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Circulation. 2007;116:2359
doi: 10.1161/CIRCULATIONAHA.107.187679
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(Circulation. 2007;116:2359.)
© 2007 American Heart Association, Inc.

Issue Highlights


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    THE COMMON LONG-QT SYNDROME MUTATION KCNQ1/A341V CAUSES UNUSUALLY SEVERE CLINICAL MANIFESTATIONS IN PATIENTS WITH DIFFERENT ETHNIC BACKGROUNDS: TOWARD A MUTATION-SPECIFIC RISK STRATIFICATION, by Crotti et al.
 
Congenital long-QT syndrome is due to mutations in ion channel–encoding genes, leading to variable clinical phenotypes of arrhythmias, syncope, and vulnerability to sudden death. In this issue of Circulation, Crotti and colleagues describe findings of a particularly severe clinical presentation in patients with a relatively common mutation in KCNQ1. Patients with this particular mutation were much more likely to have a longer QTc and experience cardiac events, including sudden cardiac death, at earlier ages in childhood as compared with other long-QT syndrome patients with different mutations on the KCNQ1 gene. This mutational "hot spot" causes a more malignant phenotype, regardless of ethnic background, even when patients were treated with β-blocker medications. These data suggest a potential role of mutation-specific risk stratification and therapeutic approaches. See p 2366.


*    SOCIOECONOMIC POSITION, RACE/ETHNICITY, AND INFLAMMATION IN THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS, by Ranjit et al.
 
Epidemiology studies have documented a higher prevalence of cardiovascular disease among populations with lower socioeconomic status. Many studies have investigated the underlying causes of this association, but some researchers have wondered if inflammation is the common biological process by which multiple behavioral and psychosocial factors mediate this increased risk. Making use of data from Multi-Ethnic Study of Atherosclerosis (MESA), which includes a large and diverse US cohort of adults 45 to 84 years of age, Ranjit and colleagues evaluated the associations of household income and education with various markers of inflammation. Moreover, they determined whether the relationships were affected by adjustment for infection, medication use, psychosocial factors, behaviors, adiposity, and diabetes. The research has the potential to identify the most . . . [Full Text of this Article]


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