Vertebral artery stenosis (VAS) is the cause of approximately 20% of ischemic strokes in the posterior circulation. There are several causes of vertebral artery stenosis, including atherosclerosis, calcification, dissections, fibromuscular dysplasia, giant cell arteritis, neurofibromatosis type 1, and bony compressions. The most common cause of VAS is atherosclerosis which is derived from the macrophage-induced oxidation of low-density lipoproteins (LDLs), alongside the accumulation of cholesterol. Calcification of the vertebral artery occurs when there is excess calcium and phosphate deposition in the vessel. Dissection of the vertebral artery can lead to the formation of a hematoma causing stenosis of the vertebral artery. Fibromuscular dysplasia can result in stenosis due to the deposition of collagen fibers in the tunica media, intima, or adventitia. Giant cell arteritis, an autoimmune disorder, causes inflammation of the internal elastic membrane resulting in eventual stenosis of the artery. Neurofibromatosis type 1, an autosomal dominant disorder, results in the stenosis of the vertebral artery due to the altered function of neurofibromin. Mechanical compression of the vertebral artery by bone can also cause stenosis of the vertebral artery. Digital subtraction angiography (DSA) is considered the current gold standard in diagnosing vertebral artery stenosis; however, its associated morbidity and mortality have led to increased use of noninvasive techniques such as duplex ultrasonography (DUS), computed tomography angiography (CTA), and magnetic resonance angiography (MRA). Currently, asymptomatic and symptomatic vertebral artery stenoses are treated by risk factor modification and medical treatment. However, it is recommended that surgical (endarterectomy, reconstruction, and decompression) and endovascular (balloon coronary, baremetal, and drug-eluting stents) treatments are also used for symptomatic vertebral artery stenosis.

Background Secondary polycythemia is an acquired condition characterized by an elevation in red blood cell (RBC) mass either in response to tissue hypoxia or inappropriate erythropoietin (EPO) secretion. It is proposed that the elevation of RBC mass in secondary polycythemia can lead to hyperviscosity and VTE. This systematic review aims to assess the relationship between secondary polycythemia and venous thromboembolism and discuss diagnostic strategies and management of secondary polycythemia and VTE. Methods This systematic review was conducted on September 2, 2022, and followed PRISMA guidelines to select and analyze relevant articles using the following databases: PubMed, ScienceDirect, and CINAHL. The queries used were  “secondary polycythemia AND venous thromboembolism,” “secondary polycythemia AND deep vein thrombosis,” “secondary polycythemia AND pulmonary embolism,” “chronic obstructive pulmonary disease AND venous thromboembolism,” “chronic obstructive pulmonary disease AND deep vein thrombosis,” “chronic obstructive pulmonary disease AND pulmonary embolism,” “high altitude AND venous thromboembolism,” “high altitude AND deep vein thrombosis,” “high altitude AND pulmonary embolism,” “smoking AND venous thromboembolism,” “smoking AND deep vein thrombosis”, “smoking AND pulmonary embolism”, “hypoventilation AND venous thromboembolism”, “hypoventilation AND deep vein thrombosis”, “hypoventilation AND pulmonary embolism”, “testosterone AND venous thromboembolism”, “testosterone AND deep vein thrombosis”, and “testosterone AND pulmonary embolism.” The search duration was set from 2012–2022. Relevant publications were selected based on the inclusion and exclusion criteria. Results The initial search generated 5,946 articles. After narrowing the search based on inclusion and exclusion criteria, 30 articles were selected for this systematic review. Conclusion We found evidence to support the relationship between secondary polycythemia and VTE. Therapies targeting the factors that lead to secondary polycythemia can correct it and prevent VTE progression. If VTE occurs as a result of secondary polycythemia, anticoagulation therapy is recommended or inferior vena cava filters if contraindicated.