Background: The integration of global longitudinal strain (GLS) with stress echocardiography (SE) represents a significant advancement in non-invasive cardiac diagnostics, particularly in the evaluation of coronary artery disease (CAD). GLS, derived from speckle-tracking echocardiography, quantifies myocardial deformation and offers superior sensitivity for detecting subclinical myocardial dysfunction compared to conventional metrics like wall motion and ejection fraction. Recent studies have validated the prognostic and diagnostic efficacy of GLS both at rest and during stress, notably enhancing the detection of obstructive and non-obstructive CAD, microvascular dysfunction, and other cardiac pathologies. Methods: This manuscript synthesizes extensive clinical data demonstrating the added value of GLS during stress echocardiography across diverse cardiac conditions—including valvular heart disease, heart failure, cardio-oncology, and pediatric cardiology. Novel metrics like longitudinal strain reserve (LSR), myocardial work indices, and post-systolic strain have further enriched risk stratification strategies. Results: The combination of GLS with SE has been shown to approximate the accuracy of invasive coronary angiography in intermediate-risk patients and in cases with equivocal traditional SE findings. Despite its clinical promise, the utility of GLS is challenged by technical limitations, including image quality dependency, inter-vendor variability, and limited applicability during high heart rate states. Conclusions: As technological refinement and standardization progress, GLS integrated with SE is poised to become a mainstay in precision cardiology, improving diagnostic yield, guiding therapeutic decisions, and enhancing patient outcomes.

Pulmonary hypertension (PH) is a complex condition in which early diagnosis remains challenging, particularly in patients with exertional symptoms and normal or borderline resting haemodynamics. Although right heart catheterisation is the diagnostic gold standard, transthoracic echocardiography is the recommended first-line non-invasive test. However, resting echocardiography provides only a static assessment and may underestimate disease severity in early or latent pulmonary vascular disease due to preserved pulmonary vascular compliance and adaptive right ventricular responses. Because pulmonary haemodynamics are intrinsically flow-dependent, pathological abnormalities may only emerge during increased cardiac output. Stress echocardiography, performed using exercise or pharmacological stress, enables dynamic evaluation of pulmonary pressure responses, cardiac output augmentation, right ventricular contractile reserve, and ventricular interaction. Increasing evidence indicates that stress echocardiography can unmask abnormal pulmonary pressure–flow relationships, impaired pulmonary vascular reserve, and reduced right ventricular–pulmonary arterial coupling that are not apparent at rest, thereby improving functional and haemodynamic characterisation in selected patients. This Diagnostic Review outlines the physiological basis for stress echocardiographic assessment of pulmonary circulation, proposes practical recommendations for patient selection and testing protocols, and provides a framework for interpretation centered on pressure–flow relationships rather than absolute pulmonary pressure thresholds. Particular attention is given to clinical scenarios with high diagnostic yield, including unexplained exertional dyspnoea, systemic sclerosis, suspected heart failure with preserved ejection fraction, at-risk relatives of patients with pulmonary arterial hypertension, selected athletes, and paediatric populations. Stress echocardiography should not be considered a standalone diagnostic test for PH but, when performed in experienced centers and integrated within structured diagnostic pathways, it represents a valuable non-invasive adjunct to guide referral for invasive haemodynamic confirmation.

Background: Reliable quantification of systemic venous congestion in acute heart failure (HF) has become feasible with the advent of the venous excess ultrasound (VExUS) score, informing therapeutic management. Nevertheless, the determinants of the VExUS score trajectory during hospitalization and the prognostic implications of persistent subclinical congestion at discharge remain poorly defined. Methods: Consecutive patients admitted for acute HF were prospectively enrolled (n = 418, 73.3 ± 11.8 years old, 59.1% male). VExUS scores were assessed at admission and prior to discharge to categorize the patients into three groups: non-congested (persistent score of 0; n = 81), improved (score reduction of ≥1 point; n = 214), and non-improved (persistent congestion without score reduction; n = 123). Baseline clinical data were collected and all the patients had a transthoracic echocardiogram on admission. All patients were followed up post-discharge and the primary endpoint was a composite of all-cause mortality or HF hospitalization. Results: Patients with non-improved VExUS exhibited a higher burden of right-sided remodeling and dysfunction including larger right chambers, lower right ventricle (RV) systolic function indices, higher RV systolic pressures and a higher prevalence of severe tricuspid regurgitation (all p < 0.001). Severe tricuspid regurgitation was the sole independent predictor of VExUS non-improvement (OR 2.86, 95% CI 1.51–5.45, p = 0.001). Non-improved VExUS (HR 1.77; 95% CI 1.17–2.67; p = 0.007), severe tricuspid regurgitation (HR 1.88; 95% CI 1.16–3.02; p = 0.010) and intravenous furosemide dose (HR 1.00; 95% CI 1.00–1.01; p = 0.011) were independent predictors of the composite primary endpoint. Inclusion of non-improved VExUS provided incremental prognostic value over models including clinical, laboratory, and echocardiographic parameters (Δχ²= 9.22; p = 0.007). Conclusions: VExUS non-improvement throughout hospitalization marks patients with worse primary endpoint Severe tricuspid regurgitation emerges as an independent determinant of VExUS non-improvement which is independently associated with poor long-term outcomes.

Background: Recreational half-marathon participation is increasing, particularly among middle-aged amateur runners, yet the interpretation of early post-race cardiac findings remains challenging in exercise-based cardiovascular health evaluation. This exploratory study assessed early post-race changes in left ventricular diastolic indices and circulating biomarkers in 20 healthy amateur runners (80% male; mean age 50.7 ± 12.3 years) after the 11th PELLA HALF MARATHON (21.1 km). Methods: Participants underwent transthoracic echocardiography and venous blood sampling within 30 days before the race and within 30 min after finishing. Diastolic assessment included the E/A ratio, tissue Doppler early diastolic myocardial velocity (e′), the E/e′ ratio, isovolumic relaxation time (IVRT), and left atrial area. Biomarkers included C-reactive protein (CRP), creatine phosphokinase (CPK), creatine kinase-MB (CK-MB), and high-sensitivity cardiac troponin I (hs-cTnI). Results: Post-race assessment showed a consistent pattern of lower early diastolic filling/relaxation indices, higher IVRT and left atrial area, and significant increases in all measured biomarkers. hs-cTnI exceeded the sex-specific 99th percentile upper reference limit in 7/20 participants (35%). Conclusions: Half-marathon completion was associated with early echocardiographic and biomarker changes in this cohort of amateur runners. These findings are consistent with acute physiological cardiac stress and may help clinicians contextualise early post-race abnormalities when advising on vigorous endurance exercise participation. However, subclinical myocardial injury cannot be excluded without serial biomarker assessment and advanced imaging, and the findings should be interpreted as exploratory because of the small convenience sample, absence of a control group, lack of hydration assessment, and single early post-race timepoint.

Heart failure (HF) is increasingly recognized as a progressive syndrome that begins long before patients develop clinical signs or symptoms, during which conventional echocardiographic parameters may fail to detect early myocardial impairment. Atrial strain imaging by speckle-tracking echocardiography has emerged as a sensitive, non-invasive tool capable of identifying subtle functional abnormalities before symptoms or structural remodeling occur. Impaired left atrial (LA) reservoir strain (LASr) serves as a sensitive marker of left ventricular (LV) diastolic dysfunction with elevated filling pressures, exercise intolerance, and HF with preserved ejection fraction, with incremental diagnostic or prognostic value reported in selected studies. Reduced LA strain is also strongly associated with atrial fibrillation (AF), valvular heart disease progression, adverse outcomes following myocardial infarction, and pulmonary vascular involvement. Although comparatively less studied, right atrial (RA) reservoir strain (RASr) reflects the haemodynamic burden of the right heart, right ventricular–pulmonary arterial coupling, and early subclinical dysfunction in cardiometabolic disease, pulmonary hypertension, and established HF. Similarly, RA strain has demonstrated potential diagnostic and prognostic value across the HF spectrum. This review summarizes contemporary evidence regarding the pathophysiological, diagnostic, and prognostic significance of LASr and RASr in unveiling subclinical dysfunction in HF. Both LA and RA strain may provide complementary information on atrioventricular coupling and may identify functional impairment and increased haemodynamic burden before overt structural remodeling becomes evident. Atrial strain assessment may therefore complement conventional echocardiography in the early detection, phenotypic characterization, and risk stratification of patients across different stages of HF.