Case Presentation:
A 31‐year‐old female presented with six hours of exertional chest pain, dyspnea, palpitations, and vomiting. Her review of systems was significant for easy bruising and bleeding gums. Physical examination was significant for epigastric tenderness and diffuse ecchymoses. Initial blood work revealed normal chemistries, a WBC of 11.3 mm3, a Hgb of 8.3 g/dl, and platelets of 8000 mm3. PT and PTT were normal. A D‐Dimer level was > 400 ng/ml and the fibrinogen level was >700 mg/dl. A peripheral smear showed 4‐5 schistocytes per high power field. Her CK was 241 u/l, CKMB was 6.3 ng/ml, and troponin I was1.15 ng/ml. The admission EKG showed normal sinus rhythm and non‐specific ST changes; a lower extremities venous duplex was negative for thrombosis. On the basis of her history, physical findings, and laboratory results, the patient was diagnosed with thrombotic thrombocytopenic purpura and non‐ST elevation myocardial infarction. Plasma exchange was initiated; however, due to her thrombocytopenia, ASA, clopidogrel, and heparin were not instituted. On hospital day #1, the troponin level dropped to 0.55 ng/ml and a TTE showed normal left ventricular size and function and normal valves. The platelet count improved with plasma exchange and steroid therapy. Tests for HIV, cold agglutinin antibodies, anti‐phospholipid antibodies, anti‐cardiolipin antibodies, and rheumatoid factor, were all negative. However, the lupus anticoagulant was detected. Cardiac catheterization was deferred during hospitalization due to the thrombocytopenia and anemia. The patient was discharged on hospital day #25 with a normal LDH and platelet count.
Discussion:
In TTP, von Willebrand Factor is synthesized normally but its subsequent cleavage is defective due to a lack of enzyme activity that breaks down vWF in the blood. In its full‐blown form, the disease consists of the pentad of microangiopathic hemolytic anemia, thrombo‐cytopenic purpura, neurologic abnormalities, fever, and renal disease. However, with the availability of plasma exchange therapy, only thrombocytopenia and microangiopathic hemolytic anemia are required to suspect the diagnosis of TTP and to initiate plasma exchange. Adequate initial response is fulfilled if neurologic signs and symptoms disappear, the platelet count climbs to greater than 50,000 mm3, and the LDH declines. Non‐ST elevation MI as a complication of TTP has rarely been reported. The etiology is suspected to be an autoimmune phenomenon resulting in microvascular thrombosis.
Conclusion:
Secondary etiologies need to be strongly considered in young patients diagnosed with acute coronary syndromes. Cardiac troponin‐I measurements should be considered as part of the initial evaluation of all patients admitted with acute TTP regardless of presenting symptoms.
Author Disclosure Block:
A. Gottesman, None; V. Ephrem, None.