For more than 50 years, oral vitamin K antagonists (VKAs) were the choice of anticoagulant for the long-term treatment and prevention of arterial and venous thromboembolic events (VTE). VKA treatment is safe and effective, if a high time in therapeutic range is achieved. However, achieving a stable, therapeutic international normalised ratio can prove challenging in the context of drug and food interactions and liver disease, resulting in either an increased risk of thromboembolism due to undertreatment or bleeding due to overtreatment.
Idiopathic pulmonary arterial hypertension (formerly referred to as primary pulmonary hypertension) is an uncommon yet progressively fatal disease defined by the presence of mean pulmonary artery pressure greater than 25mmHg at rest or greater than 30mmHg with exercise as tested by right heart catheterization in the absence of other etiologies for pulmonary hypertension.
Pulmonary arterial hypertension (PAH) is a disorder of the pulmonary circulation in which elevated pressure in the pulmonary vascular circuit, when severe, can lead to right heart failure and eventually cause death. The last three decades have seen significant advances in our understanding of this group of disorders and, with this understanding, the development of novel therapies to assist in their treatment.
Chronic thromboembolic pulmonary hypertension (CTEPH) is believed to result from single or recurrent pulmonary thromboemboli arising from sites of venous thrombosis.1 The pathogenesis of the disease has not yet been fully elucidated. Acute pulmonary embolism subsequent to deep venous thrombosis may serve as the inciting event that stimulates local factors mediating aberrant organisation of pulmonary thromboemboli characteristic for CTEPH (see Figure 1).