A 61‐year‐old man presented with episodic chest pain. He described the pain as a pressure and was associated with shortness of breath. He reported relief with sublingual nitroglycerin. He had a history of coronary artery disease treated with balloon angioplasty two years prior and chronic hepatitis C cirrhosis with a MELD of 10 without esophageal varices. Vital signs were normal. He had normal mentation with mild asterixis, Heart sounds were normal and lungs were clear. Abdominal exam demonstrated marked ascites with spider angiomata. Extremites had 1+ pitting edema to the shins. Electrocardiograph demonstrated t‐wave inversions in the lateral leads, which were unchanged from prior studies; chest x‐ray was unremarkable. Troponin was 0.32 ng/mL. Hemoglobin was 9.9 g/dL, with an MCV of 78 fL, and platelets of 25,000/mL He was started on dual anti‐platelet therapy and his troponin peak was 1.76 ng/mL. Following, he underwent nuclear perfusion demonstrating a high risk for myocardium jeopardy in the region supplied by the right coronary artery. Due to his concomitant iron deficiency and thrombocytopenia, anti‐platelet therapy was not recommended. One week following the initial presentation, he experienced similar symptoms with a troponin peak of 14.9 ng/mL. He underwent cardiac catheterization with the placement of two drug‐eluting stents in the RCA. Bare metal stent placement was not possible due to the location of the lesions. He has been symptom free since discharge and has had no episodes of bleeding.
Chest pain is a problem commonly encountered by the general internist. However due to the heterogeneity of patients and their co‐morbidities, diagnosis and treatment must be tailored. Care must be taken to balance risks and benefits before deciding on the care plan.
In general, thrombocytopenia has a myriad of causes, but is typically due to a result of multiple hits to the platelets. As in this case, the hepatitis C virus can both directly suppress the bone marrow leading to low platelet production. In addition, the virus can bind to thrombocytes forming autoantibodies against the membrane. Finally, cirrhotics can develop hypersplenism, leading to splenic sequestration and premature destruction.
In the setting of thrombocytopenia, few guidelines exist to manage these patients when presenting with acute coronary syndrome. In general, for patients with stable platelet counts above 100,000/mL, drug‐eluting stents are safe. Between 50,000 and 100,000/mL, bare metal stents are preferred; when platelets are fewer than 50,000/mL, optimal medical management is typically recommended. In patients with unstable platelet counts, bare metal is preferred over with platelets over 100,000/mL and medical management is preferred when counts are less than 100,000/mL. Retrospective case series have also demonstrated safety in stenting for acute coronary syndrome in platelet counts as low as 17,000/mL. Transplant eligible patients represent a unique subset as some require coronary intervention for medical optimization prior to transplant. Although at increased risk for bleeding, these patients have had coronary stents placed safely, and small studies have shown no increase in transfusion requirements, especially in patients without varices.
Although the management of acute coronary syndrome in thrombocytopenic patients is unclear, a better understanding of the data will assist clinicians in weighing the risks and benefits of antiplatelet therapy.
To cite this abstract:Cerreta K. Too Few — What to Do?. Abstract published at Hospital Medicine 2014, March 24-27, Las Vegas, Nev. Abstract 372. Journal of Hospital Medicine. 2014; 9 (suppl 2). https://www.shmabstracts.com/abstract/too-few-what-to-do/. Accessed April 1, 2020.