Introduction: Prevalence of nonsustained atrial fibrillation (NSAF), described as irregular atrial runs lasting shorter than 30-seconds, is higher in patients with ischemic stroke compared to stroke-free controls. Nonetheless, its role in causality of stroke and future cerebrovascular risk is still not established. Subclinical atherosclerotic burden and vascular stiffness are more prevalent, and have been shown to modify future risk of vascular events in patients with atrial fibrillation (AF). We aimed to determine the relationship between NSAF and subclinical atherosclerosis, vascular dysfunction and cerebral microvascular disease.
Methods: Sonographic carotid distensibility metrics, carotid intima-media thickness (IMT), carotid plaque burden score (Ten Cate’s), middle cerebral artery (MCA) pulsatility index (PI) and cerebral white matter disease burden (Fazekas’ periventricular and subclinical scores) were studied in 263 stroke-free control subjects. 24-hour Holter monitoring documented NSAF in 27% of study population. Abnormality limits were set as mean±standard deviation.
Results: Compared to those without NSAF (age 62±8 yr, 43% male), subjects with NSAF (age 67±9 yr, 31% male) had significantly higher total carotid plaque burden score (p=0.009) and significantly lower common carotid artery carotid distensibility (p=0.019). Maximum and averaged IMT, carotid stiffness and elastic modulus, and asymptomatic significant (≥50%) carotid artery stenosis were numerically higher. Patients with NSAF had significantly higher MCA PI (p=0.007) and numerically higher white matter disease scores. Regression analysis models showed that NSAF is one independent predictors of abnormal carotid distensibility (p=0.026) and presence of carotid plaque (p=0.023); but not for carotid plaque burden score (>4), MCA PI (>1.1) and IMT max (>0.966).
Conclusions: The presence of a significant relationship between NSAF and presence of carotid artery plaque and decreased cervical artery distensibility raises the possibility that NSAF might be a reflection of subclinical atherosclerotic burden. This crosstalk between surrogate markers might explain the higher prevalence of NSAF in ischemic stroke patients.