RESUMO
Background: Brugada syndrome (BrS) is a cardiac ion channelopathy that predisposes affected individuals to sudden cardiac death (SCD). Type 1 BrS is thought to take a more malignant clinical course than non-type 1 BrS. We hypothesized that the degrees of abnormal repolarization and conduction are greater in type 1 subjects and these differences can be detected by electrocardiography (ECG). Methods: Electrocardiographic data from spontaneous type 1 and non-type 1 BrS patients were analyzed. ECG parameters were measured from leads V1 to V3. Values were expressed as median [lower quartile-upper quartile] and compared using Kruskal-Wallis ANOVA. Results: Compared to non-type 1 BrS patients (n = 29), patients with spontaneous type 1 patterns (n = 22) showed similar (P > 0.05) heart rate (73 [64-77] vs. 68 [62-80] bpm), QRS duration (136 [124-161] vs. 127 [117-144] ms), uncorrected QT (418 [393-443] vs. 402 [386-424] ms) and corrected QT intervals (457 [414-474] vs. 430 [417-457] ms), JTpeak intervals (174 [144-183] vs. 174 [150-188] ms), Tpeak- Tend intervals (101 [93-120] vs. 99 [90-105] ms), Tpeak- Tend/QT ratios (0.25 [0.23-0.27] vs. 0.24 [0.22-0.27]), Tpeak- Tend/QRS (0.77 [0.62-0.87] vs. 0.77 [0.69-0.86]), Tpeak- Tend/(QRS × QT) (0.00074 [0.00034-0.00096] vs. 0.00073 [0.00048-0.00012] ms-1), index of Cardiac Electrophysiological Balance (iCEB, QT/QRS, marker of wavelength: 3.14 [2.56-3.35] vs. 3.21 [2.85-3.46]) and corrected iCEB (QTc/QRS: 3.25 [2.91-3.73] vs. 3.49 [2.99-3.78]). Higher QRS dispersion was seen in type 1 subjects (QRSd: 34 [24-66] vs. 24 [12-34] ms) but QT dispersion (QTd: 48 [39-71] vs. 43 [22-94] ms), QTc dispersion (QTcd: 52 [41-79] vs. 46 [23-104] ms), JTpeak dispersion (44 [23-62] vs. 45 [30-62] ms), Tpeak- Tend dispersion (28 [15-34] vs. 29 [22-53] ms) or Tpeak- Tend/QT dispersion (0.06 [0.03-0.08] vs. 0.08 [0.04-0.12]) did not differ between the two groups. Type 1 subjects showed higher (QRSd × Tpeak- Tend)/QRS (25 [19-44] vs. 19 [9-30] ms) but similar iCEB dispersion (0.83 [0.49-1.14] vs. 0.61 [0.34-0.92]) and iCEBc dispersion (0.93 [0.51-1.15] vs. 0.65 [0.39-0.96]). Conclusion: Higher levels of dispersion in conduction and repolarization are found in type 1 than non-type 1 BrS patients, potentially explaining the higher incidence of ventricular arrhythmias in the former group.
RESUMO
Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is an inherited myocardial disease characterized by fibro-fatty replacement of the right ventricular myocardium, and associated with paroxysmal ventricular arrhythmias and sudden cardiac death (SCD). It is currently the second most common cause of SCD after hypertrophic cardiomyopathy in young people <35 years of age, causing up to 20% of deaths in this patient population. This condition has a male preponderance and is more commonly found in individuals of Italian and Greek descent. To date, there is no single diagnostic test for ARVC/D and the diagnosis is made based on clinical, electrocardiographic, and radiological findings according to the Revised 2010 Task Force Criteria. In this review, we will discuss the mainstay treatment which includes pharmacotherapy, implantable cardioverter-defibrillator insertion for abortion of sudden cardiac death, and in the advanced stages of the disease cardiac transplantation.
RESUMO
BACKGROUND: There is a lack of echocardiographic studies to address the detection of atrial masses and abnormal venous connections in patients with secundum atrial septal defect (ASD) repair. This study sought to demonstrate that with proper technique, these unusual conditions could be diagnosed confidently by transthoracic echocardiography. METHOD: We performed a retrospective review of all repaired ASD patients of all ages with follow-up echocardiography done at Beijing Anzhen Hospital from year 1999 to 2005. Clinical and echocardiographic features of patients with aforementioned conditions were evaluated. RESULTS: Systematic echocardiographic protocol identified 11 patients with unusual conditions, in whom four patients had atrial masses (three atrial thrombi, one inflammatory pseudotumor) and seven patients had abnormal venous connections (two inadvertent diversion of inferior vena cava to left atrium, five previously unrecognized partial anomalous pulmonary venous connections). CONCLUSION: Atrial masses and abnormal venous connections could be diagnosed through a systematic echocardiographic approach in evaluating patients with ASD repair.