The regenerative potential of bone marrow-derived endothelial progenitor cells (EPCs) has been adapted for the treatment of myocardial and limb ischemia via ex vivo expansion. We sought to enhance EPC function by the efficient genetic modification of EPCs in a rat model of myocardial infarction. Peripheral blood EPCs were expanded and transduced, using adeno-associated virus (AAV). AAV-mediated EPC transduction efficacy was 23 ± 1.2%, which was improved by 4.0- to 7.2-fold after pretreatment with the tyrosine kinase inhibitor genistein. Adult rats (n = 7 in each group) underwent myocardial infarction by left anterior descending coronary artery occlusion, and received autologous EPCs transduced by AAV-IGF-1 or AAV-lacZ into the periinfarct area. Echocardiography demonstrated that cardiac function in the IGF-1-EPC group was significantly improved compared with the lacZ-EPC control group 12 weeks after myocardial infarction. In addition, IGF-1-expressing EPCs led to reduced cardiac apoptosis, increased cardiomyocyte proliferation, and increased numbers of capillaries in the periinfarct area. AAV expression was limited to the targeted heart region only. Pretreatment with genistein markedly improved AAV transduction of EPCs. IGF-1-expressing EPCs exhibit favorable cell-protective effects with tissue-limited expression in rat heart postinfarction.

Overlay of 3D CS anatomy defined by preprocedural cardiac CT is feasible. It allows planning of CRT implantation and live guidance of CS lead placement into a predefined target branch. Limiting the CT imaging to 40 % of the cardiac cycle phase provides optimal CS images and reduces radiation exposure. This approach may result in shorter procedural time and more optimal CS lead positioning. However, the concept remains to be confirmed by future studies.

We report a case of severe deep venous thrombosis (DVT) treated with multimodality therapy that was complicated by sepsis due to thrombus likely infected by Salmonella virchow. We review the current therapeutic options in the therapy of severe DVT and cardiovascular pathology associated with non-typhoid Salmonella.