated with ASCVD [9]. The divergence in findings could be attributed to the initial focus of the 2012 study on chronic atrophic gastritis (PGI < 70 ng/mL and PGI/PGII < 3) as a baseline for subsequent analyses. In actuality, the cardiovascular risks among the study subjects might have escalated prior to any notable change in PGI and PGII levels, which are triggered by damage to gastric chief cells. Our investigation determined that when PGR fell below 22.3, a linear negative correlation was established between PGR and RbaPWV; similarly, when PGR was under 22.5, a linear negative correlation was established between PGR and LbaPWV. These results, aligning with the 2021 study, affirm that PGR levels and atherosclerosis are interrelated.

This supports the notion that arterial stiffness is present prior to the onset of gastric mucosal atrophy, which is defined by a PGR greater than 3. Previous research has demonstrated that serum PGI levels decrease as one ages, whereas PGII levels generally increase in individuals under the age of 60 and decline in those over 60 [18]. Consequently, PGR tends to rise before the age of 60 and diminish thereafter. A study published in 2017 further indicated that PGR is influenced by additional variables such as Helicobacter pylori infection, renal function, and fasting blood glucose levels [19]. Age, renal impairment, and elevated fasting glucose are already recognized as risk factors for atherosclerosis. Henceore, these factors may act as mediators linking a decline in PGR with the onset of atherosclerosis. Notably, our research discovered that even after accounting for these and other confounding variables like gender and creatinine levels, the inverse correlation between PGR and baPWV remained significant.

Elevated intravascular pressure and increased shear stress resulting from atherosclerosis contribute to endothelial dysfunction and stimulate the production and deposition of collagen in the arterial wall, factors closely associated with atherosclerosis itself [20]. PWV is the most widely used metric for gauging arterial stiffness. Existing literature not only identifies a link between PWV and coronary atherosclerosis but also establishes a positive correlation between PWV and the severity of coronary artery disease [21, 22]. Furthermore, studies indicate that PWV correlates not just with cerebral and cerebellar vascular diseases, but also with the thickening of the carotid intima-media and the formation of carotid plaques [23,24,25]. These findings suggest that PWV is positively correlated with the progression of atherosclerosis [26]. Contrary to these trends, our research identified an inverse relationship between PGR levels and atherosclerosis. This implies that manipulating PGR levels could be a viable strategy for mitigating the progression of atherosclerosis in patients.

Our research established that PGR, a crucial marker for gastrointestinal function, also has a correlated with peripheral vascular stiffness. This observation could offer novel perspectives for the future prevention and treatment of arterial atherosclerosis. Nonetheless, the mechanisms underlying the decline in PGR levels and its subsequent influence on arterial stiffness require further investigation.

However, the study is not without limitations. Conducted at a single center and primarily involving participants from the indigenous population in southern China, he results may not be universally applicable to diverse populations in other regions. Furthermore, the study’s cross-sectional design allows for establishment for association between PGR and RbaPWV/LbaPWV but does not provide evidence for causal relationships. Consequently, future research should aim for multi-center studies to validate to the generalizability and reliability of these findings across varied populations and to further investigate the causal links between PGR and arterial stiffness.