Association Of Intracranial Artery Stenosis And Carotid Artery Disease In Patients With Nash And Normal Subjects
DOI:
https://doi.org/10.64252/tkppfg25Keywords:
NASH, Intracranial Stenosis, Carotid Artery Disease, MR Angiography, Doppler Ultrasonography, Cerebrovascular Risk, Atherosclerosis, Metabolic Syndrome, Non-Alcoholic Fatty Liver Disease, Vascular ImagingAbstract
Background: Non-alcoholic steatohepatitis (NASH), an advanced form of non-alcoholic fatty liver disease (NAFLD), is increasingly recognized not only as a hepatic disorder but also as a systemic condition with significant cardiovascular implications. Chronic metabolic inflammation, insulin resistance, and endothelial dysfunction in NASH patients are known to accelerate atherosclerosis and vascular remodeling. While the association between NASH and systemic vascular disease is well-established, its impact on cerebrovascular circulation—specifically intracranial artery stenosis (ICAS) and extracranial carotid artery disease—remains underexplored. Understanding the vascular burden in NASH patients could offer critical insight into their elevated stroke risk and support the need for comprehensive vascular screening in this population.
Aim: To assess the association between intracranial artery stenosis and carotid artery disease in patients with biopsy-proven or radiologically suspected NASH, and to compare these vascular findings with those of age- and sex-matched normal subjects using non-invasive imaging techniques.
Materials and Methods: This cross-sectional observational study included 80 adult subjects divided into two groups: Group A (40 patients with confirmed NASH based on clinical, biochemical, and imaging criteria) and Group B (40 normal controls without liver disease or cardiovascular risk factors). All subjects underwent high-resolution carotid Doppler ultrasonography to assess intima-media thickness (IMT), plaque presence, and carotid stenosis. Intracranial arterial imaging was performed using time-of-flight MR angiography (TOF-MRA) to evaluate stenosis in major arteries including the middle cerebral artery (MCA), anterior cerebral artery (ACA), and posterior circulation. Intracranial stenosis was defined as >50% luminal narrowing. Vascular parameters were compared between groups using appropriate statistical tests, with p < 0.05 considered significant.
Results: Patients with NASH demonstrated significantly higher carotid IMT (0.85 ± 0.11 mm vs. 0.63 ± 0.09 mm, p < 0.001) and greater prevalence of carotid plaques (37.5% vs. 10.0%, p = 0.004) compared to controls. Intracranial arterial stenosis was detected in 30% of NASH patients, predominantly in the MCA and vertebrobasilar arteries, whereas only 5% of controls had detectable ICAS (p = 0.003). The combined presence of both carotid atherosclerosis and intracranial stenosis was observed in 22.5% of NASH patients, suggesting a systemic pattern of vascular involvement. A positive correlation was observed between carotid IMT and the presence of ICAS (r = 0.51, p < 0.01), indicating a shared pathophysiological mechanism.
Conclusion: This study highlights a significant association between NASH and both intracranial and extracranial atherosclerotic disease. Patients with NASH exhibit a higher burden of carotid atherosclerosis and intracranial stenosis compared to normal subjects, even in the absence of traditional cardiovascular risk factors. These findings support the implementation of vascular screening protocols in patients with NASH to identify subclinical cerebrovascular disease and prevent ischemic events through early intervention.