Assessment of Residual Oxidative Stress in Patients with Well-Controlled Hypertension: A Pilot Cross-Sectional Study

<b>Background/Objectives:</b> Although hypertension is linked to oxidative stress, it remains unclear whether this pro-oxidant state persists after achieving recommended blood pressure (BP) control. This pilot study aimed to explore the presence of residual oxidative stress in patients with well-controlled hypertension compared to normotensive individuals. <b>Methods:</b> In this cross-sectional pilot study, 34 adults were enrolled: 20 normotensive controls and 14 patients with well-controlled hypertension (office BP < 140/90 mmHg). Macrovascular status was assessed by ankle-brachial index (ABI), and plasma concentrations of malondialdehyde (MDA), superoxide dismutase (SOD), catalase, tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) were measured. Hypertensive patients were further stratified by median MDA levels for subgroup analysis. <b>Results:</b> Baseline characteristics, including BP, were similar between groups. However, patients with well-controlled hypertension exhibited significantly higher plasma MDA concentrations compared to normotensive controls (9.91 ± 6.07 vs. 4.73 ± 2.34 µmol/L, <i>p</i> = 0.008). In subgroup analysis, hypertensive patients with high MDA were significantly older (<i>p</i> = 0.03) and showed a trend towards higher systolic BP (<i>p</i> = 0.05) compared to those with low MDA. No significant differences were observed in SOD or catalase activity, ABI, or inflammatory markers (all <i>p</i> > 0.05). <b>Conclusions:</b> Residual oxidative stress-as reflected by increased plasma MDA-persists in patients with well-controlled hypertension. While this oxidative state appears broadly independent of BP when viewed as a whole, it is notably more pronounced in older patients and in those with systolic BP approaching the upper limit of the controlled range. These findings support the need for comprehensive, biomarker-based risk assessment and further investigation into targeted strategies for mitigating persistent redox imbalance in hypertension.