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De subitaneis mortibus. XXIII. Rheumatoid arthritis and ankylosing spondylitis
Insights
Rheumatoid arthritis and ankylosing spondylitis can cause severe heart conduction problems, including heart block and arrhythmias. Necropsy revealed significant degeneration in the heart
Area of Science:
- Cardiovascular Pathology
- Rheumatic Diseases
- Cardiac Electrophysiology
Background:
- Investigating the cardiac conduction system in patients with rheumatic diseases is crucial for understanding sudden cardiac death.
- Rheumatoid arthritis and ankylosing spondylitis are systemic inflammatory conditions that can affect multiple organs, including the heart.
Observation:
- Necropsy examination of three patients (two with rheumatoid arthritis, one with ankylosing spondylitis) revealed significant cardiac conduction system abnormalities.
- All patients exhibited cardiac electrical instability, with two experiencing sudden death.
- Histological findings included sinus node degeneration, and degenerative disease in the atrioventricular (A-V) node and His bundle.
Findings:
- Electrophysiological abnormalities ranged from atrial fibrillation to complete heart block.
- Marked narrowing, and in some cases virtual occlusion, of the nutrient arteries supplying the A-V node and His bundle was observed.
- Sinus node degeneration was present in all cases, though sinus node arteries were not significantly abnormal.
Implications:
- These findings suggest a strong link between rheumatic disease, cardiac conduction system pathology, and potentially fatal arrhythmias.
- Understanding these pathological mechanisms may inform strategies for managing cardiac complications in patients with rheumatoid arthritis and ankylosing spondylitis.
- Comparison with cardiac findings in other connective tissue diseases like lupus, polyarteritis nodosa, and scleroderma highlights shared and distinct pathological pathways.
Abstract:
The conduction system of the heart was carefully examined at necropsy in two cases of rheumatoid arthritis and one of ankylosing spondylitis. All three patients had cardiac electrical instability and two fo the three died suddenly. The electrophysiological abnormalities of the three patients included paroxysmal atrial fibrillation in the first case, sustained atrial fibrillation with complete heart block and escape atrioventricular (A-V) junctional rhythm in the second case, and progressively increasing heart block eventually became complete in the third case. The sinus node exhibited extensive focal degeneration with and without associated inflammation in all three hearts, but the sinus node artery was not remarkably abnormal in any of these. All three hearts had important focal degenerative disease in the A-V node and His bundle, and in each of these there was marked narrowing of the local nutrient arteries, amounting to virtual occlusion in two hearts. The probable relationship of these postmortem histological findings to the electrocardiographic disturbances in each patient is discussed. Abnormalities in the cardiac conduction system of the hearts of these three patients are compared to ones previously reported for disseminated lupus erythematosus, polyarteritis nodosa, and scleroderma heart disease.
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