Polycythemia Vera Presenting as Cardiac Arrest: Novel Management Strategies

Abstract

Acute coronary syndromes (ACS) usually occur in patients with multiple cardiac risk factors. In young adults, drug use and hypercoagulable states are common causes for ACS presentations. We report a case of a man in his early 30s who was diagnosed with polycythemia vera (PV) and had a cardiac arrest due to an anterolateral ST elevation myocardial infarction. We discuss his unique management and review the evidence on the management of arterial thromboembolism in PV patients.

Myocardial infarction in young individual: A case report of polycythemia vera-induced acute inferior wall myocardial infarction

“…The case by Davis et al emphasizes the need for novel management strategies, possibly reflecting the diversity in clinical approaches. 9 Our unique case, where PV manifested as an acute MI, adds a layer of intrigue, especially given the absence of any identified blockage during the CT angiography. This observation hints at the potential resolution of thrombus following streptokinase administration, presenting a distinctive aspect in the understanding of PV-associated cardiovascular events.…”

“… 8 In contrast, Davis et al detailed a case where PV led to cardiac arrest, emphasizing the need for novel management strategies in such critical situations. 9 Additionally, Rattarittamrong et al presented a unique case of acute non-atherosclerotic STEMI in an adolescent with concurrent hemoglobin H-Constant Spring disease and PV, expanding the understanding of the disease spectrum. 10 …”

ST-Segment Elevation Myocardial Infarction and Bleeding Complications in JAK2-Negative Polycythemia

“… 9 Cases have been reported of patients with JAK2 -positive PV developing MI with single vessel involvement and cardiac arrest. 10 – 12 Although only a minority of patients with PV do not carry the alteration, this proportion is higher in familiar cases. 13 This patient tested negative for JAK2 V617F alteration; therefore, other somatic mutations involving exons 12 and 13 in the JAK2 gene 14 and inherited germline mutations involving familial or congenital polycythemia, erythropoietin receptor alteration, and high oxygen-affinity hemoglobin 9 must also be assessed.…”