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Population-based study of QT interval prolongation in patients with rheumatoid arthritis

1, 2, 3, 4, 5

 

  1. Division of Rheumatology, Mayo Clinic, Rochester, MN, USA.
  2. Departments of Medicine, Pediatrics, and Molecular Pharmacology & Experimental Therapeutics; Divisions of Cardiovascular Diseases and Pediatric Cardiology; Windland Smith Rice Sudden Death Genomics Laboratory, Mayo Clinic, Rochester, MN, USA.
  3. Division of Rheumatology, and Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.
  4. Division of Rheumatology, and Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.
  5. Division of Rheumatology, and Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.

CER7671
2015 Vol.33, N°1
PI 0084, PF 0089
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PMID: 25572282 [PubMed]

Received: 11/06/2014
Accepted : 16/09/2014
In Press: 08/01/2015
Published: 04/03/2015

Abstract

OBJECTIVES:
Patients with rheumatoid arthritis (RA) are at increased risk of cardiovascular morbidity and mortality. Heart rate corrected QT interval (QTc) (which is obtained from a 12-lead electrocardiogram (ECG) and reflects ventricular repolarisation duration) is a strong predictor of cardiovascular mortality. Our primary purpose is to determine the impact of QTc prolongation on mortality in RA patients.
METHODS:
A population-based inception cohort of patients with RA fulfilling the 1987 ACR criteria in 1988-2007 was identified, with an age- and sex-matched comparison cohort and followed until death, migration or until the end of 2008. Data were collected on ECG variables, medications known to prolong QT interval, electrolytes, cardiovascular risk factors and disease status and RA disease characteristics. Cox proportional hazards models were used to examine QTc prolongation as predictor of mortality.
RESULTS:
QTc prolongation prior to RA incidence/index date was similar in RA (15%) and non-RA (18%) subjects. During follow-up, the cumulative incidence of QTc prolongation was higher among RA (48% at 20 years after RA incidence) than non-RA (38% at 20 years after index date; p=0.004). Idiopathic QTc prolongation (excluding prolongations explained by ECG changes, medications, etc.) was marginally associated with all-cause mortality (HR: 1.28; 95% CI: 0.91–1.81, p=0.16), but was not associated with cardiovascular mortality (HR: 1.10; 95% CI:0.43–2.86, p=0.83) in RA.
CONCLUSIONS:
RA patients have a significantly elevated risk of developing QTc prolongation. However, idiopathic prolonged QTc was only marginally associated with all-cause mortality in RA patients. The clinical implications of these findings in RA require further study.

Rheumatology Article