What is the clinical evidence from this study?

Study design: Cohort. Population: Hypertrophic cardiomyopathy (n=110). Intervention: EDN2 A985G polymorphism (dominant EDN2 A allele) vs. No dominant EDN2 A allele. Primary outcome: Occurrence of atrial fibrillation (p=0.014).

January 1, 2007Open Access

A985G Polymorphism of the Endothelin-2 Gene and Atrial Fibrillation in Patients With Hypertrophic Cardiomyopathy

Resultado clave

The dominant EDN2 A allele was associated with an increased risk of atrial fibrillation in patients with hypertrophic cardiomyopathy (allele prevalence 42.3% in AF vs 16.7% in sinus rhythm; p=0.014).

Diseño del estudio

Tipo

Cohort (n=110)

PICO estructurado

Does the EDN2 A985G polymorphism increase the risk of atrial fibrillation in patients with hypertrophic cardiomyopathy?

Población

110 patients with hypertrophic cardiomyopathy (HCM) who had no clinically documented atrial fibrillation before medical treatment (86 men, mean age 53±13 years). Excluded: prior documented permanent or paroxysmal AF, myocardial infarction, severe valvular heart disease, dilated phase HCM, congenital heart disease, accessory pathway, and bundle-branch block.

Intervención

Presence of the endothelin-2 (EDN2) A985G polymorphism (A allele carrier: G/A or A/A genotype)

Comparador

Absence of the EDN2 A allele (G/G genotype)

Resultado

Occurrence of atrial fibrillation (paroxysmal, persistent, or permanent) during long-term follow-uphard clinical

The EDN2 A985 allele, along with the ACE insertion/insertion genotype and increased QRS dispersion, is an independent risk factor for the development of atrial fibrillation in patients with hypertrophic cardiomyopathy.

Resultado numérico

Tasa de eventos absoluta: 42.3% vs 16.7%

valor p: p=0.014

Resumen

BACKGROUND: It was recently suggested that the angiotensin-converting enzyme insertion/insertion genotype, which is considered to be protective against cardiovascular disease, was a significant risk factor for atrial fibrillation (AF) in patients with hypertrophic cardiomyopathy (HCM). The aim of this study was to investigate the association between the endothelin-2 (EDN2) A985G polymorphism and AF in patients with HCM. METHODS AND RESULTS: The EDN2 A985G polymorphism (rs 5800) was genotyped in 110 patients with HCM who had no clinically documented AF before medical treatment. The distribution of the EDN2 genotypes (G/G, G/A, and A/A) was 77.3%, 19.1%, and 3.6%, respectively. The EDN2 A allele frequency was 0.21 in 26 patients who subsequently developed AF during long-term follow-up and 0.11 in 84 patients who remained in sinus rhythm. The distribution of genotypes of the dominant EDN2 A allele between the two groups was significantly different by chi-square analysis (42.3% vs 16.7%, p=0.014). In a multivariate model, the A985 allele of the EDN2 gene was associated with increased adjusted risk for the occurrence of AF (p=0.018). CONCLUSION: The EDN2 A985 allele, which is considered to be protective in cardiovascular disease, may be a risk factor for AF in patients with HCM.

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