Asian Journal of Cardiology Research

Context: Thromboembolic disease is the third leading cause of cardiovascular death. In recent years, several studies have suggested the possibility of de novo thrombus formation in the pulmonary arteries without deep vein thrombus (DVT) in the lower extremities. Pulmonary artery thrombosis is a very rare diagnostic entity, typically due to embolic migration from another venous site, but it can also arise from an In situ thrombus. The aim of this study is to evaluate the clinical and echocardiographic (TTE) data of in situ pulmonary artery thrombosis (PATIS). This mini-series involves four cases observed in the intensive cardiac care unit (ICCU) at the cardiology department of Ibn Rochd University Hospital in Casablanca between January 1, 2024, and April 1, 2024.

Case Presentation: We present a mini-series of four patients, consisting of three women and one man, admitted to the ICCU for high-risk pulmonary artery thrombosis. The mean age of the patients was 64 years. Two women had neoplasms, while the man was sedentary due to bilateral lymphedema in the lower limbs. The last patient was a woman on oestro-progestative pills. Altogether, these factors appear to be the main contributors to their thromboembolic events. Clinically, all patients experienced dyspnea and angina. Bedside echocardiography revealed evidence of acute cor pulmonale associated with right ventricular dysfunction and in situ pulmonary artery thrombosis (PATIS). We administered non-fractionated heparin (NFH) immediately after diagnosing PATIS, without waiting for the results of thoracic CT angiography, and none of the patients initially received thrombolysis. The prognosis was poor, with three out of four patients dying from cardiogenic shock during hospitalization. In our opinion, the main contributing factors were comorbidities such as age, neoplastic profile, and uncontrolled diabetes.

Conclusions: While there is much theory regarding the pathophysiology of in situ pulmonary artery thrombus, the primary pathogenic factors are thought to be local pulmonary factors, including dysfunction of pulmonary vascular endothelial cells, hypoxia, and inflammation.