The Combined Effect of the Systemic Immune-Inflammation Index and Aortic Valve Calcification on Major Adverse Cardiovascular Events in Patients with Coronary Heart Disease.
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引用次数: 0
Abstract
Background: The combined effect of systemic immune-inflammation index (SII) and aortic valve calcification (AVC) on the risk of major adverse cardiovascular events (MACE) in patients with coronary heart disease (CHD) remains unclear. This study aimed to investigate their combined association with MACE in CHD.
Methods: This retrospective cohort study included 846 CHD patients. SII was calculated as platelet count × neutrophil count / lymphocyte count, and AVC status was determined by echocardiography. Patients were divided into four groups based on median SII and AVC presence: Low SII + AVC (-), High SII + AVC (-), Low SII + AVC (+), and High SII + AVC (+). Cox regression, subgroup and sensitivity analyses assessed the association between SII + AVC and MACE.
Results: Multivariate Cox regression revealed that, compared to the Low SII + AVC (-), MACE risk increased 6.542-fold in the High SII + AVC (+) group and 1.605-fold in the High SII + AVC (-) group (P < 0.05). Subgroup analysis indicated that, compared to the Low SII + AVC (-), MACE risk was significantly elevated in the High SII + AVC (-) group for patients over 60, both genders, with hypertension, hyperlipidemia, or without diabetes (P < 0.05). In the Low SII + AVC (+) group, MACE risk was elevated only in males (P < 0.05). The High SII + AVC (+) group had increased MACE risk in all subgroups except those with diabetes (P < 0.05). After excluding patients with estimated glomerular filtration rate < 60 mL/min/1.73m², the high SII + AVC (+) group remained significantly associated with increased MACE risk (P = 0.001), as did the High SII + AVC (-) group (P = 0.031).
Conclusion: The combination of SII and AVC is significantly associated with MACE risk in patients with CHD.
期刊介绍:
An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.