Optimal systolic and diastolic blood pressure threshold that associated with lower risk of white matter hyperintensity progression.

Background: The optimal control thresholds for systolic blood pressure (SBP) and diastolic blood pressure (DBP) in patients with white matter hyperintensity (WMH) are still unclear. Method: A longitudinal retrospective study of patients with brain magnetic resonance imaging (MRI) scans with intervals of more than 3 years was conducted. Blood pressure records during hospitalization and from outpatient visits between baseline and the last MRI scan were collected. The outcome was the change in total WMH from baseline to the final visit. Results: Among the 965 patients with MRI scans, 457 patients with detailed longitudinal blood pressure records were ultimately included and classified into the WMH absent group (n = 121), mild WMH group (n = 126), and moderate to severe WMH group (n = 210). Both baseline and longitudinal mean SBP, DBP, and SBP SD were significantly associated with WMH severity (p < 0.05). An average SBP of 130-140 mmHg [vs. <130 mmHg, aOR, 1.80, (95% CI, 1.05-3.07), p = 0.03] was associated with a higher risk of WMH progression. DBP ≥ 90 mmHg [vs. <80 mmHg, OR, 1.81, (95% CI, 0.88-3.74), p = 0.02, aOR, 1.54, (95% CI, 0.66-3.53), p = 0.32] was associated with a higher risk of WMH progression, but was not after adjusted for other covariates. Longitudinal BP variability was not significantly associated with WMH progression. Conclusion: Both SBP and DBP had a stronger relationship with the severity of WMH. A target mean SBP of <130 mmHg and mean DBP of <80 mmHg was associated with a lower risk of WMH progression.

Remote Ischemic Conditioning: A Potential Treatment for Chronic Cerebral Hypoperfusion.

BACKGROUND: Chronic cerebral hypoperfusion (CCH) is a clinical syndrome, which is characterized by significantly decreased cerebral blood flow (CBF). CCH is a common consequence of cerebrovascular and cardiovascular diseases and the elderly. CCH results in a series of pathological damages, increasing cell death, autophagy dysfunction, amyloid ß (Aß) peptide accumulation, blood-brain barrier (BBB) disruption, and endothelial damage, which are found in CCH models. In addition, CCH is a prominent risk factor of cognitive impairment, such as vascular dementia, and CCH contributes to the occurrence and development of Alzheimer's disease. Therefore, the treatment of patients with CCH is of great value. It has been confirmed that remote ischemic conditioning (RIC) is a safe, promising treatment for acute and chronic cerebrovascular diseases. RIC significantly increases CBF in both CCH models and patients, inhibits neuronal apoptosis, reduces Aß deposition, protects BBB integrity and endothelial function, alleviates neuroinflammation, improves cognitive impairment, and exerts neuroprotection. SUMMARY: With the development of animal models, the pathophysiological mechanisms of CCH and RIC are increasingly revealed. KEY MESSAGES: We discuss the mechanisms related to hypoperfusion in the brain and explore the potential treatment of RIC for CCH to promote its transformation and application in humans.

Are dexmedetomidine and olanzapine suitable to control delirium in critically ill elderly patients? A retrospective cohort study.

BACKGROUND: The efficacy and safety of dexmedetomidine and olanzapine for delirium control in critically ill elderly patients without ventilation or surgery are not known. METHODS: The efficacy and safety of dexmedetomidine and olanzapine for controlling delirium were evaluated in a retrospective cohort of critically illness by assessing the sedation level, drug dose/duration, combination rate with other sedatives, adverse effects, intubation rate and prognosis. RESULT: The maximum (1.61 ± 1.56 vs. 2.70 ± 1.01, p < 0.001), average (-0.57 ± 0.88 vs. 0.88 ± 0.73, p < 0.001), and minimum (-1.67 ± 1.04 vs. -1.37 ± 1.01, p = 0.014) RASS scores of 263 patients were lower after treating with dexmedetomidine than treating with olanzapine. Drug use duration (4.83 ± 2.67 days vs. 5.87 ± 3.14 days, p = 0.005) and sedative combination rates (13.56% vs. 40.00%, p = 0.003) were lower when treating with dexmedetomidine than that with olanzapine. A comparison of adverse effects between dexmedetomidine and olanzapine revealed respiratory depression (16.95% vs. 2.84%, p < 0.001), hypoxia (13.56% vs. 2.76%, p < 0.001) and hypotension (11.02% vs. 3.45%, p = 0.007). Intubation rates (22.88% vs. 12.41%, p = 0.023) and the length of hospital stay (9.30 ± 4.90 days vs. 8.83 ± 3.34 days, p < 0.001) were higher in patients treated with dexmedetomidine than that with olanzapine. Mortality rates, cognitive prognosis, and delirium recurrence rates were similar between groups. Age, severe cardiopulmonary disease, APACHE II scores, dexmedetomidine dose, minimum RASS score and sedative combination were significantly (p < 0.05) associated with the adverse effects of dexmedetomidine. Respiratory depression, hypoxia and hypotension in the olanzapine group all occurred during combination with benzodiazepines. CONCLUSIONS: Dexmedetomidine achieved more satisfactory sedative effects on delirium control, but olanzapine was safer.