**1. Introduction**

To date, stroke remains the most common cause of disability and mortality world-wide, which leads to a substantial global health burden [1]. The highest rate of stroke incidence was found in Southeast Asian countries, including Vietnam [2]. Although multilevel and multisectoral prevention strategies have been applied, the stroke recurrence (SR) rate has not changed over the years [3,4]. Moreover, the risk of SR increases over time [5], causing continuously increasing issues in societies and medical systems around the world [6], as well as in Vietnam [7]. Therefore, closing the gap in stroke prevention strategies is a high priority.

About 90% of strokes are caused by the presence of modifiable risk factors, and the regulation of core health behaviors (such as diet, physical activity, weight, and smoking) could avert about 75% of this burden [6,8]. Hypertension (HTN) is the most frequent danger for stroke and recurrent events [9,10]. Although hypertensive management is the most important primary and secondary prevention strategy for stroke, managing blood pressure in stroke patients is complex and challenging [11]. Moreover, evidence-based prevention strategies are not obviously improving modifiable risk factors and recurrent cardiovascular events (including stroke) [12]. Therefore, exploring factors that could be accessible for modifying the harmful impact of HTN on SR is necessary for prevention strategies.

Oxidative stress (OS) is characterized by the pro-oxidant–antioxidant balance (PAB) shifting toward the pro-oxidant predominance, resulting in molecular damage [13–15]. The existing evidence showed that the OS response could derive from endogenous (e.g., metabolic processes) and exogenous sources (e.g., core health behaviors), which are involved in the pathological mechanism of chronic diseases [16], including stroke [17–19]. In the endogenous aspect, OS is linked closely to chronic inflammatory disorders, which were identified as the major triggers for cardiovascular diseases (CVDs). The close interaction between OS and inflammatory response was reported regarding the overexpression of reactive oxygen species (ROS)-producing enzymes (e.g., NADPH NOXs) or aggravated inflammatory phenotypes in the absence of antioxidant defense proteins (e.g., glutathione peroxidases, heme oxygenase-1, and superoxide dismutase) [20]. Moreover, OS plays a critical role in the mechanism of CVDs through endothelial dysfunction, of which oxidative enzyme systems (e.g., xanthine oxidase and NADPH oxidase) contribute to the inactivation of nitric oxide—an endothelial regulator, leading to endothelial dysfunction [21]. In the exogenous aspect, potential diets and nutraceuticals could reduce OS and display antioxidant effects, which represents a therapeutic target in CVDs [21]. Additionally, regulating PAB could be a promising strategy for stroke therapeutics [22].

The PAB can be approached from pro-oxidative and antioxidative perspectives, and both can be considered in terms of their individual chemical constituents or their pooled effect [23]. Pro-oxidants can be from intracellular sources (such as NADPH NOXs, peroxisomes, and mitochondria) and external sources (such as pollutants, ultraviolet light, and ionizing) [24], whereas endogenous antioxidants involve the products of cellular metabolism (e.g., peroxiredoxin, catalase, and superoxide dismutase), and exogenous antioxidants involve diets and medications [24]. In the literature, the PAB has been directly estimated in saliva, urine, plasma, and serum [23], demonstrating the contribution of exogenous and endogenous agents. However, for example, serum PAB cannot reflect each agent's specific pro-oxidant and antioxidant potentials and the complex interaction between the agents. Therefore, an indirect measurement tool based on lifestyle, nutrition, and medication factors was developed and validated to evaluate the individual PAB status and its impact on health outcomes [25–27]. However, the evidence regarding the indirect estimation of PAB based on health behaviors impacting SR is limited. Therefore, we aimed to examine the relationship between health behavior-based PAB and SR. Further, the modification role of PAB in the association between HTN and SR was explored.
