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Published on: June 20, 2020
Cardiac conduction abnormalities in Reiter's syndrome
Insights
Reiter's syndrome can cause serious heart problems, including heart block and cardiomyopathy, even decades after initial infection. This B27-associated disease may target the heart, similar to joints and eyes.
Area of Science:
- Rheumatology
- Cardiology
- Immunogenetics
Background:
- Reiter's syndrome, now known as reactive arthritis, is a spondyloarthropathy.
- It is strongly associated with the B27 antigen.
- Cardiac involvement is a recognized but infrequently discussed complication.
Observation:
- Three male patients presented with cardiac conduction disturbances attributed to Reiter's syndrome.
- Two patients had long-standing, unrecognized disease (over 30 years).
- Cardiac issues included complete heart block, left bundle branch block, and cardiomyopathy.
Findings:
- A chart review of 19 patients revealed five with conduction abnormalities.
- Transient first-degree heart block was common during active disease.
- Conduction abnormalities could also manifest late, with inactive systemic symptoms.
- All affected patients were B27 antigen positive.
Implications:
- The heart may be a target organ in B27-associated spondyloarthropathies, analogous to joints and eyes.
- Cardiac manifestations can have a long latent period, complicating diagnosis.
- Further research is needed to elucidate the mechanism of cardiac involvement.
Abstract:
Reiter's syndrome was found in three men who presented with cardiac conduction disturbances. In two patients, Reiter's syndrome had been present for more than 30 years and had been previously unrecognized. These patients included a 67 year old man with complete heart block of 13 years' duration, and his son, who had left bundle branch block and chronic generalized cardiomyopathy. A chart review of 19 other patients with Reiter's syndrome who were seen at this institution disclosed five patients with conduction abnormalities. Transient first-degree heart block was the most common disturbance detected and was usually associated with active Reiter's syndrome. Some conduction abnormalities appeared after a long latent period at a time when other manifestations of Reiter's syndrome were inactive. An association with this disorder was therefore not obvious. In all five patients with Reiter's syndrome and conduction disturbances, testing for B27 antigen gave positive results. Both clinical and histopathologic changes in the heart in Reiter's syndrome are analogous to those in ankylosing spondylitis, also associated with B27 antigen. We suggest that the heart, like the joints and iris, may be a target organ for B27-associated disease by a mechanism that remains to be defined.
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