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In the past few years, the presence of fragmentation in the QRS complex has been demonstrated to be related to diseases such as myocardial fibrosis, cardiac sarcoidosis, arrythmogenic cardiopathies, acute coronary syndrome, and Brugada syndrome, among others. The detection of fragmentation in the QRS is usually carried out manually, which represents a subjective pattern recognition task that demands an effort by the clinician, increasing with the number of patients. These problems have made the process of fragmentation detection a good candidate to its automatization. In this work, we used a database with over six-thousand 12-lead ECG from Hospital Virgen de la Arrixaca de Murcia (Spain), which where digitally recorded with GE MAC5000. Affected and non-affected patients records were extracted for computerized analysis. Clinical supervision was performed for gold-standard development and for signal classification. Fragmentation detection algorithms were developed using first and second derivatives calculation in the pre-qualified segments of the signal, after fiducial point detection. The obtained results were 96.88% sensitivity, 72.92% specificity, and 82.50% accuracy. These results confirm that it is possible to automatically detect fragmentation, constituting a relevant tool to pre-qualify patients for further diagnostic-tests, and it also opens new opportunities for computerized diagnosis.

A 62-year-old woman who underwent heart transplantation 6 years later presented a regular atrial tachycardia. Electrophysiologic evaluation showed an atrial arrhythmia in the recipient atrium with 2:1 conduction to the donor atrium, with a confusing electroanatomical map. With the suspect of alternant conduction through two different breakthroughs, the map was split in two concordant maps, corresponding to two connections that were successfully ablated. Later on, a third connection was detected and therefore ablated. (PACE 2011; 1–3)

Introduction and objectives Long QT syndrome is an inherited ion channelopathy that leads to syncope and sudden death. Because of the heterogeneous phenotype of this disease, genetic testing is fundamental to detect individuals with concealed long QT syndrome. In this study, we determined the features of a family with 13 carriers of the KCNH2-H562R missense mutation, which affects the pore region of the HERG channel. Methods We identified the KCNH2-H562R mutation in a 65-year-old man with a prolonged QTc interval who had experienced an episode of torsade de pointes. Subsequently, a total of 13 mutation carriers were identified in the family. Carriers (age 48 [26] years; 46% males) underwent clinical evaluation, electrocardiography and echocardiography. Results The mean (standard deviation) QTc in carriers was 493 (42) ms (3 [23%] showed normal QTc); 6 (46%) had symptoms (4, syncope; 1, sudden death; 1, aborted sudden death [proband]). While under treatment with beta-blockers, 11 of 12 carriers (92%) remained asymptomatic at 5 years of follow-up (1 patient required left cardiac sympathectomy). The QTc shortening with beta-blockers was 50 (37) ms. There was 1 sudden death in a patient who refused treatment. Conclusions Family study is essential in the interpretation of a genetic testing result. This article describes the heterogeneous and variable phenotype of a large family with the KCNH2-H562R mutation and highlights the role of genetic study for the appropriate identification of at-risk individuals who would benefit from treatment.