Analysis of blood pressure control and circadian rhythm in hypertensive patients with cerebral infarction: A single-centre retrospective cross-sectional study

Objective: To compare ambulatory blood pressure monitoring (ABPM)-derived parameters and blood-pressure circadian rhythm types between hypertensive patients with and without cerebral infarction, and to examine their cross-sectional association with the presence of cerebral infarction. Methods: In this single-centre retrospective cross-sectional study, a total of 196 patients managed at the Affiliated Hospital of Nanjing University of Chinese Medicine from October 2024 to March 2025 were analysed and divided into an isolated-hypertension group (n = 100) and a hypertension-with-cerebral-infarction group (n = 96). In the cerebral-infarction group, ABPM was performed after the acute phase had clinically stabilised (≥2 weeks from symptom onset) in the convalescent/outpatient setting. 24-h ABPM was used to record 24-h systolic and diastolic blood pressure (24-h SBP, 24-h DBP), daytime and nighttime heart rate (dHR, nHR) and pulse pressure (PP); the daytime and nighttime systolic/diastolic coefficients of variation (dSBPcv, dDBPcv, nSBPcv, nDBPcv) and the ambulatory arterial stiffness index (AASI) were calculated. Patients were classified as dippers, non-dippers, or reverse dippers. Baseline demographic, clinical, and antihypertensive treatment characteristics were compared between groups. Multivariable logistic regression was used to identify factors independently associated with cerebral infarction; because PP is the arithmetic difference between SBP and DBP, these variables were not entered into the same model, multicollinearity was assessed using the variance inflation factor (VIF), the reference category for rhythm type was pre-specified (dipper), and sensitivity analyses were performed. Results: The two groups were comparable in baseline demographic, clinical and treatment characteristics (P > 0.05). Compared with the isolated-hypertension group, the hypertension-with-cerebral-infarction group showed significantly higher 24-h SBP, 24-h DBP, PP and nHR (P < 0.05), whereas the blood-pressure variability coefficients (dSBPcv, dDBPcv, nSBPcv, nDBPcv) and AASI did not differ between groups (all P > 0.05). The nocturnal decline in both systolic and diastolic pressure was significantly attenuated in the cerebral-infarction group (systolic 1.44% vs 7.73%; diastolic 3.01% vs 9.45%; both P < 0.001). The distribution of circadian rhythm types differed significantly between the two groups (𝜒 2 = 28.74, P < 0.001): the cerebral-infarction group was predominantly non-dipper and reverse-dipper, whereas the isolated-hypertension group was predominantly dipper and non-dipper. After adjustment, higher 24-h SBP (OR 1.06, 95% CI 1.02–1.10) and an abnormal (non-dipper or reverse-dipper) circadian rhythm (OR 4.74, 95% CI 2.04–11.00) were independently associated with cerebral infarction (P < 0.05); nHR was significant in the univariate comparison but not after multivariable adjustment, and was therefore not an independently associated factor. Conclusion: In this cross-sectional sample, the presence of cerebral infarction was associated with higher 24-h SBP, higher PP and an abnormal circadian blood-pressure rhythm. Because of the observational design, these associations do not establish causation and may, in part, reflect the effects of cerebral infarction (and of hospitalisation, autonomic dysfunction, or treatment changes) on blood-pressure regulation; prospective, temporally anchored studies are needed to clarify directionality.