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Defining the Pathways Underlying the Prolonged PR Interval in Atrioventricular Conduction Disease

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Vyšlo v časopise: Defining the Pathways Underlying the Prolonged PR Interval in Atrioventricular Conduction Disease. PLoS Genet 8(12): e32767. doi:10.1371/journal.pgen.1003154
Kategorie: Perspective
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.pgen.1003154

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Zdroje

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2. GoAS, HylekEM, PhillipsKA, ChangY, HenaultLE, et al. (2001) Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA 285 : 2370–2375.

3. KrahnAD, ManfredaJ, TateRB, MathewsonFA, CuddyTE (1995) The natural history of atrial fibrillation: incidence, risk factors, and prognosis in the Manitoba Follow-Up Study. Am J Med 98 : 476–484.

4. WolfL (1943) Familial auricular fibrillation. N Engl J Med 229 : 396–397.

5. FoxCS, PariseH, D'AgostinoRBSr, Lloyd-JonesDM, VasanRS, et al. (2004) Parental atrial fibrillation as a risk factor for atrial fibrillation in offspring. JAMA 291 : 2851–2855.

6. SinnerMF, EllinorPT, MeitingerT, BenjaminEJ, KaabS (2011) Genome-wide association studies of atrial fibrillation: past, present, and future. Cardiovasc Res 89 : 701–709.

7. DarbarD, HerronKJ, BallewJD, JahangirA, GershBJ, et al. (2003) Familial atrial fibrillation is a genetically heterogeneous disorder. J Am Coll Cardiol 41 : 2185–2192.

8. LodderEM, SciclunaBP, MilanoA, SunAY, TangH (2012) Dissection of a quantitative trait locus for PR interval duration identifies Tnni3k as a novel modulator of cardiac conduction. PLoS Genet 8: e1003113 doi:10.1371/journal.pgen.1003113.

9. RemmeCA, SciclunaBP, VerkerkAO, AminAS, van BrunschotS, et al. (2009) Genetically determined differences in sodium current characteristics modulate conduction disease severity in mice with cardiac sodium channelopathy. Circ Res 104 : 1283–1292.

10. SciclunaBP, WildeAA, BezzinaCR (2008) The primary arrhythmia syndromes: same mutation, different manifestations. Are we starting to understand why? J Cardiovasc Electrophysiol 19 : 445–452.

11. LaiZF (2009) TNNI3K could be a novel molecular target for the treatment of cardiac diseases. Recent Pat Cardiovasc Drug Discov 4 : 203–210.

12. WheelerFC, TangH, MarksOA, HadnottTN, ChuPL, et al. (2009) Tnni3k modifies disease progression in murine models of cardiomyopathy. PLoS Genet 5: e1000647 doi:10.1371/journal.pgen.1000647.

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Článok vyšiel v časopise

PLOS Genetics

2012 Číslo 12

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Autori: doc. MUDr. David Zemánek, Ph.D., MUDr. Anna Chaloupka, Ph.D.

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