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Authors: Adam Vasconcellos, Brown Medical
School, Class of 2011
Lisa Gravelin, MD, Laura Goldstein, MD, Paul Gordon, MD, Kenneth
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 patient's 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
patient's 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
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.
March Issue of IMpact