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Lýdie Izákovicova Hollá, Milan Kozák, Lýdie Izákovicova Hollá, Lubomír Krivan, Anna Vasků, Milan Sepsi, Semrád Borivoj, Jirí Vácha
Med Sci Monit 2002; 8(5): BR164-167
BACKGROUND: The endothelins are peptides with vasoconstricting and growth-promotingproperties. Endothelin-1 (ET-1) is known for its direct positive inotropic and chronotropic effects onisolated heart, and for growth effects. The aim of this pilot study was to investigate the frequencydistribution of a common polymorphism of the endothelin (ET-1) gene and its possible relation to thehemodynamic consequences of malignant ventricular arrhythmia in patients with structural heart disease.MATERIAL/METHODS: We studied 26 consecutive patients with malignant ventricular arrhythmia and implantablecardioverter defibrillators (ICD), mean age 62.7 +/- 12.2 years, mean LVEF 0.37 +/- 11. The Taq polymorphismof ET-1 was detected using our original PCR method. The PCR product with a length of 358 bp in its non-mutatedform contains a target sequence for the TaqI restrictive enzyme, while the mutated product loses thiscleavage site. RESULTS: Out of the 26 patients, 9 (34%) had recurrent palpitations and 8 (30.8%) hadsyncopes during their malignant arrhythmic episodes. 19 of the patients were receiving amiodarone afterICD implantation, 7 were not. 15 patients had the (++) and 11 had the (+ -) ET-1 genotype; none had the(- -) genotype. The risk of syncopes was associated with the (++) genotype (p=0.01). Patients with amiodaronehad a significantly higher frequency of the (++) genotype (p=0.011). CONCLUSIONS: All our results suggestedthat the presence of the (++)ET-1 genotype in patients with structural heart disease, severe left ventriculardysfunction, and malignant ventricular arrhythmia put these patients at a higher risk of hemodynamiccollapse during arrhythmic episodes.