Hypertrophic cardiomyopathy (HCM) is a cardiac muscle disorder characterized by generally asymmetric abnormal hypertrophy of the left ventricle without abnormal loading conditions (such as hypertension or valvular heart disease) accounting for the left ventricular wall thickness or mass. The incidence of sudden cardiac death (SCD) in HCM patients is about 1% yearly in adults, but it is far higher in adolescence. HCM is the most frequent cause of death in athletes in the Unites States of America. HCM is an autosomal-dominant genetic cardiomyopathy, and mutations in the genes encoding sarcomeric proteins are identified in 30–60% of cases. The presence of this genetic mutation carries more than 2-fold increased risk for all outcomes, including ventricular arrhythmias. Genetic and myocardial substrate, including fibrosis and intraventricular dispersion of conduction, ventricular hypertrophy and microvascular ischemia, increased myofilament calcium sensitivity and abnormal calcium handling, all play a role as arrhythmogenic determinants. Cardiac imaging studies provide important information for risk stratification. Transthoracic echocardiography can be helpful to evaluate left ventricular (LV) wall thickness, LV outflow-tract gradient and left atrial size. Additionally, cardiac magnetic resonance can evaluate the prevalence of late gadolinium enhancement, which when higher than 15% of LV mass is a prognostic maker of SCD. Age, family history of SCD, syncope and non-sustained ventricular tachycardia at Holter ECG have also been validated as independent prognostic markers of SCD. Arrhythmic risk stratification in HCM requires careful evaluation of several clinical aspects. Symptoms combined with electrocardiogram, cardiac imaging tools and genetic counselling are the modern cornerstone for proper risk stratification.

Physical activity is recommended for the prevention of primary and secondary cardiovascular (CV) disease as it is linked to a number of health benefits, especially CV. However, recent research suggests that high-volume, long-term endurance exercise may hasten rather than slow the coronary atherosclerosis progression. This contentious theory has generated a great discussion and is still a major source of doubt when it comes to the clinical treatment of coronary artery disease (CAD) in athletes. CAD is the primary cause of sudden cardiac death in athletes over 35 years. Thus, recent studies evaluated the prevalence of CAD in athletes and its clinical and prognostic implications. Indeed, many studies have shown a relationship between endurance sports and higher volumes of coronary calcified plaque as determined by computed tomography. However, the precise pathogenetic substrate for the existence of an increased coronary calcification burden among endurance athletes remains unclear. Moreover, the idea that coronary plaques in elite athletes present a benign morphology has been cast into doubt by some recent studies showing potential association with adverse cardiovascular events. This review aims to analyze the association between physical activity and CAD, explaining possible underlying mechanisms of atherosclerotic progression and non-ischemic coronary lesions, focusing primarily on clinical and prognostic implications, multimodal evaluation, and management of CAD in endurance athletes.

Aims: Low QRS voltages (LQRSV) are an unexpected finding in left ventricular hypertrophy, i.e. hypertrophic cardiomyopathy (HCM) or athlete’s heart. Methods and results: Prevalence and clinical correlates of LQRSV were investigated in 197 consecutive HCM patients, aged 58 ± 13 years and comparatively in 771 Olympic athletes, aged 23 ± 4. Clinical characterization included family/personal history, symptoms, New York Heart Association (NYHA) functional class, electrocardiographic pattern, ventricular arrhythmias, and cardiac magnetic resonance (CMR). Twenty-two (11%) of HCM and 18 (2.3%) of athletes presented LQRSV. At initial evaluation, in HCM, LQRSV showed no differences vs. non-LQRSV for functional class (90% vs. 91%, in Classes I and II; P = 0.983), symptoms (27% vs. 18%; P = 0.478), and ventricular arrhythmias (40% vs. 39%; P = 857) but showed larger extent of late gadolinium enhancement (LGE) at CMR (4.1 ± 1.5 vs. 1.5 ± 0.7 affected segments; P < 0.001). In athletes, LQRSV was associated with larger prevalence of inverted T-waves (22% vs. 9%; P < 0.001) and ventricular arrhythmias (28% vs. 8%; P = 0.005). In one LQRSV athlete, arrhythmogenic cardiomyopathy was identified. Over 4.5 ± 2.6-year follow-up, presence of LQRSV in HCM was associated with larger incidence of functional deterioration (31% vs. 14%; P = 0.038), stroke (22% vs. 6%; P = 0.008), and implantable cardioverter defibrillator (ICD) implant (27% vs. 10%; P = 0.015). No clinical events occurred in LQRSV athletes without initial evidence of cardiac disease. Conclusion: LQRSV are relatively common (11%) in HCM and have clinical relevance, being predictive over a medium term for a worsening functional class, incidence of stroke, and ICD implant. Instead, LQRSV are rare (2.3%) in athletes but may occasionally be a marker that raises suspicion for underlying cardiac disease at risk.

Background: The foot racing disciplines include sprints, middle distances, and long distances, which vary in terms of intensities, duration of training, and metabolic demands. The aim of our study was to evaluate the differences in morpho-functional parameters describing cardiac remodeling in a large cohort of Olympic athletes practicing the different track subspecialties. Methods: We evaluated 140 track and field (52.1% males, mean age 26.3 ± 4.3 years) Olympic athletes divided into four groups according to the distance performed: Group A (46, 32.9%): 100 and 200 mt; Group B (34, 24.3%): 400 mt; Group C (25, 17.9%): 800, 1500, and 3000 mt; Group D (35, 24.9%): 5000, 10,000 mt, and marathon distance. The athletes underwent a pre-participation screening, which included transthoracic echocardiography and exercise stress testing. Results: In Group A and in Group B, most athletes presented normal cardiac geometry (41/46, 89.1% in Group A and 31/34, 91.2% in Group B, p < 0.0001). Instead, in Groups C and D, more than half presented eccentric cardiac remodeling (13\25, 52% in Group C and 23\35, 65.7% in Group D). No significant differences were found between subspecialties in LVEF (p = 0.587), diastolic function (p = 0.431), and training hours/week (p = 0.078). Conclusions: In conclusion, the presence and extent of cardiac remodeling vary according to the distance of the discipline practiced, with the largest dimensional increase in both left and right ventricles and atria in mid- and long-distance runners and the lowest in sprinters.

Background: ESC sports classification in 2020, based on cardiac morphological adaptations, may not fully reflect also the variations in functional parameters of athletes. This study aims to characterize CPET-derived physiological parameters in elite athletes according to the ESC classification and evaluate whether this morphological classification also corresponds to a functional categorization. Methods: Elite athletes underwent pre-participation screening before the 2023 European Games and 2024 Olympic Games. Athletes were classified into four categories (skill, power, mixed and endurance). CPET was performed on a cycle ergometer using a ramp protocol, with measurements of VO₂ max, heart rate, power output and ventilatory efficiency. Results: We enrolled 1033 athletes (46.8% females; mean 25.6 ± 5.2 years old) engaged in skill (14.1%), power (33.2%), mixed (33.3%) and endurance (19.4%) disciplines. O₂ pulse showed an incremental significant increase (p < 0.0001) among sport categories (skill 14.9 ± 3.8 mL/beat; power 17.5 ± 4.6 mL/beat, mixed 19 ± 4.3 mL/beat and endurance 22.7 ± 5.8 mL/beat). The lowest ${\dot{\mathrm{V}}\mathrm{O}}_2$max was observed in skill disciplines (36.3 ± 7.9 mL/min/kg) whilst endurance ones showed the highest values (52.4 ± 9.7 mL/min/kg) (p < 0.0001). ${\dot{\mathrm{V}}\mathrm{O}}_2$max was higher in power compared to mixed (42 ± 7.7 mL/min/kg vs. 40.5 ± 5.8 mL/min/kg, p = 0.005) disciplines with an overlapping amount between some mixed and power disciplines. No differences were found for VE max (p = 0.075). Conclusions: Our study provided values of CPET parameters in elite athletes. Significant differences in CPET parameters were observed among different sports disciplines, with endurance athletes showing the highest absolute and relative values in all parameters. An overlap amount was noted between mixed and power categories, especially for relative maximal oxygen consumption.

Introduction: Metabolic syndrome (MS) is a growing global public health concern that is associated with increased risk for cardiovascular events, even in athletes. The lipid accumulation product (LAP) index and cardiometabolic index (CMI) have been shown to be efficient markers of MS in the general population; its applicability in athletes has not been discussed yet. We aimed to assess the role of LAP and CMI in predicting MS in athletes. Methods: We retrospectively enrolled 793 Olympic athletes practicing different sporting disciplines (power, skill, endurance, and mixed), classified arbitrarily into no risk (NR), low risk (LR), high risk (HR), or MS if they had 0, 1, 2, or 3 criteria for MS, respectively. Evaluations included a calculation of the LAP index, CMI, anthropometric measurements, and clinical and laboratorial variables. Results: Among our population, only 0.8% reached the criteria for MS, 9.1% were at HR for MS, 37.8% were defined as LR, and 52.3% had NR. Significant differences in anthropometric parameters and the principal components of MS criteria (blood pressure, lipidic profile, glycemia) were reported predominantly in HR athletes and those with MS (p < 0.0001). LAP and CMI presented linearly increasing values from individuals with NR to those with MS (p < 0.0001). In addition, HR and MS athletes were classified as “likely MS” (9.8%) and LR and NR athletes as “unlikely MS” (90.2%). After adjusting for potential confounders, LAP ≥ 34.66 and CMI ≥ 0.776 emerged as independent predictors for MS in the overall cohort (Hazar Ratio (HR) 7.22 [3.75–13.89], p < 0.0001, and HR 5.37 [2.96–9.73], p < 0.0001, respectively). The ROC curve revealed that these cut-offs in the general population predict MS with an area under the curve (AUC) of 0.80 and 0.79, respectively, for LAP and CMI. However, gender-related cut-offs seem to be more precise in predicting MS (LAP ≥ 38.79 for male, LAP ≥ 14.16 for female, and CMI ≥ 0.881 for male and ≥0.965 for female). Conclusion: The ROC curve analyses of LAP and CMI showed good diagnostic accuracy in predicting MS among athletes, despite the low prevalence of MS in our sample. Thus, these indexes may be used to promote screening for primary prevention and early detection of athletes at risk for MS to establish an early prevention strategy. Larger prospective studies are necessary to validate their benefit in the general population.