Radial wall strain (RWS) is an angiography-derived biomechanical index that quantifies plaque deformability from routine coronary angiography, offering a novel approach to assess plaque vulnerability beyond conventional anatomical and physiological parameters. This narrative review synthesizes current evidence on the pathophysiological basis, clinical applications, and prognostic implications of RWS in coronary artery disease. Recent studies have demonstrated that elevated RWS values are associated with established markers of plaque vulnerability, including thin-cap fibroatheromas and large lipid cores, as well as increased risk of major adverse cardiovascular events. Furthermore, RWS has emerged as a promising tool for identifying vulnerable plaques in non-flow-limiting lesions and predicting in-stent restenosis, demonstrating incremental prognostic value when combined with angiography-derived physiological indices such as the quantitative flow ratio. By integrating biomechanical assessment with conventional physiological and morphological characterization, RWS may enhance risk stratification and guide clinical decision-making in percutaneous coronary intervention. While current evidence is encouraging, prospective randomized trials are needed to validate RWS-guided management strategies and establish optimal cutoff values for clinical implementation.

Acute pulmonary embolism (PE) is a major cause of cardiovascular mortality, and managing patients at risk of deterioration despite anticoagulation is challenging. Transcatheter interventions, including catheter-directed thrombolysis (CDT) and mechanical thrombectomy (MT), aim to rapidly unload the right ventricle while limiting the bleeding risk of systemic thrombolysis. Their use long preceded robust evidence, but recent randomised trials have changed this. In normotensive patients with right ventricular dysfunction and elevated cardiac biomarkers, low-dose CDT, with or without ultrasound, reduced early clinical deterioration in two trials with differing eligibility criteria: HI-PEITHO required troponin elevation and at least two additional markers of cardiorespiratory compromise, whereas PRAGUE-26 required troponin or natriuretic peptide elevation. No statistically significant difference in major bleeding was detected, although mortality did not improve and intracranial haemorrhage occurred. MT accelerated right ventricular recovery versus anticoagulation and, in an open-label trial against CDT, improved a composite driven by deterioration and intensive care use. Guidelines predate most of these data and differ between continents: the 2019 European Society of Cardiology guideline and European consensus documents reserve transcatheter treatment mainly for high-risk PE with contraindicated or failed thrombolysis and for rescue after deterioration, whereas the 2026 American Heart Association/American College of Cardiology guideline allows its consideration in incipient cardiopulmonary failure. This review summarises techniques, evidence and recommendations, and it discusses patient selection, comparative effectiveness and long-term outcomes. Pending updates, decisions should be individualised by multidisciplinary PE response teams.

Background: Obesity is increasing worldwide and remains a major contributor to cardiovascular morbidity and mortality. It is strongly associated with hypertension, dyslipidemia, diabetes mellitus, endothelial dysfunction, and chronic inflammation, all of which promote coronary artery disease and acute coronary syndrome (ACS). Despite this well-established risk profile, multiple studies have described an “obesity paradox,” suggesting that obese patients may experience better outcomes after percutaneous coronary intervention (PCI) for ACS than normal-weight individuals. Objective: This narrative review aims to discuss the pathophysiological basis of the obesity paradox and to synthesize contemporary evidence regarding the relationship between body mass index (BMI), major adverse cardiovascular events (MACE), and mortality after PCI in patients presenting with ACS. Results: Contemporary observational cohorts consistently suggest a non-linear relationship between BMI and MACE outcomes after PCI. Overweight and mildly obese patients often demonstrate lower crude mortality and fewer MACE, whereas underweight patients consistently show the poorest prognosis. However, after adjustment for age, left ventricular ejection fraction (LVEF), renal function, frailty, and nutritional status, obesity is less consistently associated with improved outcomes. Overweight status appears to be more reproducibly associated with better prognosis than obesity itself. Conclusions: The obesity paradox is likely driven less by a true protective effect of excess adiposity and more by younger age at presentation, preserved physiological reserve, lower frailty burden, and the limitations of BMI as a marker of cardiovascular risk. Underweight status emerges as the strongest predictor of adverse outcomes. Nutritional assessment and body composition should complement BMI in risk stratification after ACS.