Immune reconstitution inflammatory syndrome (IRIS) describes the initial clinical deterioration some patients manifest upon initiation of effective antiretroviral therapy (ART) for HIV infection. In this report we describe a case of IRIS manifesting as polyarticular gout, a previously unreported rheumatological manifestation of IRIS. A 53-year-old HIV-infected man with a history of intermittent attacks of gout and an initial CD4 count of 112 cells/microL and a viral load of >100,000 copies/mL presented to our institution with severe, refractory, polyarticular gout approximately 4 weeks after initiating ART. At this point, the patient demonstrated significant gains in his CD4 counts (103 cells/microL) and a greater than 3 log decline in his HIV-1- viral load. This episode was prolonged lasting for approximately 10 weeks and required hospitalization for the management of pain and control of inflammation. The temporal associations of this attack with the initiation of ART and the observed immunologic reconstitution make IRIS a clinical possibility.Monosodium urate crystals through their interactions with interleukin 1- beta, and neutrophilic synovitis play a critical role in the pathophysiology of gout. Defects in both neutrophil and macrophage function and imbalances in the cytokine milieu are documented in HIV infected patients. The introduction of ART results in restoration of neutrophil and macrophage function, declines in levels of the anti-inflammatory cytokine IL-10, and increases in levels of proinflammatory cytokines including IL-1 beta, which may provide the necessary milieu for the precipitation of attacks of severe polyarticular gout in the context of ART initiation.

Aortic insufficiency from iatrogenic valve perforation from nonaortic valve operations is rarely reported despite the prevalence of these procedures. Rapid diagnosis of these defects is essential to prevent deterioration of cardiac function. In this paper, we describe a young man who reported to our institution after two open cardiac surgeries with new aortic regurgitation found to be due to an iatrogenic perforation of his noncoronary aortic valve cusp. This defect was not appreciated by previous intraoperative transesophageal echocardiography and was inadequately visualized on follow-up transthoracic and transesophageal echocardiograms. In contrast, cardiac gated computed tomography clearly visualized the defect and its surrounding structures. This case highlights the utility of cardiac gated computed tomography for cases of suspected valvular perforation when echocardiography is not readily available or inadequate imaging is obtained.

Objective: To investigate the risk of major adverse cardiac events (MACE) in patients with a history of bare metal stent (BMS) restenosis who undergo subsequent bare metal stenting of a geographically distinct, de novo coronary lesion. Methods: We conducted a retrospective review of 72 BMS procedures performed in geographically distinct, de novo coronary lesions in patients with a history of previous BMS placement at least 3 months prior to the second, index stent procedure. Patients with a history of in-stent restenosis (ISR) were compared with those who had no ISR in their initial stent. Results: Restenosis in the initial BMS was associated with a significant increase in MACE after placement of the index BMS (OR 20.0, 95% CI 3.86–103.58, p < 0.0001). This association was independent of traditional clinical and angiographic risk factors for restenosis. Conclusions: Restenosis of a previously placed BMS is strongly associated with MACE after placement of a subsequent BMS in a de novo coronary lesion.

Brugada syndrome (BrS) is a common occult cause of sudden cardiac arrest in otherwise healthy-appearing adults. The pathognomonic electrocardiographic pattern may be unmasked only by certain medications, many of which are unknown. We report a case of a depressed but otherwise healthy man with an asymptomatic right bundle branch block on electrocardiography who experienced antidepressant-induced BrS and ultimately recovered with transcranial magnetic stimulation (TMS). After an initial trial of nortriptyline, the patient's depressive symptoms improved; however, he experienced a syncopal event and was subsequently diagnosed as having BrS. Cross titration to bupropion, which had not previously been known to exacerbate BrS, was followed by another cardiac event. As a result, the patient was referred for TMS as a substitute for pharmacotherapy. After 31 TMS sessions over 8 weeks, the patient demonstrated significant improvement by subjective report and objective reduction in his Patient Health Questionnaire-9 scores from 10 (moderate) to 1 (minimal). Transcranial magnetic stimulation is a Food and Drug Administration-approved nonpharmacologic treatment for depression. Given the potential lethality of BrS with known and unknown psychopharmacologic agents, providers should consider TMS as first-line therapy in this patient population. Bupropion should be added to the list of agents known to exacerbate this disease.

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