Literature DB >> 19468786

Low creatine kinase is associated with a high population incidence of fainting.

Lizzy M Brewster1, Gideon Mairuhu, Karin Ganzeboom, Nynke van Dijk, Gert A van Montfrans, Wouter Wieling.   

Abstract

OBJECTIVE: Vasoconstrictor capacity, skeletal muscle tone, and renal sodium retention are involved in the pathogenesis of fainting. As muscle contractility and ion transport are highly energy-demanding processes, we hypothesized that a low activity of the energy-generating enzyme creatine kinase (CK) is associated with a higher risk of fainting. The aim of this observational study was to explore the association of vasovagal syncope with low CK.
METHODS: A random sample of 1,000 subjects aged 34-60 years was drawn from the general population, with 442 subjects eventually included in the study. Data on fainting history were collected with the investigators blinded to participants' CK level. We prepared this report according to the "Strengthening the Reporting of Observational Studies in Epidemiology" (STROBE) statement. The main outcome was the lifetime cumulative incidence of vasovagal syncope in subjects with low versus high-normal serum CK after a 3 days rest.
RESULTS: The proportion of fainters within the high CK group was 29 out of 130 (22%) versus 121 out of 312 (39%) in the low CK group; a 73% greater occurrence of fainting with low CK (P = 0.0005). This finding was consistent across recurrent fainters, and in men and women.
INTERPRETATION: Low CK is associated with a 73% higher incidence of fainting in a random population sample. The association is biologically plausible, as CK enhances cardiovascular and skeletal muscle contractility and salt retention. The presented data suggest that low CK activity is a potential new risk factor for vasovagal syncope.

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Year:  2009        PMID: 19468786      PMCID: PMC2720582          DOI: 10.1007/s10286-009-0013-6

Source DB:  PubMed          Journal:  Clin Auton Res        ISSN: 0959-9851            Impact factor:   4.435


  27 in total

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Review 2.  Physiology of renal sodium transport.

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2.  Response to creatine kinase and pressor response to orthostatic tolerance.

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