Hypertrophic remodeling and increased arterial stiffness in patients with intracranial aneurysms

ObjectiveBecause an underlying arteriopathy might contribute to the development of intracranial aneurysms (IAs), we assessed the elastic properties of proximal conduit arteries in patients with IA.MethodsIn 27 patients with previous ruptured IA and 27 control subjects matched for age, gender and BMI, we determined arterial pressure, internal diameter, intima-media thickness (IMT), circumferential wall stress (CWS) and elastic modulus (wall stiffness) in common carotid arteries using applanation tonometry and echotracking. Moreover, carotid augmentation index (AIx, arterial wave reflections) and carotid-to-femoral pulse wave velocity (PWV, aortic stiffness) were assessed.ResultsCompared with controls, patients with IA exhibited higher brachial and carotid systolic and diastolic blood pressures, with similar brachial but higher carotid artery pulse pressure (35 ± 6 mm Hg vs. 41 ± 8 mm Hg, P = 0.014). Moreover, patients have higher PWV (7.8 ± 1.2 m s−1 vs. 8.3 ± 1.1 m s−1, P = 0.048) and AIx (15.8 ± 10.8% vs. 21.1 ± 8.5%, P < 0.001) which contributes to increase carotid blood pressures. Furthermore, carotid IMT was higher in patients (546 ± 64 μm vs. 642 ± 70 μm, P < 0.001) without difference in diameter suggesting an adaptive hypertrophy. However, patients display a lower CWS (61.6 ± 9.2 kPa vs. 56.9 ± 10.3 kPa, P = 0.007) and no correlation between IMT and pulse pressure (r = 0.152, P = NS) in contrast to controls (r = 0.539, P < 0.001) showing the contribution of a pressure-independent process. Finally, despite this lesser CWS, elastic modulus was increased in patients (310 ± 105 kPa vs. 383 ± 174 kPa, P = 0.026).ConclusionThis study demonstrates that patients with IA display a particular carotid artery phenotype with an exaggerated hypertrophic remodeling and altered elastic properties. Thus, a systemic arteriopathy might contribute, together with the arterial wall fatiguing effect of the increased pulsatile stress, to the pathogenesis of IA.