Abstract
Background
Compression therapy has traditionally been regarded as a treatment for venous disease. However, growing experimental and clinical evidence shows that its effects extend beyond the venous system, influencing tissue fluid balance, lymphatic function, arterial perfusion, microcirculation, and inflammation. This suggests that its clinical benefits arise from a global effect on the compressed structures rather than from isolated vascular effects.
Study Aim
to highlight two key concepts: first, that the effects of compression depend not only on resting pressure but also on its dynamic behavior and stiffness; and second, that compression acts simultaneously on all structures within the compressed segment, irrespective of the primary clinical indication.
Methods
We critically reviewed and integrated evidence from experimental studies, imaging, clinical investigations, randomized controlled trials, systematic reviews, consensus documents, and international guidelines into a mechanism-based framework. Rather than adopting a disease-oriented approach, the review organized the evidence around the biological targets through which compression exerts its therapeutic effects.
Results
Compression therapy works by delivering a controlled mechanical stimulus to the entire compressed segment, thereby improving venous hemodynamics, lymphatic drainage, microvascular function, and arterial perfusion, while regulating inflammation. These interconnected mechanisms explain the efficacy of compression across different vascular disorders. Therapeutic benefit depends on compression characteristics, including not only interface pressure but, most importantly, material stiffness, dynamic pressure changes during movement, treatment duration, and patient adherence. The review also shows that much of the heterogeneity in the literature reflects methodological limitations rather than conflicting biological effects.
Conclusions
Compression therapy should be viewed as a biomechanical intervention that restores tissue homeostasis, with vascular changes reflecting coordinated downstream responses. This integrated framework offers a unifying explanation of its biological effects, supports individualized treatment planning, and identifies priorities for improving the design and interpretation of future clinical studies.