The main goals for urologists during the coronavirus disease 2019 (COVID-19) pandemic are to prevent their patients from getting COVID-19, protect themselves as health care professionals, and deliver optimal urology care [1]. While prioritisation strategies are being proposed [2,3], further measures are warranted for multifaceted action plans towards optimal perpetuation of urology care during the pandemic [4]. Urological telemedicine can lead to (1) fewer patient contacts, (2) lower infection rates among the staff, and (3) continuation of urological care by quarantined urologists [5]. However, the proportion of patients eligible for telemedicine, their wish to use telemedicine, and their demographic risk profile for acquiring a severe pandemic infection are unknown. In this context, we tested the potential of telemedicine in urology. We evaluated patients' eligibility for telemedicine according to the physician and examined the patients' perspective by evaluating their willingness for telemedicine.

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Objective Extracellular matrix (ECM) of neointima formed following angioplasty contains elevated levels of versican, loosely arranged collagen, and fragmented deposits of elastin, features associated with lipid and macrophage accumulation. ECM with a low versican content, compact structure and increased elastic fiber content can be achieved by expression of versican variant V3, which lacks chondroitin sufate (CS) glycosaminoglycans (GAG). We hypothesized that V3-expressing arterial smooth muscle cells (ASMC) can be utilized to form a neointima resistant to lipid and macrophage accumulation associated with hypercholesterolemia. Methods and Results ASMC transduced with V3 cDNA were seeded into ballooned rabbit carotid arteries and animals fed a chow diet for four weeks, followed by a cholesterol-enriched diet for four weeks, achieving plasma cholesterol levels of 20–25mmol/L. V3 neointimae at eight weeks were compact, multilayered and elastin-enriched. They were significantly thinner (57%) than control neointimae, contained significantly more elastin (118%), less collagen (22%) and less lipid (76%), and showed significantly reduced macrophage infiltration (85%). Mechanistic studies demonstrated that oxidized LDL stimulated the formation of this monocyte binding ECM which was inhibited in the presence of V3 expressing ASMC. Conclusion These results demonstrate that expression of V3 in vessel wall creates an elastin-rich neointimal matrix that in the presence of hyperlipidemia is resistant to lipid deposition and macrophage accumulation.