Athlete’s heart is generally regarded as a physiological adaptation to regular training, with specific morphological and functional alterations in the cardiovascular system. Development of the noninvasive imaging techniques over the past several years enabled better assessment of cardiac remodeling in athletes, which may eventually mimic certain pathological conditions with the potential for sudden cardiac death, or disease progression. The current literature provides a compelling overview of the available methods that target the interrelation of prolonged exercise with cardiac structure and function. However, this data stems from scientific studies that included mostly male athletes. Despite the growing participation of females in competitive sport meetings, little is known about the long-term cardiac effects of repetitive training in this population. There are several factors—biochemical, physiological and psychological, that determine sex-dependent cardiac response. Herein, the aim of this review was to compare cardiac adaptation to endurance exercise in male and female athletes with the use of electrocardiographic, echocardiographic, and biochemical examination, to determine the sex-specific phenotypes, and to improve the healthcare providers’ awareness of cardiac remodeling in athletes. Finally, we discuss the possible exercise-induced alternations that should arouse suspicion of pathology and be further evaluated.

Physical training is gaining popularity among amateurs. Males and females exhibit different cardiac adaptation to exercise. The aim of the study was to compare the incidence of electrocardiographic abnormalities before and after the marathon between sexes. 12-lead electrocardiogram was performed in 40 male (39±8 years) and 27 female (40±7 years) amateur runners: 2–3 weeks before (Stage 1) and immediately after (Stage 2) the marathon. Abnormalities in the resting (Stage 1) and exercise (Stage 2) electrocardiograms were compared between sexes. At rest left atrial enlargement was more frequent in females than males (48 vs. 20%; p<0.05). The incidence of right atrial enlargement was significantly more common at Stage 2 than 1, both in men (43 vs. 0%; p<0.001) and in women (48 vs. 4%; p=0.001). Significant increase of P-wave amplitude was found in male runners after the marathon (0.12±0.05 vs. 0.21±0.09 mV; p<0.001 Stage 1 vs. 2), but was absent in females. QTc prolongation was observed in both sexes, however to a higher degree in males (p<0.05 for the interaction stage and sex). Although both male and female amateur marathon runners exhibit abnormalities in resting and exercise electrocardiograms, men present more exercise-induced electrocardiographic changes, which might indicate a higher propensity for post-marathon arrhythmias. Electrocardiographic screening in amateurs should be considered.

Introduction: Sport is known to have beneficial influence on cardiovascular system. However, activities of high intensity such as marathon running may adversely affect cardiac morphology and function, especially in the heterogenous group of amateur athletes. As males and females exhibit discrepancies in cardiac response to training, we aimed to compare exercise-induced myocardial alterations between sexes among 61 amateur marathon runners, with the use of evolving echocardiographic techniques and cardiac biomarkers.Methods: The study followed three stages: 2–3 weeks prior the marathon (Stage 1), at the finish line (Stage 2) and 2 weeks after the run (Stage 3). Echocardiographic examination along with blood analyses for biomarkers of cardiac injury and overload [creatine kinase, high sensitivity cardiac troponin I, heart-type fatty acid binding protein, B-type natriuretic peptide, galectin-3 (Gal-3), endothelin-1 (ET-1), interleukin-6 and neopterin] were performed at each stage.Results: After the marathon there was a transient increase in right ventricular (RV) size and concomitant decrease in left ventricular (LV) volumes, leading to a significant increase of RV end-diastolic volume (RVEDV)/LVEDV ratio (0.91 ± 0.21 vs. 1.10 ± 0.22, p < 0.001 in males; 0.73 ± 0.17 vs. 1.02 ± 0.22, p < 0.001 in females). Although at Stage 2 RV contractility decreased, while LV ejection fraction (LVEF) remained at the same level in both sexes, men had greater tendency for LVEF reduction (p < 0.05 for the interaction sex and stage). The concentrations of biomarkers were higher after the run in both study groups, except for ET-1 and neopterin, which increased post-race only in males. The larger training-related rise in Gal-3 level correlated with the greater drop in LVEF at Stage 2 (r = −0.42; p < 0.05). Less-trained marathoners with lower VO₂max values after the race showed higher levels of Gal-3 post-run (r = −0.29; p < 0.05).Conclusion: Marathon running induces transient cardiac remodelling, more pronounced in male than female athletes. Structural and functional changes assessed by echocardiography correspond with biochemical alterations. Galectin-3 was the best biomarker to reflect overload changes. Cardiovascular screening in amateur runners should be implemented to identify subjects requiring further evaluation.

Radiotherapy (RT) may have a cardiotoxic effect on the heart and cardiovascular system. Postulated mechanisms mediating these complications include vascular endothelium damage and myocardial fibrosis. The aim of our study was to assess endothelial damage and myocardial fibrosis in the early period after RT on the basis of cardiac biomarkers and in relation to the radiation dose applied to individual heart structures in patients treated for non-small-cell lung cancer. This single-center prospective study included consecutive patients with lung cancer (LC) who were referred for treatment with radiochemotherapy (study group) or chemotherapy (control group). The study protocol included performing an echocardiographic examination, a standard ECG examination, and collecting blood samples for laboratory tests before starting treatment for lung cancer in the first week after completing RT (after four cycles of chemotherapy in the control group) and after 12 weeks from the end of treatment. The study included 23 patients in the study group and 20 patients in the control group. Compared to the baseline values, there was a significant increase in total cholesterol concentration in the study group immediately after the end of RT, which persisted for three months after the end of therapy. After taking into account the use of statins in the analysis, it was found that an increase in total cholesterol concentration after oncological treatment was observed only among patients who did not use statins. Taking into account the assessment of myocardial fibrosis markers, there were no significant changes in the concentration of matrix metallopeptidase 9 (MMP-9) and tissue inhibitors of metalloproteinases 1 (TIMP-1) in the study group. In patients treated with radiochemotherapy, there was a significant increase in the concentration of intercellular adhesion molecule 1 (ICAM-1) immediately after RT, when compared to the baseline. After taking into account the use of statins, an increase in ICAM-1 concentration immediately after RT was observed only in patients who did not use statins. There was also a significant correlation between the radiation dose received by the left anterior descending coronary artery (LAD) and left circumferential coronary artery, and vascular cell adhesion protein 1 (VCAM-1) concentration measured at three months after the end of RT. Immediately after completion of radiotherapy, a significant increase in the level of ICAM-1 is observed indicating endothelial damage. The radiation dose to coronary arteries should be minimized, as it correlates with the concentration of VCAM-1. The use of statins may prevent the increase in total cholesterol and ICAM-1 concentration after irradiation for lung cancer; however, further studies designed for this specific purpose are necessary to confirm the effectiveness of statins in this area.

In patients with idiopathic ventricular fibrillation (VF), recurrent implantable cardioverter-defibrillator (ICD) shocks might increase mortality risk and reduce patients’ quality of life. Catheter ablation of triggering ectopic beats is considered to be an effective method. We present a patient with recurrent VF, caused by the “R on T” premature ventricular complexes. In the presented case radiofrequency catheter ablation efficiently eliminated arrhythmia trigger, which was possible to detect thanks to the intracardiac electrocardiograms (ECG’s) stored in the ICD.

Background: Anticancer treatment is associated with many side effects, including those involving the cardiovascular system. While many studies are available on the effects of radiotherapy (RT) on the left ventricle (LV), studies are lacking on the early effects of RT on the structure and function of the right ventricle (RV). Our study aims to assess, using modern echocardiographic techniques, the effect of irradiation on RV systolic function in the mid-term follow-up of patients undergoing RT for lung cancer (LC). Methods: This single-center, prospective study included consecutive patients with LC who were referred for treatment with definite radiotherapy and chemotherapy (study group) or chemotherapy only (control group). Results: The study included 43 patients with a mean age of 64.9 ± 8.1 years. Cancer treatment-related RV toxicity (CTR-RVT) was found in 17 patients (40%). Early reductions in TAPSE values were observed among patients in the study group (20.3 mm vs. 22.1 mm, p = 0.021). Compared to baseline, there was a significant reduction in RV global longitudinal strain (RV GLS) in the study group immediately after the treatment (−21.1% vs. −18.4%, p = 0.02) and also at 3 months after RT (−21.1% vs. −19.1%, p = 0.021). A significant reduction in the RV FWLS value was also observed at 3 months after the end of the treatment (−23.8% vs. −21.8, p = 0.046). There were no significant changes in the three-dimensional right ventricular ejection fraction (3DRVEF) during the follow-up. We found a correlation (p = 0.003) between the mean dose of radiation to the RV and 3DRVEF when assessed immediately after RT. The mean dose of radiation to the heart correlated with RV free-wall longitudinal strain (RV FWLS) immediately after RT (p = 0.03). Conclusions: RV cardiotoxicity occurs in nearly half of patients treated for lung cancer. TAPSE is an important marker of deterioration of RV function under LC treatment. Compared to 3DRVEF, speckle tracking echocardiography is more useful in revealing deterioration of RV systolic function after radiotherapy.