Abstract
The mechanism underlying atherosclerotic ischemic events within the middle cerebral artery (MCA) is unclear. High structural stress induced by blood pressure might be a potential aetiology as plaque rupture occurs when such mechanical loading exceeds its material strength. To perform reliable analyses quantifying the mechanical loading within a plaque, the local blood pressure is needed. However, data on MCA blood pressure is currently lacking. In this study, the arterial pressure proximal to the stenotic site in the MCA was measured in 15 patients scheduled for intervention. The relationships between these local measurements and pre-intervention and intra-intervention non-invasive arm measurements were assessed. The impact of luminal stenosis on the local blood pressure was quantified. Compared with the pre-intervention arm measurement, the intra-intervention arm pressure decreased significantly by 23.9 ± 11.8 and 9.3 ± 14.7 % at diastole and systole, respectively. The pressure proximal to the stenosis was much lower than the pre-intervention arm measurement (diastole: 65.3 ± 15.7 vs 82.0 ± 9.7, p < 0.01; systole: 81.1 ± 15.9 vs 133.9 ± 18.7, p < 0.01; unit: mmHg). The systolic pressure in the MCA in patients with stenosis <70 % (n = 6) was significantly higher than the value in patients with stenosis ≥70 % (n = 9) (92.0 ± 7.3 vs 73.9 ± 16.1, p = 0.02; unit: mmHg), as was pulse pressure (22.8 ± 6.4 vs 11.1 ± 8.3, p = 0.01; unit: mmHg). However, diastolic pressure remained unaffected (69.2 ± 9.3 vs 62.8 ± 19.0, p = 0.58; unit: mmHg). In conclusion, the obtained results are helpful in understanding the local hemodynamic environment modulated by the presence of atherosclerosis. The local pressure measurements can be used for computational analysis to quantify the critical mechanical condition within an MCA lesion.
Highlights
Intracranial atherosclerosis has become one of the major subtypes of stroke, accounting for around 8–10 % of strokes in western societies [1] and 33–55 % of strokes in Asian populations [2, 3]
Both of these decreased as middle cerebral artery (MCA) stenosis severity increased
The systolic and pulse pressures decreased as the stenosis increased
Summary
Intracranial atherosclerosis has become one of the major subtypes of stroke, accounting for around 8–10 % of strokes in western societies [1] and 33–55 % of strokes in Asian populations [2, 3]. Around 40 % of symptomatic intracranial atherosclerosis is located in the middle cerebral artery (MCA) [4]. The mechanisms underlying stroke related to intracranial atherosclerosis are varied and may include cerebral hypoperfusion, Jiang et al BioMed Eng OnLine (2016) 15:67 artery-to-artery embolism, plaque extension over small penetrating artery ostia or a combination of aforementioned [5,6,7]. Similar to carotid atherosclerotic disease, luminal stenosis is the primary criterion for assessing disease severity in MCA atherosclerosis. Severe luminal stenosis results in flow restriction [8, 9], leading to insufficient cerebral perfusion which has been shown to be predictive for subsequent ischemic events [10]. Further analyses are needed for a better understanding the mechanism underlying the ischemic events caused by MCA atherosclerosis
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