A 69-year-old man with unprovoked PE 2 months prior was referred to Cardiovascular Medicine Clinic for exertional dyspnea despite consistently therapeutic anticoagulation with warfarin. Although the dyspnea and chest pressure associated with his diagnosis of PE improved initially with anticoagulation, these symptoms never resolved completely and became progressively worse. He had presented to his local Emergency Department 1 month earlier with chest pressure and dyspnea. A contrast-enhanced chest computed tomogram (CT) was performed and demonstrated no new PE. He was instructed to continue warfarin and follow-up with his Primary Care Physician, who subsequently referred him for cardiovascular evaluation. On physical examination, he had a heart rate of 105 beats per minute, blood pressure of 113/76 mmHg, respiratory rate of 22 breaths per minute, and an oxygen saturation of 90 % on room air. Although his lungs were clear to auscultation, his cardiac examination was remarkable for tachycardia, a loud sound of pulmonic closure (P2), and a III/VI holosystolic murmur at the left lower sternal border that increased with inspiration. Because of his history of PE and physical examination findings, a transthoracic echocardiogram was performed to evaluate for pulmonary hypertension. The echocardiogram demonstrated RV dilation and moderate tricuspid regurgitation (Fig. 11.1) with a severely elevated estimated pulmonary artery systolic pressure of 84 mmHg (Fig. 11.2). A contrast-enhanced chest CT demonstrated extensive chronic bilateral PE consistent with chronic thromboembolic pulmonary hypertension (Fig. 11.3). After definitive therapy with surgical pulmonary thromboendarterectomy, the patient’s exertional dyspnea completely resolved.