Evaluation of possible CPVT Evaluation of possible CPVT should be referred to a cardiologist. An exercise stress ECG such as an exercise treadmill test may be diagnostic in CPVT. Infusion of intravenous catecholamines (isoproterenol) during ECG monitoring or CPVT genetic testing may confirm the diagnosis in questionable cases.1 44 Brugada syndrome BrS is a primary electrical disease which is characterised by the distinctive ECG pattern of ‘high take-off“ ST segment elevation in the right precordial leads and predisposes to ventricular fibrillation and sudden death in the absence of clinically demonstrable structural heart disease.45 Loss-offunction defects in the SCN5A gene, which encodes for the -subunit of the sodium channel, accounts for approximately 20–25% of BrS and approximately 40% of BrS accompanied by prolonged PR intervals.1 45–47 Prevalence and contribution as a cause of SCD The syndrome is estimated to account for up to 4% of all sudden deaths in the general population and 5–20% of sudden deaths victims with a structurally normal heart at autopsy.20 45 Ventricular fibrillation and sudden death in patients with BrS occurs more commonly during rest and sleep and is unrelated to exercise. Diagnostic criteria In 2002, a consensus conference endorsed by the Heart Rhythm Society and the European Heart Rhythm Association proposed ECG criteria for the diagnosis of BrS.48 Three types of Brugada ECG (Br-ECG) patterns were defined: the ‘diagnostic’ (type 1) which is characterised by a ‘coved-type’ ST segment elevation in the right precordial leads, and the ‘non-diagnostic’ (types 2 and 3) which show a ‘saddleback’ configuration. (figure 8) The type 1 Br-ECG may be unmasked or worsened by sodium channel blockers such as ajmaline, flecainide and procainamide.49 Higher placement of the V1 and V2 electrodes in the second intercostal space (rather than the fourth intercostal space) also can precipitate a type 1 Brugada ECG pattern. Conversion of type 2 and 3 Br-ECG to type 1 by sodium channel blocker administration is considered diagnostic for a positive Brugada ECG pattern and is used in clinical practice for diagnosis and management of BrS according to current guidelines.49 ECG findings in Brugada syndrome Type 1 Brugada pattern ECG is defined as a high-take off and downsloping ST segment elevation ≥2 mm followed by a negative T-wave in at least two contiguous leads (V1–V3) (figure 8). Type 2 and 3 Brugada pattern ECGs have a ‘saddleback’ appearance with J-point elevation ≥2 mm, ST segment elevation >1 mm in type 2 and ≤1 mm in type 3, and either a positive or biphasic T-wave (figure 8). The downsloping ST elevation in Brugada type-1 ECG should be distinguished from the ‘convex’ ST segment elevation characteristic of early repolarisation in a trained athlete (figure 9). Measuring the ST elevation at the start of the ST segment/ J-point (STJ) and 80 ms after the start of the ST segment (ST80) can help differentiate the slope of the ST segment. In Brugada type-1 pattern the downsloping ST segment will have a STJ/ ST80 ratio >1. In early repolarisation patterns in an athlete the initial upsloping of the ST segment will produce a STJ/ST80 ratio <1 (figure 9). Evaluation of possible brugada syndrome Patients with a type 1 Brugada pattern ECG should be referred to a cardiac electrophysiologist for further evaluation and management. Ventricular pre-excitation The PR interval is the time required for the electrical impulse to travel from the sinus node through the AV node to the Purkinje fibres, and it is measured from the beginning of the P wave to the beginning of the QRS. Ventricular pre-excitation occurs when an accessory pathway of electrical activation bypasses the AV node. As a result, there is abnormal conduction to the ventricle (pre-excitation) with shortening of the PR interval and widening of the QRS. This is evident on the ECG as the Wolf–parkinson–White (WPW) pattern. Prevalence and contribution as a cause of SCD WPW pattern occurs in approximately 1 : 1000 athletes.50 The presence of an accessory pathway can predispose an athlete to sudden death if the athlete also goes into atrial fibrillation. Rapid conduction of atrial fibrillation across the accessory pathway can result in ventricular fibrillation. The risk of sudden death associated with asymptomatic WPW pattern in most population-based studies is 0.1% per year in adults.51 There is evidence to suggest a higher risk of sudden death in asymptomatic children and younger adults with WPW pattern.52–54 Overall, WPW accounted for 1% of cardiovascular deaths in a long-term registry of sudden death in athletes.4 Diagnostic criteria and ECG findings in ventricular pre-excitation WPW pattern is defined as a short PR interval (<120 ms), nummer 5 | november 2013 | Sport & Geneeskunde 27 Pagina 26
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