Coronary Atherosclerosis and Subclinical Cerebral Small Vessel Disease: A Robust Association Beyond Intracranial Atherosclerosis and Cardiac Systolic Function

Background This study investigates the associations between asymptomatic coronary atherosclerosis and subclinical cerebral small vessel disease (CSVD) in a community‐based population, considering potential confounding by intracranial atherosclerosis and cardiac systolic function. Methods Community‐dwelling residents from the PRECISE (Polyvascular Evaluation for Cognitive Impairment and Vascular Events) study in Lishui City, China (n=3021; mean age, 61.2±6.4 years; 46.4% male), underwent assessment of coronary and intracranial atherosclerotic burden via coronary computed tomography angiography and high‐resolution magnetic resonance imaging. CSVD burden and imaging markers (white matter hyperintensities, lacunes, enlarged perivascular spaces, and cerebral microbleeds) were evaluated. Results Advanced coronary atherosclerosis was significantly associated with higher total CSVD burden (adjusted common odds ratio [cOR], 1.54 [95% CI, 1.18–2.01]; P =0.002) after adjusting for age, sex, and vascular risk factors. Heavier coronary atherosclerosis was linked to increased odds of lacunes (adjusted OR, 2.52 [95% CI, 1.59–3.97]; P <0.001), WMHs burden (adjusted OR, 1.46 [95% CI, 1.06–2.02]; P =0.020), modified WMHs burden (adjusted cOR, 1.47 [95% CI, 1.12–1.93]; P =0.005), and moderate‐to‐severe basal ganglia‐enlarged perivascular spaces (adjusted OR, 1.70 [95% CI, 1.17–2.48]; P =0.005), but not cerebral microbleeds ( P >0.05). These associations remained after further adjusting for left ventricular ejection fraction and intracranial atherosclerosis. Mendelian randomization analyses suggested a potential role of chronic inflammation in linking coronary atherosclerosis and CSVD. Conclusions This community‐based study demonstrates an association between advanced coronary atherosclerosis and CSVD that persists after accounting for intracranial atherosclerosis and cardiac systolic dysfunction. Mendelian randomization analyses provide preliminary evidence suggesting that chronic inflammation may contribute to this association. Longitudinal studies incorporating circulating inflammatory markers are warranted to clarify these associations.