Patients with rheumatoid arthritis (RA) have higher aortic stiffness and cardiovascular risk. Tumor necrosis factor alpha (TNF-a) antagonists reduce inflammation in RA and are indicated for the treatment of patients with severe active rheumatoid disease. However, it is debatable if they have favorable effects on cardiovascular health. The present meta-analysis evaluates the effect of TNF-a antagonists on aortic stiffness and wave reflections, predictors of cardiovascular events and mortality, in RA patients. A search of PubMed, Cohrane, and Embase databases was conducted to identify studies into the effect of TNF-a antagonists on aortic stiffness in RA patients. Aortic stiffness and wave reflections were assessed by aortic (carotid-femoral [cf]) pulse wave velocity (PWV) and augmentation index (AIx), respectively. cfPWV significantly improved following TNF-a antagonist treatment (mean change: -0.53 m/s, 95% CI: -0.833 to -0.218, p = 0.001), independently of age and clinical response to treatment. A more prominent reduction in cfPWV was associated with etanercept/adalimumab (mean difference: -0.62 m/s, 95% CI: -0.968 to -0.272 m/s, p < 0.001) versus infliximab (mean difference: -0.193 m/s, 95% CI: -0.847 to 0.462 m/s, p = 0.564). TNF-a antagonist treatment induced a significant improvement in AIx (mean change: -1.48%, 95% CI: -2.89 to -0.078%, p = 0.039), but this reduction was influenced by age and clinical response to treatment. The balance of evidence suggests that TNF-a antagonists may have a beneficial effect on aortic stiffness and, therefore, on cardiovascular risk. However, larger, longitudinal studies are warranted to confirm such findings.
Rheumatoid arthritis (RA) is associated with increased cardiovascular morbidity and mortality attributed to traditional cardiovascular risk factors and/or the chronic systemic inflammation. We investigated the effect of a TNF antagonist (adalimumab-ADA) on aortic stiffness in RA patients. We studied 18 RA patients with active disease despite therapy with disease modifying antirheumatic drugs (DMARDs), treated with ADA (alone or in combination with DMARDs) for 12 weeks. Disease activity markers as well as aortic stiffness indices (carotid-femoral pulse wave velocity-PWV, augmentation index-AIx), were measured at baseline and at the end of treatment. Eighteen RA patients treated with methotrexate (MTX) were included as controls. Patients were categorized as responders (decrease of Disease Activity Score-DAS28 > 1.2) or nonresponders. There was a statistically significant decrease in PWV (from 8.18 ± 2.03 to 7.01 ± 1.78 m/s, p = 0.00006) and DAS28 (from 6.65 ± 1.22 to 4.69 ± 1.46, p = 0.00007) in RA patients treated with ADA. The decrease in PWV was observed both in responders (n = 12) and nonresponders (n = 6). Multivariate analysis showed that the decrease of PWV was independent of changes in disease activity or other parameters. There was no significant change in PWV in patients treated with MTX (from 8.87 ± 1.91 to 8.41 ± 2.17, p = 0.29). No significant change in AIx or traditional cardiovascular risk factors was observed. Treatment with ADA significantly reduced aortic stiffness in RA patients regardless of their response to therapy. These findings imply a direct protective effect of ADA in vascular wall in RA patients.
Background Guillain-Barré syndrome is an autoimmune disorder in which autoantibodies mainly affect the peripheral nervous system. Autonomic dysfunction is a common and severe complication of Guillain-Barré syndrome. Cardiomyopathy, though, is a rare complication in Guillain-Barré syndrome, with only a few cases reported in the literature. Case Presentation We present a case of a 65-year-old Greek woman with Guillain-Barré syndrome who developed cardiomyopathy shortly after admission to the intensive care unit due to respiratory deterioration. Her estimated left ventricular ejection fraction upon admission was 20%. The result of coronary angiography was negative for coronary artery disease, and cardiac magnetic resonance imaging excluded myocarditis. Her clinical condition improved with supportive therapy, and her estimated left ventricular ejection fraction at discharge was normal. Conclusions Clinicians should be aware of this potentially lethal complication of Guillain-Barré syndrome and the therapeutic options, because early diagnosis can improve prognosis. Routine electrocardiographic and echocardiographic assessments should be performed in patients with Guillain-Barré syndrome presenting with hemodynamic instability.
Background Aneurysm formation is a possible, but rare, complication of granulomatosis with polyangiitis, known as Wegener’s granulomatosis. Urgent diagnosis and therapy is very important because a ruptured aneurysm could be life threatening. Case presentation We, therefore, present the case of a 63-year-old Greek man who was diagnosed with granulomatosis with polyangiitis and retroperitoneal hematoma due to ruptured aneurysm in renal artery and upper pancreaticoduodenal artery. His clinical course was complicated by acute renal failure and acute respiratory failure due to alveolar hemorrhage. Emergency coil embolization was performed. Postembolization recovery was uneventful; no bleeding occurred. The patient underwent mechanical ventilation and continuous veno-venous hemofiltration and received combined immunosuppression and supportive therapy, but eventually died 30 days after admission to hospital from severe septic shock and multiple organ failure. Conclusion Endovascular treatment is the therapy of choice, especially for patients with ruptured aneurysms that are hemodynamically stable. Early diagnosis is very important, as urgent embolization and early initiation of immunosuppression therapy are the treatment of choice.
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