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Winning Abstracts from the 2010 Medical Student Abstract Competition: Spontaneous Calcific Coronary Embolus From A Degenerative Calcific Aortic Valve: A Rare Cause Of Acute STEMI

Authors: Adam Vasconcellos, Brown Medical School, Class of 2011
Lisa Gravelin, MD, Laura Goldstein, MD, Paul Gordon, MD, Kenneth Korr, MD

Case Presentation: A 79-year-old man presented with 3 hours of substernal chest pain. The patient had no prior history of chest pain or coronary artery disease. His pulse was 74 and his blood pressure was 104/70. Cardiovascular exam was notable for a grade II/VI mid peaking systolic ejection murmur at the upper sternal border and a soft second heart sound. Carotid upstrokes were delayed with transmitted murmurs from the aortic area. His initial ECG showed ST segment elevations in the anterior leads. Cardiac enzymes were within normal limits but his hemoglobin was 8.3 and his stool was guaiac negative. Diagnostic coronary angiography revealed total occlusion of the Left Anterior Descending (LAD) coronary artery with an abrupt cutoff in the distal third of the vessel and no other significant coronary stenoses. The aortic valve was heavily calcified with a peak transvalvular gradient of 45mmHg. Emergency coronary intervention with an aspiration thrombectomy catheter was performed and a large, whitish, firm and relatively intact specimen was removed from the LAD and sent for pathologic evaluation. Repeat coronary angiography revealed Thrombolysis In Myocardial Infarction (TIMI) grade 3 flow throughout the entire LAD with no angiographic evidence of plaque rupture or residual stenosis. The patient was now chest pain free with resolution of ST segment elevations and no further coronary intervention was performed. Cardiac enzymes peaked the following morning with a CPK of 1108, MB index of 5.5, and Troponin of 58.51. The remainder of the patientís hospital course was unremarkable and he was discharged 5 days later. Pathologic examination of the specimen revealed that it was not thrombus, but rather a calcific fragment likely originating from the stenotic aortic valve.

Discussion: Coronary embolization is an exceedingly rare cause of STEMI and has been reported in the setting of endocarditis, prosthetic valve thrombosis, following cardiac surgery, and after invasive and interventional cardiac procedures including valvuoplasty and coronary interventions. Several studies suggest that the incidence of calcific coronary emboli from degenerative calcific aortic stenosis may be higher than has been generally recognized [1-3], but clinically this has been difficult to document. Coronary intervention with an aspiration thrombectomy catheter was instrumental in re-establishing coronary blood flow and it eliminated the need for coronary stent placement and dual anti-platelet therapy in this patient with an unexplained anemia. Furthermore, it permitted the diagnosis of coronary embolization as the etiology of this patientís STEMI which was later demonstrated pathologically to be a calcific fragment presumably from the stenotic aortic valve. This case underscores the importance of considering coronary embolization as an etiology of STEMI and utilizing an aspiration thrombectomy catheter as the initial step in coronary intervention. The subsequent pathological findings add support to previous studies linking coronary embolization to degenerative calcific aortic stenosis.

References:
1.
Charles RG, Epstein EJ, Holt S, et al. Coronary embolism in valvular heart disease. Q J Med 1982; 202: 147-61.
2. CSalka S, Almassi GH, Leitschuh ML. Spontaneous coronary artery embolus associated with calcific aortic stenosis. Chest 1994; 105: 1289-90.
3. C Mansur AJ, de Miranda RC, Grinberg M, et al. Calcific aortic stenosis presenting as acute myocardial infarction. J Cardiovasc Surg (Torino) 1990; 31: 310-2.

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