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Abstract Number: 2617

Electrocardiogram Abnormalities Related to Antimalarials in Systemic Lupus Erythematosus

Taneisha McGhie1, Paula Harvey2, Jiandong Su1, Nicole Anderson3, George A. Tomlinson4 and Zahi Touma5, 1University of Toronto, Toronto Western Hospital, Toronto, ON, Canada, 2Cardiology, Women's College Hospital, University of Toronto, Toronto, ON, Canada, 3Rheumatology, University of Toronto, Toronto Western Hospital, Toronto, ON, Canada, 4Medicine, Mount Sinai Hospital, Toronto, ON, Canada, 5Rheumatology, University of Toronto, Division of Rheumatology, Institute of Health Policy, Management and Evaluation, Toronto, ON, Canada

Meeting: 2017 ACR/ARHP Annual Meeting

Date of first publication: September 18, 2017

Keywords: Antimalarial drugs and systemic lupus erythematosus (SLE)

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Session Information

Date: Tuesday, November 7, 2017

Title: Systemic Lupus Erythematosus – Clinical Aspects and Treatment Poster III: Therapeutics and Clinical Trial Design

Session Type: ACR Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose:

Anti-malarials (AM), such as hydroxychloroquine (HCQ) and chloroquine (CQ), have long been used for the treatment of systemic lupus erythematosus (SLE). However, despite their general safety, both drugs have the potential to cause serious toxicity. These drugs have significant lysosomal affinity and induce the prominent development of autophagic vacuoles in several tissues. Cardiotoxicity with potential conduction/structural abnormalities on electrocardiogram (ECG) have been reported with AM.  We aimed to study whether cumulative AM is associated with ECG abnormalities.

Methods:

A standard resting supine ECG was performed on consecutive patients attending the Lupus Clinic since 2012.  ECGs were analyzed and tracings were coded by a single cardiologist blinded to identifying data and previous AM exposure on the basis of the Minnesota criteria. ECG abnormalities were grouped into structural [left ventricular hypertrophy or atrial enlargement] and conduction abnormalities [prolonged corrected QT interval (QTc), short PR interval, left bundle branch block (LBBB), right bundle branch block (RBBB) and atrioventricular block (AVB), bradycardia, tachycardia, premature atrial complex, ectopic atrial rhythm, atrial fibrillation, premature ventricular complex and ventricular bigeminy].

Clinical and laboratory variables from the baseline (corresponds to the ECG visit) were studied as potential factors associated with ECG abnormalities. Associations between cumulative AM [calculated after equating 3.0 mg of CQ with 6.5 mg of HCQ] and ECG abnormalities (structural or conduction) were assessed using logistic regression analysis (after adjusting for baseline patient characteristics) and in a nested case control study (1:3) [matching for sex, SLE duration at ECG within 5 years, ECG testing year within 5 years and hypertension status].

Results:

Of 453 patients treated with AM, the median cumulative AM was 1207 grams at ECG. The mean age at ECG was 49.2 ± 13.8 years and SLE duration was 19.8 ± 10.4 years. CQ or HCQ had been used by 409 (90.3%) before the ECG.

Conduction abnormalities were more prevalent than structural abnormalities, 71 (15.7%) vs. 58 (12.8%). AM cumulative dose did not show a statistical significant association with ECG structural abnormalities, (OR 1.82, p=0.07) while it was protective for conduction ECG abnormalities (OR 0.42, p=0.006) (table 1).

The nested case control analysis also found that AM cumulative dose is protective against conduction ECG abnormalities (OR 0.36; 95% CI: 0.17-0.75; p=0.007). SLE duration was a risk factor for both structural and conduction ECG abnormalities.

Conclusion:  

This study suggests an association between cumulative AM dose above the median (1207 g) and structural ECG abnormalities. More importantly, cumulative AM decreases the odds of ECG conduction abnormalities.

 

Table 1:  Multivariable logistic regression analysis for structural or conduction abnormalities

ECG Abnormality

       Variables

OR 95% CI

p value

ECG structural abnormality

SLE duration at ECG test (years)

1.03 (1.004, 1.06)

0.0248

Hypertension vs. normotension

      

2.21 (0.98, 4.99)

0.0567

eGFR at ECG (each 10 mL/min/173 m2)

0.83 (0.76, 0.92)

0.0002

 

Cumulative AM dose prior to ECG higher than median dose (1207 grams)

 

1.82 (0.95, 3.47)

0.0707

ECG conduction abnormality

SLE duration at ECG test

1.03 (1.01, 1.06)

0.0080

Hypertension

1.66 (0.85, 3.25)

0.1357

Pulmonary hypertension

Treatment with N-CBB

or beta-blockers

 

2.37 (0.82, 6.80)

2.75 (1.42, 5.33)

0.1090

0.0026

 

Cumulative prednisone 3 years before ECG (each 100 grams)

 

1.05 (1.01, 1.09)

0.0147

Cumulative AM prior to ECG higher than median dose (1207 grams)

0.42 (0.22, 0.77)

0.0057

N-CCB; non-dihydropyridine calcium channel blocker


Disclosure: T. McGhie, None; P. Harvey, None; J. Su, None; N. Anderson, None; G. A. Tomlinson, None; Z. Touma, None.

To cite this abstract in AMA style:

McGhie T, Harvey P, Su J, Anderson N, Tomlinson GA, Touma Z. Electrocardiogram Abnormalities Related to Antimalarials in Systemic Lupus Erythematosus [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/electrocardiogram-abnormalities-related-to-antimalarials-in-systemic-lupus-erythematosus/. Accessed .
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