Workflow and Patient Satisfaction in Treating Peripheral Arterial Disease in the Office-Based Setting.

Contemporary concepts in health-care reform promote a shift in the provision of care away from hospitals in favor of the more cost-effective and efficient use of outpatient facilities including ambulatory surgery centers and office-based procedure centers particularly in the care of cardiovascular disease. This article reviews the experience of patients and specialists in caring for patients with peripheral arterial disease in an office-based care setting.

Initial experience with the ambulatory management of acute iliofemoral deep vein thrombosis with May-Thurner syndrome with percutaneous mechanical thrombectomy, angioplasty and stenting.

Objective: Patients undergoing intervention for acute iliofemoral deep vein thrombosis (IFDVT) with May-Thurner syndrome (MTS) typically require inpatient (IP) hospitalization for initial treatment with anticoagulation and management with pharmacomechanical thrombectomy. Direct oral anticoagulants and percutaneous mechanical thrombectomy (PMT) devices offer the opportunity for outpatient (OP) management. We describe our approach with these patients.

A telephone call 1 week after hospitalization can identify risk factors for vascular surgery readmission.

Objective: Compared with other populations, patients who undergo vascular surgery have higher 30-day hospital readmission rates of up to 25%. Postdischarge telephone call assessments have demonstrated utility in patients with significant medical comorbidities and traditionally high readmission rates. Therefore, we hypothesized that a 1-week postdischarge telephone call evaluation can identify risk factors for readmission among vascular surgery patients.

Bone morphogenetic protein-2 decreases microRNA-30b and microRNA-30c to promote vascular smooth muscle cell calcification.

Background: Vascular calcification resembles bone formation and involves vascular smooth muscle cell (SMC) transition to an osteoblast-like phenotype to express Runx2, a master osteoblast transcription factor. One possible mechanism by which Runx2 protein expression is induced is downregulation of inhibitory microRNAs (miR).

Methods And Results: Human coronary artery SMCs (CASMCs) treated with bone morphogenetic protein-2 (BMP-2; 100 ng/mL) demonstrated a 1.