A recent study discussed a case report of a 43-year-old male athlete with progressive exercise limitation after experiencing a pulmonary embolism (blockage of a pulmonary blood vessel), but without signs of pulmonary hypertension. The study was published in the journal BMC Pulmonary Medicine, and is titled “Case report: Subjective loss of performance after pulmonary embolism in an athlete – beyond normal values.”
Chronic thromboembolic pulmonary hypertension (CTEPH) is a progressive disease caused by a wall-adherent, fibrotic thrombus (a clot) in the pulmonary circulation, despite the use of oral anticoagulation medicines. For patients whose CTEPH is operable, surgical removal of persistent thrombi is highly recommended by pulmonary endarterectomy. However, without the presence of pulmonary hypertension, the therapy of chronic thromboembolic disease (CTED) is challenging.
At this time, there is not enough significant background cases on therapeutic approaches for CTED with normal hemodynamics. In some selected cases, such as athletes, lower exercise tolerance and dyspnea can be related to the extent of persistent pulmonary perfusion defects and dead space ventilation, despite having expected or increased exercise capacity and normal pulmonary hemodynamics.
The athlete in this case report experienced progressive exercise limitation for eight months. Six months earlier, he had a pulmonary embolism and was treated with oral anticoagulation therapy. A pulmonary ventilation and perfusion scan indicated severe ventilation and perfusion distortion. A chest computed tomography and pulmonary angiography pointed out bilateral wall-adherent thrombotic material, while pulmonary hemodynamics were normal. His maximal oxygen uptake exceeded predicted values, but exercise ventilatory efficiency was not normal compared to a healthy athlete.
The patient successfully underwent pulmonary endarterectomy. At 5 and 12 months post-surgery, his maximal exercise capacity and ventilatory efficiency improved compared to his preoperative status, and his subjective exercise tolerance returned to normal.
According to the authors, this report emphasizes that significant CTED can be present without relevant pathologic changes in pulmonary hemodynamics at rest. Cardiopulmonary deficiency can be masked by a high level of physical fitness, therefore normal values of maximal exercise capacity do not exclude pulmonary vascular disease in trained people.
Although pathophysiological considerations suggest a beneficial treatment effect, more data is needed to evaluate the risks of pulmonary endarterectomy in patients with CTED and normal pulmonary hemodynamics. Patients should be thoroughly informed of their options and be treated only at expert centers. Successful surgery can result in beneficial, sustained treatment, even in patients who have normal pulmonary hemodynamics.
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