Key result
Higher Lp(a) linked to ~24% lower risk of acute lacunar infarction.
Why the study?
Studies on the correlation between serum lipoprotein(a) levels and acute lacunar infarction remain inconclusive.
Are serum lipoprotein(a) levels associated with the presence of acute lacunar infarction in a Chinese population?
Case-Control (n=1,978)
Are serum lipoprotein(a) levels associated with the presence of acute lacunar infarction in a Chinese population?
Answers are grounded in this paper and cite their sources.
Lower serum lipoprotein(a) levels are independently associated with the presence of acute lacunar infarction, suggesting a distinct mechanism compared to typical atherosclerotic cardiovascular diseases.
Background Serum lipoprotein(a) [Lp(a)] is a well-established risk factor for atherosclerotic cardiovascular diseases. However, studies on the correlation between Lp(a) and acute lacunar infarction (ALI) remain inconclusive. We conducted a case-control study to investigate the association between serum Lp(a) levels and ALI in a Chinese population. Methods We consecutively enrolled 989 patients with ALI (719 males, 270 females; mean age 64.63 ± 11.97 years) and an equal number of sex-matched controls with available brain MRI from the Departments of Neurology and Geriatrics. Univariate and multivariable binary logistic regression analyses were used to examine the relationships between Lp(a) concentrations and the presence of ALI. Results Serum Lp(a) levels were significantly lower in the ALI group compared to controls. Multivariable logistic regression revealed an independent inverse association between Lp(a) levels and the presence of ALI (odds ratio [OR], 0.76; 95% confidence interval [CI], 0.66–0.87; P < 0.001. The trend held across age and sex subgroups (age ≥ 60 years: OR, 0.71; 95% CI, 0.60–0.84; P < 0.001; age < 60 years: OR, 0.76; 95% CI, 0.59–0.98; P = 0.034; males: OR, 0.80; 95% CI , 0.69–0.94; P = 0.007; females: OR, 0.68; 95% CI, 0.53–0.88; P = 0.003). For lesion locations, inverse associations existed in the basal ganglia and brainstem/cerebellum lesions, but not in the subcortical white matter. Conclusions This study demonstrates that lower serum Lp(a) levels are independently associated with the presence of ALI. The clinical implications and underlying biological mechanisms of this observation warrant further investigation.
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Chen et al. (2026) conducted a case-control in Acute lacunar infarction (ALI) (n=1,978). Serum lipoprotein(a) [Lp(a)] levels vs. Sex-matched controls was evaluated on Presence of acute lacunar infarction (OR 0.76, 95% CI 0.66-0.87, p=<0.001). Serum Lp(a) levels demonstrated an independent inverse association with the presence of acute lacunar infarction (OR 0.76; 95% CI 0.66-0.87; P<0.001).
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