• 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • A type saddle back type


    A type 2 (“saddle-back type”) or type 3 ST-segment elevation cannot substitute for a type 1, unless converted to type 1 with fever or sodium drug challenge. A drug challenge–induced type 1 can be used to diagnose BrS only if accompanied by 1 of the criteria specified above. Type 2 is characterized by ST-segment elevation ≥0.5mm (generally ≥2mm in V2) in ≥1 right precordial lead (V1−V3), followed by a convex ST. The ST segment is followed by a positive T wave in V2 and variable morphology V1. Type 3 is characterized by either a saddleback or coved appearance with an ST-segment elevation o1 mm. Placement of the right precordial leads in more cranial positions (in the 3rd or 2nd intercostal space) in a 12-lead resting ECG or 12-lead Holter ECG increases the sensitivity of ECG [51–53]. It is recommended that tolterodine tartrate ECG recordings be obtained in the standard and superior positions for the V1 and V2 leads. Veltman et al. [54]. showed that RVOT localization using magnetic resonance imaging (MRI) correlates with type 1 ST-segment elevation in BrS and that lead positioning according to RVOT location improves the diagnosis of BrS. Interestingly, in most cases a type I pattern was found in the 3rd intercostal space in the sternal and left parasternal positions [54]. In reviewing ECGs of a large cohort of BrS patients, Richter et al [55]. concluded that lead V3 does not yield diagnostic information in BrS. A proposed diagnostic score system for BrS, referred to as the Proposed Shanghai BrS Score, is presented in Table 2. These recommendations are based on the available literature and the clinical experience of the Task Force members [8,56–60]. Weighting of variables is based on expert opinion informed by cohort studies that typically do not include all variables presented. Thus, rigorous, objectively weighted coefficients were not derived from large-scale risk factor and outcome- informed datasets. Nonetheless, the authors believed that some inferential weighting would be of benefit when applied to patients. As with all such recommendations, they will need to undergo initial and ongoing validation in future studies.
    Pharmacologic tests and other diagnostic tools When there is clinical suspicion of BrS in the absence of spontaneous type 1 ST-segment elevation, a pharmacologic challenge using a sodium channel blocker is recommended. A list of agents used for this purpose is presented in Table 1 (also see The test is considered positive only if a type 1 ECG pattern is obtained, and it should be discontinued in case of frequent ventricular extrasystoles or other arrhythmias, or widening of the QRS 4130% over the baseline value [6]. As an alternative, the “full stomach test” has been proposed for diagnosing BrS [61]. In this case, ECGs are performed before and after a large meal. The use of “high electrodes” increases the sensitivity for recognizing spontaneous type I ST-segment elevation at night or after heavy meals [62]. A type 1 ST-segment elevation recorded using a Holter is a spontaneous type 1, and it is reasonable to assume that a spontaneous type 1 recorded by Holter at night or after a large meal has more value—both diagnostic and prognostic—than a drug-induced type 1. Drug challenge is not indicated in asymptomatic patients displaying the type 1 ECG under baseline conditions because of the lack of the additional diagnostic value. These provocative drug tests are also not recommended in cases in which fever has been documented to induce a type I ECG, other than for research purposes. Much debate has centered around the definition of a false-positive sodium channel block challenge [63]. The consensus is that a false-positive is difficult to define because of the lack of a gold standard. The development of a type 1 ST-segment elevation in response to sodium block challenge should be considered as probabilistic, rather than binary, in nature. As will be discussed later, a similar approach is recommended in evaluating the ability of genetic variants to promote the BrS phenotype.