Case Report Figure 5: Microscope Slide (20x) Hematoxylin and Eosin Stain
The American Heart Hospital Journal
Other data suggest that the incidence of calcific coronary embolization from degenerative calcific aortic stenosis may actually be somewhat more common, but concur that in most instances the patient may remain asymptomatic due to the small size of the embolus and the subsequent infarcted territory.1–3
Khetarpal et al. describe diagnostic criteria for spontaneous cerebral embolism in the absence of iatrogenic causation from invasive cardiac procedure as:
1. Absence of embologenic calcified lesions at Doppler examination of the cervical vessels;
Fibrinous plaque (pink) with focal dystrophic calcification (purple) and occasional red blood cells. The slide is notable for the absence of organizing thrombus.
2. Presence of calcified aortic valve stenosis confirmed by echocardiography with good left ventricular function; and 3. Exclusion of other sources of cerebral thromboembolism.2
Embolization from a stenotic aortic valve may be calcific or non-calcific in nature. Non-calcific embolization results from complications of turbulent flow and thrombus formation.2 Increased risk of calcific embolization from calcific aortic stenosis has been seen more commonly with bicuspid valves and other congenital valve abnormalities, as well as3
from
It has been suggested that there is an inherently increasing risk of spontaneous calcific embolization as aortic valves become more severely calcified.2
invasive procedures such as cardiac catheterization or valve surgery.7
In autopsy series, approximately one-third of patients with calcific aortic valves demonstrate histopathologic evidence of systemic calcific emboli involving cerebral, coronary, renal, retinal, and peripheral arteries. Only one-fifth of these were found to have occurred spontaneously.2
In an
autopsy series from Holley et al., the incidence of calcific coronary embolization, presenting as a clinically significant event was extraordinarily rare. Only 10 of 163 patients (6 %) with calcific aortic stenosis demonstrated embolic material within a major coronary artery, and none of those demonstrated pathologic evidence of a clinically significant myocardial infarction.8
Steiner and Hlava’s series supports this observation. They examined 31 hearts 58
Charles et al., applying a similar strategy to coronary emboli, assert that, in assigning embolic phenomena as causation for an acute myocardial infarction, “the combination of acute myocardial infarction with angiographically normal coronary arteries and an underlying source for embolism constitutes circumstantial evidence for a diagnosis of coronary embolism”.1
Findings of “abrupt occlusion of
specific coronary arteries” with other coronaries appearing patent and free of evidence of atherosclerotic disease or growth of collateral vessels further supports this diagnosis.10
The patient described in this report certainly meets these criteria including clinical presentation of acute anterior wall myocardial infarction, angiographic evidence of abrupt LAD coronary occlusion in the absence of other significant coronary atherosclerosis, and fluoroscopic evidence of a heavily calcified aortic valve without evidence of calcification of the ascending aorta or coronary arteries. Coronary intervention with an aspiration thrombectomy catheter removed the embolic material and re-established coronary blood flow. Subsequent angiography did not demonstrate evidence of plaque rupture or a significant residual stenosis, thus obviating the need for stent placement and dual anti-platelet therapy in this patient with an unexplained anemia and a potentially increased risk of bleeding complications. The subsequent pathological findings revealed
Spontaneous Calcific Coronary Embolus From a Degenerative Calcific Aortic Valve Summer 2011
with significant calcification of one or both left heart valves from patients who had not previously been operated on or studied invasively. Among 24 cases with calcific aortic valves, only one, a 39-year-old patient with a unicuspid aortic valve, demonstrated macroscopic evidence of a calcific coronary embolus. Radiologic evaluation further demonstrated the existence of calcific emboli (intracoronary or interventricular) in nine of the 24 cases, but only one involved a patient with senile calcific aortic stenosis.9
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