How to perform a successful drug-coated balloon angioplasty? Tips and tricks.

Drug-coated balloons (DCB) offer an excellent alternative to stents as the antiproliferative drugs are delivered via balloons and hence there is no permanent implant of metal or polymer. This rationale applies perfectly in in-stent restenosis (ISR) as we want to avoid another layer of metal in a previously failed stent. However, their use has also been extended to de novo lesions especially in patients and lesion subsets where stents are not ideal. There is an increased desire toward expanding this further and studies are now being done which are testing DCB in large-caliber vessels. As the use of DCB is escalating, we felt the importance of writing this article whereby we aim to provide important tips and tricks when using DCB especially for the operators who are in the early phase or have the desire of embarking this technology. From our experience, the DCB-angioplasty substantially differs on several aspects from DES-angioplasty. We have provided several case bases examples including algorithm when using DCB in ISR and de novo lesions.

The evolution and revolution of drug coated balloons in coronary angioplasty: An up-to-date review of literature data.

European Society of Cardiology (ESC) guidelines gave class I A indication for use of DCB in in-stent restenosis. However, no indication exists for the usage of DCB in de novo lesions. Although the current generation DES offer excellent results, as we embark more complex lesions such as calcified lesion and chronic total occlusion, restenosis and stent thrombosis are higher and tend to increase within the years. There is increasing desire to leave nothing behind to abolish the risk of restenosis and stent thrombosis and hence the absorbable scaffolds were introduced, but with disappointing results. In addition, they take several years to be absorbed. Drug coated balloons offer an alternative to stents with no permanent implant of metal or polymer. They are already in use in in Europe and Asia and they have been approved for the first time in the United States for clinical trials specifically for restenotic lesions. There is emerging data in de novo lesions which have shown that DCB are noninferior and in some studies maybe even superior to current generation DES especially in small vessels. In this article, we provide a comprehensive review of the literature on this expanding technology focussing on the evidence in both re-stenotic and de novo lesions.

Cross-Priming Dendritic Cells Exacerbate Immunopathology After Ischemic Tissue Damage in the Heart.

BACKGROUND: Ischemic heart disease is a leading cause of heart failure and despite advanced therapeutic options, morbidity and mortality rates remain high. Although acute inflammation in response to myocardial cell death has been extensively studied, subsequent adaptive immune activity and anti-heart autoimmunity may also contribute to the development of heart failure. After ischemic injury to the myocardium, dendritic cells (DC) respond to cardiomyocyte necrosis, present cardiac antigen to T cells, and potentially initiate a persistent autoimmune response against the heart. Cross-priming DC have the ability to activate both CD4+ helper and CD8+ cytotoxic T cells in response to necrotic cells and may thus be crucial players in exacerbating autoimmunity targeting the heart. This study investigates a role for cross-priming DC in post-myocardial infarction immunopathology through presentation of self-antigen from necrotic cardiac cells to cytotoxic CD8+ T cells. METHODS: We induced type 2 myocardial infarction-like ischemic injury in the heart by treatment with a single high dose of the ß-adrenergic agonist isoproterenol. We characterized the DC population in the heart and mediastinal lymph nodes and analyzed long-term cardiac immunopathology and functional decline in wild type and Clec9a-depleted mice lacking DC cross-priming function. RESULTS: A diverse DC population, including cross-priming DC, is present in the heart and activated after ischemic injury. Clec9a-/- mice deficient in DC cross-priming are protected from persistent immune-mediated myocardial damage and decline of cardiac function, likely because of dampened activation of cytotoxic CD8+ T cells. CONCLUSION: Activation of cytotoxic CD8+ T cells by cross-priming DC contributes to exacerbation of postischemic inflammatory damage of the myocardium and corresponding decline in cardiac function. Importantly, this provides novel therapeutic targets to prevent postischemic immunopathology and heart failure.

Pelvic floor examination performed by medical students: a model to obtain consent.

Student-led clinical examinations, including pelvic floor examinations, are an integral part of clinical training and can be beneficial to both students and patients alike. However, our experience and previous literature catalog numerous obstacles in obtaining consent for student-led pelvic floor examinations. Although some of these factors may not be modifiable, it is evident that efforts can be made to overcome those that are. An examination of these obstacles can help to provide a clear and succinct template to overcoming them: we propose a "5-Rs" framework that may bridge the apparent gap between the students' need to practice and obtain valid consent.