Spontaneous Calcific Coronary Embolus From a Degenerative Calcific Aortic Valve - A Rare Cause of Acute ST Segment Elevation Myocardial Infarction

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This case report describes pathology-proven spontaneous coronary embolization from a calcific aortic valve resulting in an acute ST segment elevation myocardial infarction. It serves as an important reminder that, especially for elderly patients with coexisting aortic valvular disease, initial treatment for abrupt coronary artery occlusion with aspiration thrombectomy catheterization is standard of care.

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Segment elevation myocardial infarction (STEMI) and other acute coronary syndromes occur most commonly as a consequence of plaque rupture within a coronary artery. By contrast, coronary embolization is often perceived as an exceedingly rare cause of acute coronary events but has been reported in the setting of endocarditis, prosthetic valve thrombus, following cardiac surgery, and after invasive and interventional cardiac procedures including valvuloplasty and coronary angioplasty. Several studies suggest that the incidence of calcific coronary embolus from degenerative calcific aortic stenosis may be higher than has been generally recognized.1–3 We report the first case of a spontaneous calcific embolus occluding the left anterior descending (LAD) and causing an acute STEMI in an elderly patient with degenerative calcific aortic stenosis as confirmed from pathological examination of the retrieved embolic specimen.

Case Report

A 79-year-old man presented to the Emergency Department of the Miriam Hospital with three hours of substernal chest pain and electrocardiographic (ECG) evidence of an acute anterior wall STEMI. The patient had no prior history of chest pain or coronary artery disease (CAD). He had a right middle cerebral artery cerebrovascular accident in 2004 and his only medications were aspirin/dipyridamole 25/200 mg twice daily and an unspecified antihypertensive. He was otherwise a vague historian with a questionable history of hypertension, and hyperlipidemia, and he received his general medical care at the Providence Veterans Medical Center (VAMC).

Physical examination revealed a well-developed, elderly gentleman in moderate distress with chest pain. His pulse was 74 bpm and regular and his blood pressure was 104/70 mmHg. His lungs were clear. There was no jugular vein distension. Carotid upstrokes were delayed with transmitted murmurs from the aortic focus. Cardiovascular exam was notable for a II/VI mid peaking systolic ejection murmur at the upper sternal border and a soft S2. Neurologic exam was remarkable for a dense left upper extremity hemiplegia. His ECG showed ST segment elevations in the anterior leads. Initial creatine kinase and troponin were within normal limits. Hemoglobin and hematocrit were 8.3 mg/dl and 26 % with microcytic, hypochromic indices. His stool was guaiac negative. We subsequently learned that he had a chronic microcytic anemia with a negative gastrointestinal (GI) work-up at the VAMC six months earlier. After some discussion with the patient and his wife it was decided to proceed to emergent diagnostic cardiac catheterization and possible coronary intervention.

Diagnostic coronary angiography revealed an abrupt cutoff in the distal LAD with mild luminal irregularities proximally and no other significant coronary stenoses. The aortic valve was moderately calcified with a peak transvalvular gradient of 45 mmHg.

The decision was made to proceed to coronary intervention with aspiration thrombectomy and angioplasty and to avoid stent placement if possible. An EBU 4.0 Launcher guiding catheter, a Sport ST wire and an Export aspiration catheter were easily deployed. Very little material was retrieved from the aspiration catheter and the guiding catheter developed a dampened waveform, could not be aspirated and had to be removed with the guidewire. When the guiding catheter was flushed a large, firm, and relatively intact, presumably embolic, specimen was obtained and sent to pathology. Repeat coronary angiography revealed a thrombolysis in myocardial infarction (TIMI) grade three flow throughout the entire LAD, with minimal residual luminal narrowing distally at the site of prior total occlusion and no angiographic evidence of plaque rupture. The patient was now chest-pain free with resolution of ST segment elevations. We briefly considered performing intravascular ultrasound (IVUS), but since the angiographic result appeared so stable and our original plan was to avoid stent placement it was felt that IVUS would require re-instrumentation of the LAD and would probably add little clinically. The procedure was terminated at that point and the patient was transferred to the Coronary Care Unit in a stable condition. A 2D echocardiogram later that day revealed a depressed left ventricular ejection fraction at 30–35 % with apical akinesis, as well as a severely calcified aortic valve. Cardiac enzymes peaked the following morning with a creatine phosphokinase (CPK) of 1108 IU/l, CK-MB of 60.4, MB index of 5.5, and a troponin of 58.51. A subsequent ECG, on hospital day three, was unchanged. The remainder of the patient’s hospital course was uneventful and he was discharged on hospital day four.


The material obtained from the LAD was a 0.5 x 0.2 x 0.2 cm grey-yellow soft tissue fragment, which was entirely microscopically examined. Sections show (referring to higher power photomic) pink fibrinous plaque with focal purple calcification and a few scattered red blood cells. No recent or organized thrombus was identified, and, therefore, this was presumed to be embolic, possibly from the calcific aortic valve.


Although STEMI and other acute coronary syndromes occur most commonly as a consequence of atherosclerotic plaque rupture within a coronary artery, a variety of other pathologic processes can also result in coronary occlusion and subsequent myocardial infarction.4,5 Coronary embolization has been described in the setting of valvular and prosthetic valvular heart disease, infective endocarditis, atrial fibrillation, intracardiac shunts, dilated cardiomyopathy, and from iatrogenic causes during cardiac catheterization and valve surgery.1,4–6 Seventy-five percent of embolic infarcts are anterior in location, demonstrating LAD occlusion, as a consequence of preferential diastolic flow into the left coronary artery due to the shape, structure, and closure pattern of the aortic valve cusps.

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 invasive procedures such as cardiac catheterization or valve surgery.7 It has been suggested that there is an inherently increasing risk of spontaneous calcific embolization as aortic valves become more severely calcified.2

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 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

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:

  • Absence of embologenic calcified lesions at Doppler examination of the cervical vessels;
  • Presence of calcified aortic valve stenosis confirmed by echocardiography with good left ventricular function; and
  • Exclusion of other sources of cerebral thromboembolism.2

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 focal dystrophic calcification with notable absence of thrombus, further supporting the diagnosis of calcific coronary embolization as the etiology of this patient’s STEMI.

Notable case studies demonstrating clinically significant calcific emboli originating from stenotic aortic valves include a spontaneous calcific embolus presumably derived from a calcific stenotic bicuspid aortic valve occluding the second circumflex marginal coronary artery,3 a spontaneous calcific embolus occluding a distal branch of the left circumflex artery resulting in an acute myocardial infarction,11 and a spontaneous calcific embolism from a calcific stenotic aortic valve occluding a retinal artery.12 To our knowledge, this is the first documented and pathologically supported case of a calcific embolus spontaneously dislodging from a senile calcific stenotic aortic valve and resulting in total occlusion of the LAD, presenting as a STEMI.


This case demonstrates the importance of recognizing distinctive pathologic causes of acute STEMI other than plaque rupture and localized thrombus formation within a coronary artery. The possibility of coronary embolization as an alternative etiology must be considered, particularly when abrupt coronary occlusion is observed in the absence of other coronary atherosclerosis, and in the setting of other underlying sources of embolization. This is especially true for elderly patients with co-existing aortic valvular disease.9 Initial treatment for acute coronary artery occlusion with an aspiration thrombectomy catheter13 is now the recognized standard of care for all patients with abrupt coronary occlusion, regardless of the etiopathology. In this particular case it afforded the additional benefit of avoiding stent placement and dual antiplatelet therapy in a patient with potentially increased bleeding risk and other comorbidities.


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