Purpose: Hypertension-induced alterations in cerebral blood flow (CBF) precede overt cerebrovascular structural damage. This study classified SBP control into four threshold ranges based on clinical staging criteria for hypertension, with particular focus on elucidating the differential effects of long-term SBP management on CBF dynamics.
Methods: Randomized controlled trials (RCTs) were collected. Data were retrieved from four databases, spanning their inception until 3 October 2024. Independent data extraction was conducted, and the risk of bias was assessed. First, an overall assessment of the impact of SBP control on CBF was carried out. Second, studies were assigned into four subgroups: 120-129, 130-139, 140-159, and at least 160 mmHg. And then, subgroup was analyzed to explore effects of different SBP control on CBF. The effects of CBF were compared between intensive (120-129 mmHg) and standard SBP control (130-139 mmHg).
Results: The meta-analysis included 12 RCTs with 1100 participants. Four long-term trials (33.33%) were identified as high risk with attrition bias due to dropout rates exceeding 20%. Overall, SBP control, both acute and long-term, improved CBF [standardized mean difference (SMD), 0.17; 95% confidence interval (CI) 0.02-0.31; P = 0.02, I2 = 39%] with moderate robustness. Specially, long-term SBP control improved CBF (SMD, 0.15; 95% CI 0.01-0.29; P = 0.04, I2 = 37%) with low robustness, due to the change of P value when removing a large-sample trial. Intensive SBP control, maintaining 120-129 mmHg, significantly increased long-term CBF (SMD, 0.21; 95% CI 0.07-0.34; P = 0.003, I2 = 0%) with low heterogeneity and high robustness. In contrast, long-term SBP control above 130 mmHg did not lead to significant change in CBF. Although intensive SBP control showed a nonsignificant improvement in CBF compared with standard SBP control, it demonstrated a promising effect size (SMD 2.17; P = 0.07).
Conclusion: This review suggests that intensive SBP control might provide a potential advantage on CBF improvement and deceleration of cerebral small vessel disease (CSVD) development, and might affect cognitive function but requires further verification in the hypertensive population.
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