Key result
Protein C deficiency linked to acute MI from total LAD occlusion in a young male.
Why the study?
Although protein C deficiency is known to cause venous thromboembolism, its role in arterial thrombus and premature myocardial infarction in young patients with minimal cardiovascular risk is less recognized.
Case Report (n=1)
No
Protein C deficiency should be considered as a possible cause of acute, premature myocardial infarctions in young patients with minimal or no traditional cardiovascular risk factors.
MI in protein C deficiency may signal arterial risk; hypothesis-generating and leaves open extension beyond VTE.
Protein C is a Vitamin K derivative that plays an essential role in anticoagulation. Protein C deactivates clotting factors Va and VIIIa; therefore, a deficiency in this protein leads to over expression and activation of these factors and essentially a hypercoagulable, prothrombotic state. Although studies have shown that the cardinal manifestation of protein C deficiency is venous thromboembolism, we present a case of a patient in his third decade with a myocardial infarction on a background of protein C deficiency and minimal cardiovascular risk factors. Similar cases of patients presenting with arterial thrombus on background of protein C deficiency have been reported; therefore, it is imperative to acknowledge protein C deficiency as a possible cause of acute, premature myocardial infarctions in young patients with minimal or no risk for cardiovascular disease.
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Mansour et al. (2019) conducted a case report in Myocardial infarction and Protein C deficiency (n=1). Protein C deficiency was evaluated. A 32-year-old male with protein C deficiency and minimal cardiovascular risk factors presented with an acute myocardial infarction due to total thrombotic occlusion of the left anterior descending artery.
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