Via computational fluid dynamics models, a recent study has offered insights into the relevance of balancing two key mechanisms of haemodynamic deterioration—plaque burden and compromised perfusion—with regard to blood pressure management in symptomatic intracranial atherosclerotic stenosis (ICAS) patients.
“This research elucidates the role of haemodynamic impairment of blood pressure in symptomatic ICAS-related stroke mechanisms, underscoring the necessity to conduct haemodynamic assessments when managing blood pressure in symptomatic ICAS,” write study authors Haiqiang Qin, Zixiao Li (both Capital Medical University, Beijing, China) et al, concluding the publication of their findings in the journal Stroke.
In a subsequent commentary article—also published in Stroke—Giuliana Pollaci (Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy) states that haemodynamic impairment may have a “significant influence” on the mechanisms behind strokes of atherosclerotic origin, and describes the role of blood pressure in determining ICAS-related haemodynamics as a “double-edged sword”.
“If high, luminal stenosis could generate differences in pressure across the proximal and distal ends of a plaque, contributing to the mechanical burden on the area of plaque, whereas low blood pressure may compromise blood flow,” Pollaci explains. “Due to this double role, to unravel the relationship between blood pressure and mechanisms of ICAS-related stroke, it is necessary to study regional ICAS-specific blood pressure profiles considering regional haemodynamics.”
Qin, Li et al note in their initial research article that—in an attempt to elucidate the potentially “crucial” role haemodynamic impairment of blood pressure could play in symptomatic ICAS-related stroke mechanisms—they performed computed fluid dynamics modelling using the Newton-Krylov-Schwarz method across 339 symptomatic ICAS patients in the third China National Stroke Registry from 2015 to 2018.
The authors relay that—as per the major outcome measures of their study—a total of 184 cortex-involved infarcts (54.3%) and 70 borderzone-involved infarcts (20.6%) were identified. They also report that multivariable logistic analysis revealed a correlation between the upper quartile of translesional systolic blood pressure (SBP) drop and an increase in cortex-involved infarcts (odds ratio [OR], 1.92; 95% CI, 1.03–3.57), and a potential correlation between the lower quartile of post-stenotic mean arterial pressure (MAP) and an increase in borderzone-involved infarcts (OR, 2.07; 95% CI, 0.95–4.51). Furthermore, the investigators found a negative correlation between SBP drop and post-stenotic MAP (p<0.001).
“In generating haemodynamic impairment, simulating blood pressure modifications suggested that ensuring adequate blood pressure to maintain sufficient post-stenotic MAP appears preferable to the reverse approach, due to the prolonged plateau period in the association between the translesional SBP drop and cortex-involved infarcts, and the relatively short plateau period characterising the correlation between post-stenotic MAP and borderzone-involved infarcts,” Qin, Li et al add.
The researchers ultimately conclude that, while blood pressure management in these patients “poses challenges”, their findings provide further insights and may therefore equip clinicians with more effective strategies for addressing this issue via a haemodynamic approach.
“Future research is encouraged to investigate the causal links between the haemodynamic impairment of blood pressure and stroke events in symptomatic ICAS,” they continue. “Additionally, investigations into how haemodynamic impairment interacts with plaque features and collateral circulation are also warranted.”
“This study includes the largest cohort of patients with symptomatic ICAS to undergo [computational fluid dynamics] analysis with an individualised boundary condition to date,” Pollaci avers. “Some limitations are linked to the fact that their investigation was confined to the effect of regional pressure on ICAS; of course, information on the collateral circulation, as well as vulnerability of plaques, might have influenced risk of plaque rupture or hypoperfusion.”
Providing a similar closing sentiment to Qin, Li et al, Pollaci also comments that future studies with a “comprehensive approach” to refining the understanding of this phenomenon are needed.
