Value of preparticipation cardiovascular evaluation of master athletes by self-reported symptoms and cardiovascular risk-score.

The risk of sudden cardiac death (SCD) is increased during endurance competitive sports. Coronary artery disease (CAD) is the most common cause of SCD in master athletes ≥ 35 years old (MAs). To reduce the risk of SCD self-assessment of symptoms by questionnaire, and evaluation of cardiovascular risk-score, are recommended as pre-participation cardiovascular evaluation (PCVE). We aimed to examine whether PCVE predicts CVD in MAs with or without increased risk as measured by validated score instruments.We performed a single-site observational cohort study of healthy MAs based on findings at PCVE. They were allocated in two different groups: those MAs with reported symptoms on the questionnaire and/or with elevated cardiovascular risk score were allocated to a symptom group (SG), while MAs with no symptoms, nor raised risk score were defined as control group (CG). Thereafter, all were examined with extended examinations: resting-ECG, cardiorespiratory exercise testing and echocardiography.Total, 81 (18 women) MAs participated in the study. There were no differences at baseline between SG (n = 39) and CG (n = 42); sex (p = 0.11), age (55.0 ± 9.8 vs. 51.9 ± 11.1 years; p = 0.18), maximal oxygen uptake (49.8 ± 7.6 vs. 51.6 ± 7.0 ml/kg/min; p = 0.26), resting heart rate (61.4 ± 12.8 vs. 60.2 ± 11.0/min; p = 0.66), training hours/week (7.0 ± 3.2 vs. 7.1 ± 3.1; p = 0.88). After further examination, sixteen (20%) MAs were found with CVD: 12 in SG, 4 in CG (p = 0.024). The negative predictive value and specificity of the PCVE were 90% and 58%, respectively.Negative findings on PCVE by questionnaire and cardiovascular risk-score may be a strategy to exclude subjects from preparticipation screening, thus saving resources.

Genotype-phenotype correlation in arrhythmogenic right ventricular cardiomyopathy-risk of arrhythmias and heart failure.

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is predominantly caused by desmosomal genetic variants, and clinical hallmarks include arrhythmias and systolic dysfunction. We aimed at studying the impact of the implicated gene(s) on the disease course. METHODS: The Nordic ARVC Registry holds data on a multinational cohort of ARVC families. The effects of genotype on electrocardiographic features, imaging findings and clinical events were analysed. RESULTS: We evaluated 419 patients (55% men), with a mean follow-up of 11.2±7.4 years. A pathogenic desmosomal variant was identified in 62% of the 230 families: PKP2 in 41%, DSG2 in 13%, DSP in 7% and DSC2 in 3%. Reduced left ventricular ejection fraction (LVEF) ≤45% on cardiac MRI was more frequent among patients with DSC2/DSG2/DSP than PKP2 ARVC (27% vs 4%, p<0.01). In contrast, in Cox regression modelling of patients with definite ARVC, we found a higher risk of arrhythmias among PKP2 than DSC2/DSG2/DSP carriers: HR 0.25 (0.10-0.68, p<0.01) for atrial fibrillation/flutter, HR 0.67 (0.44-1.0, p=0.06) for ventricular arrhythmias and HR 0.63 (0.42-0.95, p<0.05) for any arrhythmia. Gene-negative patients had an intermediate risk (16%) of LVEF ≤45% and a risk of the combined arrhythmic endpoint comparable with DSC2/DSG2/DSP carriers. Male sex was a risk factor for both arrhythmias and reduced LVEF across all genotype groups (p<0.01). CONCLUSION: In this large cohort of ARVC families with long-term follow-up, we found PKP2 genotype to be more arrhythmic than DSC2/DSG2/DSP or gene-negative carrier status, whereas reduced LVEF was mostly seen among DSC2/DSG2/DSP carriers. Male sex was associated with a more severe phenotype.

No adverse association between exercise exposure and diffuse myocardial fibrosis in male endurance athletes.

The potential association between endurance exercise and myocardial fibrosis is controversial. Data on exercise exposure and diffuse myocardial fibrosis in endurance athletes are scarce and conflicting. We aimed to investigate the association between exercise exposure and markers of diffuse myocardial fibrosis by cardiovascular magnetic resonance imaging (CMR) in endurance athletes. We examined 27 healthy adult male competitive endurance athletes aged 41 ± 9 years and 16 healthy controls in a cross sectional study using 3 Tesla CMR including late gadolinium enhancement and T1 mapping. Athletes reported detailed exercise history from 12 years of age. Left ventricular total mass, cellular mass and extracellular mass were higher in athletes than controls (86 vs. 58 g/m2, 67 vs. 44 g/m2 and 19 vs. 13 g/m2, all p < 0.01). Extracellular volume (ECV) was lower (21.5% vs. 23.8%, p = 0.03) and native T1 time was shorter (1214 ms vs. 1268 ms, p < 0.01) in the athletes. Increasing exercise dose was independently associated with shorter native T1 time (regression coefficient - 24.1, p < 0.05), but expressed no association with ECV. Our results indicate that diffuse myocardial fibrosis has a low prevalence in healthy male endurance athletes and do not indicate an adverse dose-response relationship between exercise and diffuse myocardial fibrosis in healthy athletes.