Sick sinus syndrome pathophysiology: Difference between revisions
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Sick sinus syndrome revolves around an improperly propagated signal from the sinoatrial node. Some of the causes for this propagation abnormality include degenerative fibrosis of the SA node, abnormalities in ion-channel conduction, and and a remodeling of the node itself. As a disease of the elderly, it is most commonly thought to be secondary to the age-related idiopathic fibrosis of the nodal tissue. | Sick sinus syndrome revolves around an improperly propagated signal from the sinoatrial node. Some of the causes for this propagation abnormality include degenerative fibrosis of the SA node, abnormalities in ion-channel conduction, and and a remodeling of the node itself. As a disease of the elderly, it is most commonly thought to be secondary to the age-related idiopathic fibrosis of the nodal tissue.<ref name="pmid23939447">{{cite journal| author=Semelka M, Gera J, Usman S| title=Sick sinus syndrome: a review. | journal=Am Fam Physician | year= 2013 | volume= 87 | issue= 10 | pages= 691-6 | pmid=23939447 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23939447 }} </ref> Studies on familial and congenital presentations of sick sinus syndrome have revealed genetic contributions to dysfunctional ion channels.<ref name="pmid14523039">{{cite journal| author=Benson DW, Wang DW, Dyment M, Knilans TK, Fish FA, Strieper MJ et al.| title=Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A). | journal=J Clin Invest | year= 2003 | volume= 112 | issue= 7 | pages= 1019-28 | pmid=14523039 | doi=10.1172/JCI18062 | pmc=198523 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14523039 }} </ref> Recent research has revealed a higher incidence of SSS in carriers of a rare variant of the MYH6 gene, which encodes the alpha heavy chain subunit of cardiac myosin, further delineating a possible genetic basis to the disease. <ref name="pmid21378987">{{cite journal| author=Holm H, Gudbjartsson DF, Sulem P, Masson G, Helgadottir HT, Zanon C et al.| title=A rare variant in MYH6 is associated with high risk of sick sinus syndrome. | journal=Nat Genet | year= 2011 | volume= 43 | issue= 4 | pages= 316-20 | pmid=21378987 | doi=10.1038/ng.781 | pmc=3066272 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21378987 }} </ref> | ||
== References == | == References == | ||
Revision as of 18:43, 28 September 2016
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Sick sinus syndrome revolves around an improperly propagated signal from the sinoatrial node. Some of the causes for this propagation abnormality include degenerative fibrosis of the SA node, abnormalities in ion-channel conduction, and and a remodeling of the node itself. As a disease of the elderly, it is most commonly thought to be secondary to the age-related idiopathic fibrosis of the nodal tissue.[1] Studies on familial and congenital presentations of sick sinus syndrome have revealed genetic contributions to dysfunctional ion channels.[2] Recent research has revealed a higher incidence of SSS in carriers of a rare variant of the MYH6 gene, which encodes the alpha heavy chain subunit of cardiac myosin, further delineating a possible genetic basis to the disease. [3]
References
- ↑ Semelka M, Gera J, Usman S (2013). "Sick sinus syndrome: a review". Am Fam Physician. 87 (10): 691–6. PMID 23939447.
- ↑ Benson DW, Wang DW, Dyment M, Knilans TK, Fish FA, Strieper MJ; et al. (2003). "Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A)". J Clin Invest. 112 (7): 1019–28. doi:10.1172/JCI18062. PMC 198523. PMID 14523039.
- ↑ Holm H, Gudbjartsson DF, Sulem P, Masson G, Helgadottir HT, Zanon C; et al. (2011). "A rare variant in MYH6 is associated with high risk of sick sinus syndrome". Nat Genet. 43 (4): 316–20. doi:10.1038/ng.781. PMC 3066272. PMID 21378987.