Hypercoagulable Workup in Thrombotic Cardiovascular Diseases.

Abstract

Heart disease was the leading cause of death, whereas stroke was the fifth leading cause of death, in the United States in 2015. Arterial obstruction underpins myocardial infarction (MI) and stroke in patients. However, a minority of patients have no obstructive arterial disease found on angiography (termed myocardial infarction with nonobstructive coronary arteries [MINOCA], 6%),1 or source of embolus determined after extensive evaluation (termed cryptogenic stroke and embolic stroke of undetermined source, 30%).2 In MINOCA, potential causes include occult plaque rupture, coronary dissection, coronary embolism, vasospasm, microvascular disease, and thrombophilia.1 In cryptogenic stroke and embolic stroke of undetermined source, potential causes include occult atrial fibrillation, atrial cardiomyopathy, paradoxical embolism/patent foramen ovale, malignancy, and thrombophilia.2 Thrombophilia, inherited or acquired, results in increased risk of venous or arterial thrombosis. Hematologists are often asked to look for thrombophilia in patients with MINOCA, cryptogenic stroke, or embolic stroke of undetermined source, but the clinical utility of a thrombophilia workup in these scenarios is questionable. Recent studies indicate an intimate interaction between the hemostatic system and the vasculature, directly between coagulation factors and the endothelium, and indirectly via the complement and bradykinin systems. A plethora of experimental data implicates a potential role for platelets and the coagulation system in atherogenesis and atherothrombosis.3 Several heritable thrombophilic defects have been described involving various components of the coagulation system. Among these, factor V Leiden and prothrombin gene G20210A mutation …