Key result
The alpha2C-adrenoceptor deletion polymorphism was associated with significantly reduced event rates in patients with dilated cardiomyopathy (RR 0.167; 95% CI 0.041-0.685; P=0.012).
Why the study?
Does the alpha2CDel322-325 polymorphism improve event-free survival in patients with dilated cardiomyopathy?
Cohort (n=345)
No
Does the alpha2CDel322-325 polymorphism improve event-free survival in patients with dilated cardiomyopathy?
Relative Risk: 0.167 (95% CI 0.041–0.685)
p-value: p=0.012
The alpha2C-adrenoceptor deletion polymorphism is a strong, independent predictor of improved event-free survival in patients with dilated cardiomyopathy on guideline-directed medical therapy.
No takes yet. Share an insight, caveat, or question.
Should not yet guide genotyping or therapy in dilated cardiomyopathy; leaves open whether the polymorphism improves risk stratification in prospective studies.
Regitz‐Zagrosek et al. (2005) conducted a cohort in Dilated cardiomyopathy (DCM) (n=345). alpha2C-adrenoceptor deletion polymorphism (alpha2CDel322-325) vs. Absence of the deletion polymorphism was evaluated on First event (death, heart transplantation, or implantation of a left ventricular assist device) (RR 0.167, 95% CI 0.041-0.685, p=0.012). The alpha2C-adrenoceptor deletion polymorphism was associated with significantly reduced event rates in patients with dilated cardiomyopathy (RR 0.167; 95% CI 0.041-0.685; P=0.012).
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