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Background Recently, novel interest in low QRS voltages was prompted by the observation that low QRS voltages are present in arrhythmogenic cardiomyopathy patients, even before occurrence of symptoms/events. Aim The purpose of this study was to assess prevalence and clinical correlates of low QRS voltages in Olympic athletes, evaluated and followed-up within our cardiovascular screening programme. Methods Five hundred and sixteen athletes consecutively examined (2010–2011) were included in this study. A low QRS voltage was defined as amplitude of QRS <0.5 mV in limb and/or <1.0 mV in precordial leads. Cardiovascular evaluation included 12-lead and exercise electrocardiogram, echocardiography and, selectively, additional tests to confirm diagnosis. Athletes were followed-up for 5 ± 2 (1–9) years. Results The majority of athletes (493; 96%) showed normal/increased R/S-wave voltages, but 23 (4%) had low QRS voltages. No differences were observed in low QRS voltage athletes compared to normal/increased QRS voltages for QRS duration, QTc and PR intervals, left ventricular cavity size and mass, or gender and sport participated. However, premature ventricular beats, occurred more frequently in low QRS voltages (39% vs 7%; p < 0.001), with patterns suggesting origin from left or right free wall. No diseases or events were registered in low QRS voltage athletes over the follow-up. Conclusions In Olympic athletes, the prevalence of low QRS voltages was 4%. Athletes with low QRS voltages did not differ from other athletes according to sport participated in or cardiac dimensions. However, more frequently (39% vs 7%) they showed premature ventricular beats, originating from either the left or right free ventricular wall. Therefore, long-term follow-up with serial clinical evaluations is needed in low QRS voltage athletes, in order to definitely clarify the clinical significance.

Background Low-QRS voltages (LQRSV) are an unexpected finding in left ventricular (LV) hypertrophy, i.e, hypertrophic cardiomyopathy (HCM) or athlete’s heart. Methods 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, NYHA functional class, ECG pattern, ventricular arrhythmias and cardiac magnetic resonance (CMR). Results 22 (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 class I-II; p=0.983), symptoms (27% vs. 18%; p=0.478), ventricular arrhythmias (40% vs. 39%; p=857), but showed larger extent of LGE at CMR (4.1±1.5 vs. 1.5±0.7 affected segments; p&lt;0.001). In athletes, LQRSV was associated with larger prevalence of inverted T-waves (22% vs. 9%; p&lt;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 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.

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.