Long-term patency of aorto-biiliac endoprosthesis for critical lower limb ischaemia in Takayasu arteritis after complicated angioplasty with a drug-coated balloon: Effect of dual antiplatelet therapy combined with tocilizumab.

Takayasu arteritis is a chronic granulomatous vasculitis of unknown aetiology affecting the aorta and its major branches. Critical limb ischaemia may occur and eventually require surgical intervention. Surgical outcomes are influenced by disease activity, age, and comorbidities. We report a 43-year-old woman with Takayasu arteritis and stenosis of the left common iliac artery and occlusion of the left external iliac artery with limiting vascular claudication, who underwent angioplasty of the iliac artery with drug-eluting stent while being treated with infliximab. The artery ruptured a week later but was contained by the ilio-psoas muscle. She required subsequent stent placement to correct the lesion. Treatment comprised aspirin and clopidogrel, and the biological was switched to monthly intravenous tocilizumab. During an 8-year follow-up, serial imaging examinations showed a patent aorto-biiliac endoprosthesis, without evidence of thrombosis or restenosis. Clinically, the patient denies vascular claudication and pulses remain palpable in the left lower limb. This case highlights the risks inherent to these procedures in patients with large artery vasculitis and reinforces that the effectiveness of endovascular intervention can be increased by detailed preoperative evaluation, associated with a drug strategy including immunomodulatory and antiplatelet therapy as directed by the multispecialty team. Periodic imaging examinations are required because of the reported high rate of restenosis.

Risk of Cardiac Lesion with Chronic and Acute Use of Loperamide-An Integrative Review.

Loperamide is a synthetic opioid commonly used as an antidiarrheal due to its activation of u-opioid receptors in the myenteric plexus. In therapeutic doses, it inhibits peristalsis and has anti-secretory and anti-motility effects, until metabolized by intestinal and hepatic CYP3A4 and CYP2C8 into inactive metabolites. Furthermore, loperamide also inhibits L-type voltage-gated calcium (Ca2+) channels, increases action potential duration, and can induce arrhythmias and even cardiotoxicity, particularly when taken in extremely high doses. Thus, the aim of this study was to perform an integrative review of the available evidence in the recent literature on the cardiac risks of acute and chronic use of loperamide. In electrocardiogram (ECG) analysis, the most common finding was QTc prolongation in 27 cases, followed by QRS prolongation, first-degree atrioventricular (AV) block, torsades de pointes, ventricular tachycardia, and right bundle branch block. As for the symptoms encountered, syncope, weakness, palpitations, lightheadedness, shortness of breath, nausea, vomiting, bradycardia, and cardiac arrest were the most common. Loperamide can inhibit hERG voltage-gated potassium (K+) channels (Kv11.1), leading to the prolongation of repolarization, QTc interval prolongation, and increased risk of torsades de pointes. In addition, loperamide can inhibit voltage-gated sodium (Na+) channels (Nav1.5), impairing electrical cardiac conduction and potentiating QRS interval widening. Therefore, QTc prolongation, torsades de pointes, and other ECG alterations are of particular concern regarding loperamide toxicity, particularly when overdosed.