ABSTRACT
Background: Tumour necrosis factor (TNF)-alpha inhibition is a core therapeutic avenue for a broad range of inflammatory and autoimmune disorders including rheumatoid arthritis and inflammatory bowel disease, as well as dermatological conditions such as hidradenitis suppurativa. Adalimumab has become one of the most common TNF-alpha-inhibiting agents, which is used for many of these conditions. Treatment with such agents is associated with numerous systemic side effects, though cardiac complications remain relatively rare. These include reports of pericarditis and pericardial effusions1-3. Case summary: A 63-year-old lady was referred to the outpatient respiratory clinic with a 1-year history of increasing breathlessness, on a background of 4 years of treatment with adalimumab for Stage III hidradenitis suppurativa. A high-resolution computed tomography (CT) thorax revealed evidence of pericardial calcification. Subsequent left and right heart catheterization study revealed equalization of intraventricular pressures, consistent with constrictive pericarditis. A QuantiFERON test was negative, and rheumatological serology was unremarkable. The patient was initially managed conservatively with close follow-up, before undergoing surgical pericardectomy when she developed signs of cardiac failure. Discussion: Adalimumab is associated with a range of systemic side effects, though cardiac complications are relatively rare. This case highlights a potentially novel complication associated with prolonged adalimumab therapy. Given that there are reports in the literature of pericarditis and pericardial effusions associated with TNF-alpha inhibition1-3, it is reasonable to hypothesize that the calcific constrictive pericarditis seen in this case may demonstrate a novel cardiac phenomenon associated with this therapy, given the lack of any traditional aetiological factors.
ABSTRACT
A 22-year-old woman was referred with exertional dyspnoea and chest tightness 3 weeks following a diagnosis of COVID-19. Evaluation revealed a resting sinus tachycardia and criteria for postural orthostatic tachycardia syndrome were met. After non-pharmacological interventions failed to yield symptomatic improvement, ivabradine was commenced. This intervention was followed by a substantial improvement in the patient's exercise tolerance and energy levels and an objective reduction in supine and standing heart rate.
