Abstract

Acute Pulmonary Embolism (PE) is a life-threatening condition and the common cause of death is due to obstruction of main pulmonary vessels by the embolus, resulting in pulmonary hypertension followed by right-sided heart failure. Acute PE often occurs in some patients with hereditary and acquired factors predisposing them at a risk for the development of thrombotic events. The hereditary hypercoagulable state due to genetic mutations, such as deficiency of protein C and protein S, involves an increased risk of recurrent venous thromboembolism.

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