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FRI0154 Increased risk of qt interval prolongation in rheumatoid arthritis patients compared to the general population: a population-based study
  1. K. Chauhan1,
  2. M. J. Ackerman2,
  3. C. Crowson3,
  4. E. L. Matteson1,
  5. S. E. Gabriel3
  1. 1Rheumatology
  2. 2Cardiology
  3. 3Health Science Research, Mayo Clinic, Rochester, United States


Background Patients with rheumatoid arthritis (RA) have increased risk of sudden cardiac death (SCD), not entirely explained by RA disease characteristics. The 12-lead electrocardiogram (ECG) derived heart- rate corrected QT interval (QTc) is an index of ventricular repolarization. Recently, QT prolongation has been established as a risk factor for all cause cardiovascular (CV) mortality including SCD

Objectives To compare the rate of QT prolongation in RA patients with an age- and sex-matched cohort of non-RA subjects

Methods Using a population based incident cohort of RA patients (1987 ACR criteria), diagnosed between 1988-2007, we retrospectively collected ECG data for heart rate (HR), QRS interval, QT interval, heart rate corrected QT (QTc) calculated using the Bazett’s formula, atrial fibrillation, atrial flutter, supraventricular tachycardia (SVT), bundle branch block (BBB), paced rhythm, and ST-T wave changes. The same data were also collected for an age- and sex-matched cohort of patients without RA selected from the same population with index date corresponding to the RA incident date. Prolonged QTc was defined as per the American Heart Association (AHA) guidelines: QTc ≥ 450 msec in males, ≥ 460 msec in females; marked prolonged QT defined: QTc: ≥ 500 msec if QRS < 120 msec or ≥ 550 msec if QRS > 120 msec. Cumulative incidence adjusted for the competing risk of death and Cox models were used to compare the development of QT prolongation over time between the 2 cohorts

Results The study population included 650 RA and 650 non-RA patients. 518 RA and 499 non-RA subjects (mean age 58 years, 68% females) had ≥1 ECG during a mean follow-up of 10 years (total person years: 5291 in RA and 5417 in non-RA). Prior to RA incidence/index date, 3474 ECGs were available for RA, 3561 for non RA subjects. The proportion of patients with QT prolongation prior to RA incidence/index date was similar in two groups (16% in RA vs. 15% in non-RA, p=0.65). During follow-up, 5606 ECGs were available for RA, 5220 for non-RA subjects, QT prolongation occurred in 187 RA and 146 non-RA subjects. 20 years after RA incidence/index date, the cumulative incidence of prolonged QT interval was 62% (standard error [SE] 4%) in RA compared to 54% (SE 4%) in non-RA group (p=0.015). RA patients had significantly more ST-T wave changes during follow-up compared to non-RA (RA: 39%, SE 4%; Non-RA:24%, SE 3%; p<0.001). No differences were observed in rates of development of marked prolonged QTc, BBB, paced rhythm, atrial fibrillation and flutter, SVT or low HR (HR<50). Patients with RA had an increased risk of developing QT prolongation during follow-up compared to non-RA subjects (hazard ratio: 1.45; 95% CI: 1.17-1.81; p<0.001 adjusted for age and sex) it was mildly attenuated (hazard ratio: 1.36; 95% CI: 1.08-1.7; p=0.008) after adjusting for: HR <50, HR > 100, BBB, paced rhythm, atrial flutter, atrial fibrillation, SVT and ST-T wave changes

Conclusions Rheumatoid arthritis patients have a significantly higher chance of developing a QTc that exceeds the published guideline definition of “prolonged QTc”. Further research is needed to establish whether the increased risk of QT prolongation may contribute to the increased risk of sudden death in RA patients

Disclosure of Interest None Declared

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