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Internal Medicine Journal 2018-Oct

Serum albumin level and abnormal corrected QT interval in patients with coronary artery disease and chronic kidney disease.

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Cheng-Ching Wu
Yung-Chuan Lu
Teng-Hung Yu
Chao-Ping Wang
Wei-Chin Hung
Wei-Hua Tang
I-Ting Tsai
Fu-Mei Chung
Yau-Jiunn Lee
Jin-Jia Hu

Ključne riječi

Sažetak

BACKGROUND

Lower concentrations of serum albumin appear to be associated with an increased risk of all-cause and cardiovascular mortality, coronary heart disease, heart failure and stroke. However, little is known about the relationship between serum albumin level and prolonged QT interval.

OBJECTIVE

To investigate whether lower serum albumin is associated with prolonged QT interval by recording 12-lead electrocardiography in patients with coronary artery disease and chronic kidney disease.

METHODS

This study included 1383 consecutive patients with coronary artery disease and chronic kidney disease (841 with acute coronary syndrome and 542 with elective percutaneous coronary intervention patients) who were enrolled in a disease management programme. Twelve-lead electrocardiography was recorded in each subject. We assessed the relationship between albumin levels (both as a continuous variable and stratified by tertile) at admission and corrected QT (QTc) prolongation.

RESULTS

Patients with abnormal QTc interval had lower serum albumin levels than those with normal and borderline QTc intervals. Statistically significant negative associations were observed between serum albumin levels and QTc interval (β = -0.211, P < 0.0001). Using multivariate and trend analyses, a lower concentration of serum albumin was independently associated with QTc prolongation in both the patients with acute coronary syndrome and elective percutaneous coronary intervention patients.

CONCLUSIONS

Concentrations of serum albumin were significantly lower in the patients with an abnormal QTc interval and were associated with QTc prolongation. Further studies are needed to clarify whether lower serum albumin plays a role in the pathogenesis of QTc prolongation.

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