Publications by authors named "Wisam Khider"

Background: Residual and significant postinfarction left ventricular (LV) dysfunction, despite technically successful percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI), remains an important clinical issue. In preclinical models, low-dose insulin-like growth factor 1 (IGF1) has potent cytoprotective and positive cardiac remodeling effects. We studied the safety and efficacy of immediate post-PCI low-dose intracoronary IGF1 infusion in STEMI patients.

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We evaluated the therapeutic efficacy of a novel drug eluting stent (DES) inhibiting inflammation and smooth muscle cell (SMC) proliferation. We identified CX3CR1 as a targetable receptor for prevention of monocyte adhesion and inflammation and in-stent neointimal hyperplasia without interfering with stent re-endothelization. Efficacy of AZ12201182 (AZ1220), a CX3CR1 antagonist was evaluated in inhibition of monocyte attachment in vitro.

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We report a case of a patient admitted with an acute ST elevation myocardial infarction following occlusion of his right coronary artery, successfully treated with thrombectomy and percutaneous coronary intervention (PCI). Coronary angiography and multislice CT revealed a single right coronary artery with two anomalous branches (constituting the left coronary system); one branch passed between the pulmonary trunk and the aorta before dividing into three separate branches, while the other anomalous branch passed anterior to the pulmonary trunk, consistent with a Yamanaka R-IIIC classification. The course of this Yamanaka R-IIIC subtype is unusual as both anomalous branches combine to form a dual origin left anterior descending artery.

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Mesenchymal stem cells (MSCs) are currently under investigation as tools to preserve cardiac structure and function following acute myocardial infarction (AMI). However, concerns have emerged regarding safety of acute intracoronary (IC) MSC delivery. This study aimed to characterize innate prothrombotic activity of MSC and identify means of its mitigation toward safe and efficacious therapeutic IC MSC delivery post-AMI.

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