Heart failure (HF) is a clinical syndrome with high morbidity and mortality, and its prevalence is rapidly increasing. Galectin-3 (Gal-3) is an important factor in the pathophysiology of HF, mainly due to its role in cardiac fibrosis, inflammation, and ventricular remodeling. Fibrosis is a hallmark of cardiac remodeling, HF, and atrial fibrillation development. This review aims to explore the involvement of Gal-3 in HF and its role in the pathogenesis and clinical diagnostic and prognostic significance. We report data on Gal-3 structure and molecular mechanisms of biological function crucial for HF development. Over the last decade, numerous studies have shown an association between echocardiographic and CMR biomarkers in HF and Gal-3 serum concentration. We discuss facts and concerns about Gal-3’s utility in acute and chronic HF with preserved and reduced ejection fraction for diagnosis, prognosis, and risk stratification. Finally, we present attempts to use Gal-3 as a therapeutic target in HF.

Galectin-3 is a biomarker of fibrosis, inflammation and oxidative stress, and its role in heart remodelling and exercise intolerance has not been conclusively proven in heart failure (HF) patients with reduced ejection fraction (rEF). We prospectively assessed 67 consecutive patients with symptomatic HF and left ventricular (LV) EF ≤ 35% during optimal medical therapy, with a mean serum galectin-3 concentration of 15.3 ± 6.4 and a median of 13.5 ng/mL. The group with galectin-3 concentrations greater than or equal to the median had significantly worse right ventricular (RV) systolic function parameters (s′, TAPSE), higher pulmonary artery systolic pressure, more advanced tricuspid regurgitation and lower RV-to-pulmonary circulation coupling index, while no significant differences were found in LV parameters. Moreover, this group achieved significantly lower parameters in cardiopulmonary exercise testing. Significant negative correlations were found between galectin-3 concentration and RV parameters and exercise capacity parameters and have persisted after adjustment for glomerular filtration rate, but not all of them have persisted after adjustment for NT-proBNP. Multivariate regression analysis revealed that TAPSE (β coefficient: − 0.605; p < 0.001) and heart rate at peak exercise (β coefficient: − 0.98; p = 0.009) were independently related to galectin-3 concentration. Elevated galectin-3 concentration in patients with HFrEF might indicate concomitant RV dysfunction and exercise intolerance.

Cardiopulmonary exercise testing (CPET) is an important diagnostic tool in contemporary clinical practice. This document presents an expert opinion from the Working Group on Cardiac Rehabilitation and Exercise Physiology of the Polish Cardiac Society concerning the indications, performance technique, and interpretation of results for CPET in adult cardiology. CPET is an electrocardiographic exercise test expanded with exercise evaluation of ventilatory and gas exchange parameters. It allows for a global assessment of the exercise performance including the pulmonary, cardiovascular, hematopoietic, neuropsychological, and musculoskeletal systems. It provides a noninvasive dynamic evaluation during exercise and is a reference modality for exercise capacity assessment. Moreover, it allows the measurement of numerous prognostic parameters. It is useful in cardiology, pulmonology, oncology, perioperative assessment, rehabilitation as well as in sports medicine and in the evaluation of healthy people. This test not only helps to diagnose the causes of exercise intolerance but also supports the evaluation of the treatment. New opportunities are offered by combining CPET with imaging such as exercise stress echocardiography. These tests are complementary and synergistic in their diagnostic and prognostic strength.

Background: Cryoballoon‐based pulmonary vein isolation (CB‐PVI) has been widely used for the treatment of atrial fibrillation. Although generally safe and effective, the procedure may be associated with pulmonary vein (PV) stenosis and bronchial or esophageal injury. The mechanisms leading to these complications have not been studied in detail. Our aim was to examine acute effects of cryoballoon on the pulmonary vessel and right heart pressures as well asPVwall morphology.Methods and Results: In 8 patients (5 men, mean age 55±14 years) undergoingCB‐PVI, pressure in eachPVwas measured by catheter located inside thePVdirectly before and afterCB‐PVI. The right atrial, right ventricular, and pulmonary artery pressures as well as pulmonary arterial wedge capillary pressure in the pulmonary artery branch corresponding to targetPVwere also measured. Morphological changes inPVswere assessed using intravascular ultrasonography.There were no significant differences inPVpressures before and after ablation. The pulmonary arterial wedge capillary pressure significantly increased during cryoapplication (left superior: 20±10 versus 29±8.5 mm Hg,P=0.004; left inferior: 24±10 versus 32±6 mm Hg,P=0.012; right superior: 25±9 versus 35±10 mm Hg,P=0.002; right inferior: 24±10 versus 37±12 mm Hg,P=0.0036). The right atrial and pulmonary artery pressures increased significantly afterCB‐PVI(9±6 versus 13±8 mm Hg,P=0.004, and 20±9 versus 24±10 mm Hg,P=0.048, respectively). Intravascular ultrasonography showed acute edema and dissection‐like changes causing relative lumen narrowing in 90% ofPVs.Conclusions: CB‐PVIcauses significant rise in pulmonary artery and right atrial pressures as well asPVwall damage. The clinical significance of these findings warrants further investigations.

Background: Chronotropic incompetence in patients taking beta-blockers is associated with poor prognosis; however, its impact on exercise capacity (EC) remains unclear. Methods: We analyzed data from consecutive patients taking beta-blockers referred for cardiopulmonary exercise testing to assess EC. Chronotropic incompetence was defined as chronotropic index (CI) ≤ 62%. Results: Among 140 patients all taking beta-blockers (age 61 ± 9.7 years; 73% males), 64% with heart failure, chronotropic incompetence was present in 80.7%. EC assessed as peak oxygen uptake was lower in the group with chronotropic incompetence, 18.3 ± 5.7 vs. 24.0 ± 5.3 mL/kg/min, p < 0.001. EC correlated positively with CI (β = 0.14, p < 0.001) and male gender (β = 5.12, p < 0.001), and negatively with age (β = −0.17, p < 0.001) and presence of heart failure (β = −3.35, p < 0.001). Beta-blocker dose was not associated with EC. Partial correlation attributable to CI accounted for more than one-third of the variance in EC explained by the model (adjusted R² = 59.8%). Conclusions: In patients taking beta-blockers, presence of chronotropic incompetence was associated with lower EC, regardless of the beta-blocker dose. CI accounted for more than one-third of EC variance explained by our model.

Cardiac rehabilitation (CR) is indicated in all patients after acute myocardial infarction (AMI) to improve prognosis and exercise capacity (EC). Previous studies reported that up to a third of patients did not improve their EC after CR (non-responders). Our aim was to assess the cardiac and peripheral mechanisms of EC improvement after CR using combined exercise echocardiography and cardiopulmonary exercise testing (CPET-SE). The responders included patients with an improved EC assessed as a rise in peak oxygen uptake (VO₂) ≥ 1 mL/kg/min. Peripheral oxygen extraction was calculated as arteriovenous oxygen difference (A-VO₂Diff). Out of 41 patients (67% male, mean age 57.5 ± 10 years) after AMI with left ventricular ejection fraction (LVEF) ≥ 40%, 73% improved their EC. In responders, peak VO₂ improved by 27% from 17.9 ± 5.2 mL/kg/min to 22.7 ± 5.1 mL/kg/min, p < 0.001, while non-responders had a non-significant 5% decrease in peak VO₂. In the responder group, the peak exercise heart rate, early diastolic myocardial velocity at peak exercise, LVEF at rest and at peak exercise, and A-VO₂Diff at peak exercise increased, the minute ventilation to carbon dioxide production slope decreased, but the stroke volume and cardiac index were unchanged after CR. Non-responders had no changes in assessed parameters. EC improvement after CR of patients with preserved LVEF after AMI is associated with an increased heart rate response and better peripheral oxygen extraction during exercise.