![]() Premature ventricular contractions (PVCs) originating from the right ventricle typically show an LBBB pattern with a predominantly negative QRS complex in V1. Low voltage in limb leads, defined as a QRS amplitude ≤5 mm in each of the limb leads (I, II and III), also can be suggestive of ARVC (figure 11). Prolonged S wave upstroke may be present in up to 95% of patients with ARVC in the absence of RBBB. The S wave upstroke is measured from the nadir of the S wave to the end of the QRS (including epsilon wave if present). 49 This feature is most commonly observed among ARVC patients with mild QRS prolongation (100–120 ms). ![]() 49ĭelayed S wave upstroke of >55 ms in leads V1–V3 in the absence of complete RBBB represents a minor diagnostic criterion for ARVC (figure 11). The presence of epsilon waves in the right precordial leads V1–V3 represents a major diagnostic criterion for ARVC. Epsilon waves are challenging to detect and appear as a small negative deflection just beyond the QRS in V1–V3 (figure 10). 49 Thus, TWI involving at least two consecutive precordial leads, excluding V1, should prompt further investigation in the athlete.Įpsilon waves are defined as distinct low-amplitude potentials localised at the end of the QRS complex. TWI extending beyond V3 is uncommon in patients with RBBB and represents a minor diagnostic criterion for ARVC. 28 In the presence of complete RBBB, right precordial (V1–V3) TWI is more likely secondary to RBBB rather than a sign of underlying ARVC. 49 In Italian children ≥14 years with TWI in the anterior precordial leads beyond V2 (ie, V3 or V4), 3 of 26 (11%) fulfilled diagnostic criteria for ARVC (1 definitive, 2 borderline). TWI in V1–V3 or beyond in individuals >14 years of age (in the absence of complete RBBB) represent a major diagnostic criterion for ARVC, while TWI confined to just leads V1 and V2 in individuals >14 years of age (in the absence of complete RBBB) represents a minor diagnostic criterion. 50 TWI occasionally extends to the left precordial leads V5–V6 or inferior limb leads II, III and aVF. TWI in the anterior precordial leads (V1–V3/V4) is present in approximately 85% of patients with ARVC in the absence of RBBB (figures 10 and 11). If there is primarily LV involvement, the TWI involves the lateral precordial leads and the premature ventricular beats can have an RBBB morphology. 45 50 51 ECG abnormalities include TWI in the anterior precordial leads, epsilon waves, delayed S wave upstroke, lowvoltage in limb leads and premature ventricular beats with an LBBB morphology and superior axis. Over 80% of patients with ARVC will have an abnormal ECG. 49 The diagnosis is fulfilled in the presence of two major criteria, one major plus two minor criteria, or four minor criteria from different groups. The original (1994) and the revised (2010) Task Force Criteria for diagnosis of ARVC are based on major and minor criteria encompassing familial/genetic, ECG, arrhythmic, morphofunctional ventricular and histopathological features. 44 45 Contribution as a cause of SCDĪccording to data from the Veneto region of Italy where postmortem investigation of young sudden death victims is performed systematically, ARVC is a leading cause of sport-related sudden death accounting for approximately one-fourth of fatalities in young competitive athletes.3 Data from the USA, notably without a mandatory registry for SCD in athletes, suggest that ARVC is a less common cause of SCD. 46–48 The prevalence of familial ARVC is estimated at 1 : 2000–1 : 5000 persons. 44 45 In addition, there is emerging evidence that intense endurance sports may lead to a similar phenotype (with similar prognosis) in the absence of desmosomal mutations, so-called exercise-induced ARVC, which may be the result of increased RV wall stress during exercise. Mutations in the desmosomal genes account for approximately 50% of ARVC cases. Variants with predominantly LV involvement are described in about 10% of patients (hence the alternative term of arrhythmogenic cardiomyopathy). Progressive dilation/dysfunction predominantly involves the right ventricle with involvement of the left ventricle in late-stage disease. Deel II: Arrhythmogenic right ventricular cardiomyopathyĪRVC is an inherited heart muscle disease characterised by fibro-fatty replacement of right ventricular myocardium and corollary life-threatening ventricular arrhythmias or SCD, mostly in young people and athletes. Voor de complete introductie zie Sport & Geneeskunde 3-2013, pag. Hierin kunt u lezen dat differentiatie tussen fysiologie en pathologie op het ECG bij een sporter soms zeer moeilijk kan zijn, vooral omdat het ECG van een sporter bedrieglijk veel kan lijken op dat van iemand met CMP. In dit deel wordt het ECG bij sporters met een cardiomyopathie onder de loep genomen. ![]() Na publicatie (met toestemming) van de eerste twee delen van de “ECG bundel”, overgenomen uit BJSM 2013 in Sport & Geneeskunde, volgt hier het tweede deel van deel 3.
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