Prospective Comparison of Plasma Biomarker and Traditional Risk Factor Profiles for Incident Isolated Atherosclerotic Disease and Incident Isolated Abdominal Aortic Aneurysm

Abstract

Background: Traditional risk factors for atherosclerotic disease (AD) are well-known, of which some are relevant also for abdominal aortic aneurysms (AAA). The present study compares the importance of plasma biomarkers and traditional risk factor profiles for incident AD without concomitant AAA (isolated AD) and AAA without concomitant AD (isolated AAA) during long-term follow-up.Methods: In the Malmö Diet and Cancer Study—cardiovascular cohort, 5,381 participants were free from atrial fibrillation or flutter, AD (coronary artery disease, atherothrombotic ischemic stroke, carotid artery disease, or peripheral artery disease), and AAA underwent blood sampling under standardized fasting conditions between 1991 and 1994. Cox proportional hazards regression analysis was used to calculate hazard ratios (HR) with 95% CIs.Results: During a median follow-up of 23.1 years, 1,152 participants developed isolated AD, and 44 developed isolated AAA. Adjusted HR for lipoprotein-associated phospholipase A2 (mass) (HR 1.53, 95% CI 1.14–2.04 vs. HR 1.05, 95% CI.99–1.12) was higher for incident isolated AAA compared to incident isolated AD, respectively. Mid-regional pro-adrenomedullin (MR-proADM) was associated with incident isolated AD (HR 1.17, 95% CI 1.1–1.25) and incident isolated AAA (HR 1.47, 95% CI 1.15–1.88). MR-proADM was correlated (r = 0.32; p < 0.001) to body mass index (BMI), and BMI was associated with increased risk of incident isolated AAA (HR 1.43, 95% CI 1.02–2). No participant with diabetes mellitus (DM) at baseline developed isolated AAA (0/44), whereas DM was associated with an increased risk of isolated AD (HR 2.57, 95% CI 2.08–3.18). Adjusted HR for male sex (HR 4.8, 95% CI 2.42–9.48, vs. HR 1.76, 95% CI 1.56–1.98) and current smoking (HR 4.79, 95% CI 2.42–9.47 vs. HR 1.97, 95% CI 1.73–2.23) were higher in the incident isolated AAA group compared to the incident isolated AD group, respectively.Conclusions: The data supports the view that components of vascular inflammation and cardiovascular stress drives AAA development, whereas glycated cross-links in abdominal aortic wall tissue may have a plausible role in reducing AAA risk in individuals with DM.

Burden of Aortic Aneurysm and Its Attributable Risk Factors from 1990 to 2019: An Analysis of the Global Burden of Disease Study 2019

“…A Mendelian randomization study showed that BMI did not impact aortic aneurysms ( 42 ). But a prospective study showed that BMI was related to a rising risk of incident isolated AAA ( 43 ). High BMI or obesity would lead to atherosclerosis and hypertension, which were important incentives for aortic aneurysm ( 44 , 45 ).…”

Current Prognostic Biomarkers for Abdominal Aortic Aneurysm: A Comprehensive Scoping Review of the Literature

“…For example, several studies have demonstrated that it can be used as an early marker of heart failure and hypertrophic cardiomyopathy [ 63 , 64 , 65 ]. Two studies conducted by Acosta et al in 2018 [ 11 ] and 2021 [ 34 ] investigated MR-proANPs association with AAA; however, both studies noted no significant association between the biomarker level and incidence of AAA.…”

“…Due to its proteolytic activity, AAA has been hypothesized to potentially be associated with AAA. Acosta et al [ 34 ] investigated the association between Cystatin C levels and AAA; however, they noted no significant association between Cystatin C and the incidence of AAA.…”

“…Instead, mid-regional proADM (MR-proADM), the precursor of ADM, is used as a surrogate biomarker [ 189 ]. Finally, MR-proADM has been associated with predicting both carotid artery disease and AAA [ 34 ].…”

Kardiovaskuläre Folgen des Rauchens

“…Aus dem bisher Gesagten geht der große Einfluss des Rauchens auf das gesamte kardiovaskuläre System hervor. Betrachtet man den Einfluss des Rauchens auf die Entwicklung abdomineller Aortenaneurysmen (AAA), so ist das Risiko, ein solches zu entwickeln, bei Rauchern im Vergleich zu Nichtrauchern noch einmal deutlich höher (HR 4,79) als für die Entwicklung eines isolierten CKS, ischämischen Schlaganfalls oder einer PAV (HR 1,97; [ 2 ]).…”