ASSOCIATION OF INFLAMMATION AND ATHEROGENIC DYSLIPIDEMIA WITH INCIDENT CARDIOMETABOLIC DIASEASE: A LONGITUDINAL COHORT STUDY
03 medical and health sciences
0302 clinical medicine
DOI:
10.1097/01.hjh.0001022264.98015.4d
Publication Date:
2024-05-22T10:12:52Z
AUTHORS (5)
ABSTRACT
Objective:
Inflammation and atherogenic dyslipidemia promote each other establishing a vicious circle. This study aimed to examine their joint association with cardiometabolic disease (CMD) and whether the temporal relationship between them is associated with risk of CMD.
Design and method:
This study included 78,211 participants without history of cardiovascular disease and diabetes mellitus at baseline in 2006. We categorized the participants into six groups according to their C-reactive protein (CRP, <1,1–3, or >=3 mg/L) level and atherogenic index of plasma (AIP, <-0.08 or >=-0.08). Incident CMD was defined as the first occurrence of a CMD event during follow-up, including cardiovascular disease (including myocardial infarction, coronary revascularization, heart failure, ischemic stroke, and hemorrhagic stroke) and type 2 diabetes mellitus (T2DM). Cox regression models were used to estimate the risk of CMD across CRP-AIP groups. The temporal relationship between CRP and AIP was assessed by cross-lagged analysis in the 53,715 participants who attended the resurvey in 2010. The association of this temporal relationship with subsequent CMD risk was examined by mediation analysis.
Results:
After adjusting for potential confounders, increased CRP and elevated AIP were cumulatively associated with a higher risk of CMD, where participants with a CRP of >=3 mg/L and an AIP of >=-0.08 had a hazard ratio of 1.63 (95% confidence interval [CI], 1.55–1.71) for CMD, 1.43 (95% CI, 1.33-1.55) for cardiovascular disease, and 1.71 (95% CI, 1.60-1.82) for T2DM, compared with those with low CRP and AIP values. (Table 1). In cross-lagged analysis, the standard regression coefficient from baseline CRP to follow-up AIP was greater than that from baseline AIP to follow-up CRP (0.069 [95% CI, 0.061–0.077] versus 0.014 [95% CI, 0.005–0.023], P difference <0.001) (Table 2). Furthermore, AIP partially mediated the effect of CRP on incident CMD. The mediation effect was 15.56% (95% CI, 12.87–18.25) for CMD, 10.03% (95% CI, 6.19–13.88) for cardiovascular disease, and 18.82% (95% CI, 15.36–22.28) for T2DM (Figure 1).
Conclusions:
CRP and AIP were additively associated with risk of CMD. Increased CRP might precede elevated AIP, and AIP partially mediated the association between CRP and incident CMD.
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