* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download conduction abnormalities in arrhythmogenic right
Survey
Document related concepts
Transcript
CONDUCTION ABNORMALITIES IN ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY Stefan Peters - St.Elisabeth Hospital Salzgitter, Cardiology, Germany According to an article of Tabib et al., published in 2003, in more than 60% of cases fibrosis was found within structures of the conduction system of 200 autopsy cases with arrhythmogenic (right ventricular) cardiomyopathy-dysplasia (ARVC-D). The question is whether conduction abnormalities belong to the electrocardiographic spectrum of ARVC/D. Method: The very first ECG without medication was analysed with regard to conduction abnormalities (AV block 1° or 2° or 3°), right bundle branch block or need for pacemaker implantation of 376 patients with modified ISFC/ESC criteria of ARVC-D (210 males, mean age 46.4 ± 11.7 years). Results: Symptomatic AV block II° and III° were present in 6 patients and in additional 3 patients with provocable electrocardiographic Brugada pattern. A complete right bundle branch block as the initial electrocardiographic finding was found in 5 patients. Only nine patients presented with AV-block I°. The incidence of conduction abnormalities and complete right bundle branch block was only 6 %. Conclusions: The rate of fibrosis of the conduction system as described in the paper of Tabib cannot be confirmed, as the incidence of conduction abnormalities in only 6%. Fibrofatty changes of the conduction system were found in 7% of cases which correspond to the rate of conduction abnormalities. This finding can be seen in the light of rare non-desmosomal gene mutations encoding lamin A/C, titin, TMEM protein 43 and possibly cardiac sarcoidosis mimicking ARVC/D. Complete right bundle branch block is possibly the result of rare desmin gene mutations. AV block I° is more prevalent in Brugada syndrome and belongs to the electrocardiographic spectrum of this syndrome in SCN5A mutations.