Handgrip strength asymmetry is independently associated with systolic blood pressure in adults without established cardiovascular disease: a cross-sectional analysis

Introduction Handgrip strength asymmetry (HSA) has recently emerged as a marker of impaired neuromuscular integrity and reduced physiological reserve. However, its relationship with systolic blood pressure (SBP), particularly in adults without established cardiovascular disease, remains insufficiently explored. This study aimed to evaluate the association between HSA and SBP and to investigate the potential role of HSA as a complementary functional marker for elevated SBP. Methods This retrospective cross-sectional study included 366 adults aged 45–75 years without established cardiovascular disease (e.g., coronary artery disease, heart failure, cerebrovascular disease, or peripheral arterial disease). Participants with hypertension, diabetes mellitus (DM), and dyslipidemia were eligible for inclusion. HSA was calculated as the percentage difference between dominant and non-dominant handgrip strength relative to the maximal value. The association between HSA and SBP was assessed using Spearman correlation analysis and multivariable linear regression models adjusted for age, sex, body mass index (BMI), smoking status, DM, and non-HDL cholesterol. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the discriminatory ability of HSA for identifying elevated SBP (≥ 140 mmHg). Results HSA showed a moderate positive correlation with SBP ( r = 0.479, p < 0.001). In multivariable linear regression analysis, HSA remained independently associated with SBP ( β = 0.422, p < 0.001). ROC analysis demonstrated good discriminatory ability for identifying elevated SBP (AUC = 0.792; 95% CI 0.745–0.840; p < 0.001). The optimal HSA cut-off was 12.39%, yielding a sensitivity of 83% and a specificity of 65%. Conclusions HSA was independently associated with SBP in adults without established cardiovascular disease. Prospective longitudinal studies are required to determine whether HSA predicts incident hypertension and cardiovascular outcomes and to establish its potential clinical utility in cardiovascular risk assessment.