Abstract

Abstract Permanent pacemaker (PPM) implantation can lead to thromboembolic events at different times after the procedure. According to literature, 1.7% of patients with pulmonary embolism have an implantable cardiac device. This frequency is higher than reported so far, from 0.16 to 0.47% of the total population. The pathophysiologic mechanism of pulmonary embolism in chronic thromboembolic pulmonary hypertension (CTEPH) is multifactorial. Recently, there is evidence that not only the organisation of thrombotic deposits in the proximal pulmonary arterial vessels is important, but also the development of small vessel disease, which plays an important role in the evolution and progression of the disease. The role of thrombosis in medical devices in contact with blood flow, such as stents, vascular grafts, heart valves, has been well studied and documented in scientific literature on biomaterials. It is clear that implantable cardiac devices such as pacemakers, similarly to other foreign surfaces exposed to blood flow, promote blood clotting and complement activation. Numerous studies to date have addressed the potential risk of distal vascular involvement of pulmonary circulation in the presence of a pacemaker, but none has conclusively proven this hypothesis. Over the last decade, there has been significant progress in the therapeutic potential of CTEPH. Pulmonary endarterectomy remains the only therapeutic method that can lead to lasting clinical improvement in these patients while achieving a good quality of life. This method is operational, with high financial value and is associated with the presence of a highly specialised team of specialists. This justifies the search for ways to prevent the onset of the disease rather than treat the consequences.

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