Mechanobiology has emerged as a unifying framework for understanding how mechanical forces and tissue physical properties regulate cellular function, metabolism, and disease progression. Mechanical forces are fundamental regulators of cellular behaviour and tissue homeostasis. Growing evidence indicates that disturbances in mechanobiological signalling contribute to both metabolic disorders and cardiovascular diseases, two highly prevalent and interrelated groups of conditions. This review aims to synthesize current evidence on mechanobiological mechanisms linking metabolic dysfunction and cardiovascular pathology, with particular emphasis on shared pathways involved in tissue remodelling, inflammation, and disease progression. Shared pathogenic mechanisms, including chronic low-grade inflammation, oxidative and endoplasmic reticulum stress, and lipotoxicity, further reinforce the bidirectional relationship between metabolic and cardiovascular disorders. Moreover, advances in mechanobiological imaging and the usage of mechanobiological biomarkers are more commonly regarded as promising tools for early detection of the disease and risk stratification. It is worth mentioning that targeting mechanosensitive pathways may support the development of personalised diagnostic strategies and novel therapeutic approaches addressing both metabolic and cardiovascular components of disease, which may result in a breakthrough.

Intermediate-high-risk (IHR) pulmonary embolism (PE) remains one of the most challenging clinical phenotypes in contemporary PE management. Although haemodynamically stable at presentation, these patients remain at significant risk of clinical deterioration, right ventricular failure, and haemodynamic decompensation. Current management primarily relies on anticoagulation and close surveillance, while routine reperfusion therapy remains controversial due to the balance between potential haemodynamic benefit and bleeding risk. Catheter-based reperfusion strategies, including catheter-directed thrombolysis and mechanical thrombectomy, have emerged as potential alternatives to systemic thrombolysis in selected patients. However, despite growing procedural adoption, important uncertainties remain regarding optimal patient selection, timing of intervention, and comparative effectiveness. Current evidence demonstrates consistent short-term improvements in surrogate haemodynamic parameters, but robust evidence for reductions in mortality, recurrent PE, chronic thromboembolic complications, or long-term functional impairment remains limited. This narrative review critically evaluates contemporary catheter-based reperfusion strategies in IHR PE, focusing on methodological limitations of the current evidence base and unresolved challenges in clinical decision-making. It highlights the limitations of existing risk stratification models and the heterogeneity of IHR PE, where static risk categories often fail to capture dynamic clinical deterioration. Future progress in this field will likely depend on improved patient selection, refined risk assessment, and personalised reperfusion strategies supported by high-quality comparative trials.