Calcific embolus resulting in ST elevation myocardial infarction: A rare complication of mitral annular calcification

Abstract

Coronary embolism is an uncommon mechanism of myocardial infarction in comparison with atherosclerotic plaque rupture. We present a unique case of an anterior ST elevation myocardial infarction as a result of coronary embolism, the source of which appears to be calcific debris from mitral annular calcification (MAC). Although embolic phenomena in the setting of MAC has been documented previously, particularly in the setting of acute ischemic stroke, to our knowledge this is the first reported case in the literature where MAC alone appears to have resulted in a coronary embolic event.

<Learning objective: Myocardial infarction as the result of embolic coronary phenomena is uncommon. Thrombotic emboli in the setting of atrial fibrillation, paradoxical emboli in the setting of structural heart defects, and cardiac masses are among the most common causes of coronary embolism. We make the argument that debris from mitral annular calcification may also serve as an uncommon mechanism of embolic phenomena.>

Introduction

Acute myocardial infarction (MI) as the result of embolic phenomena is an uncommon mechanism of coronary ischemia. Emboli in the setting of atrial fibrillation, cardiac masses, and paradoxical emboli in the setting of structural heart defects are frequent culprits in these circumstances [1]. Although mitral annular calcification (MAC) has been associated with other embolic phenomena, most notably embolic stroke [2], [3], debris from MAC has not been known previously to be an embolic source in the setting of an acute coronary syndrome. We present what we believe to be the first reported case of an acute MI that occurred as the result of embolized calcium from the mitral annulus.

Case report

A 78-year-old woman with a history of severe MAC, paroxysmal atrial fibrillation without anticoagulation, pulmonary hypertension, and scleroderma presented to the emergency department with severe crushing sub-sternal chest pain, light-headedness, and malaise that started 12 h prior to presentation. In the emergency department she had a blood pressure of 111/86 mmHg, heart rate of 92 beats per minute, 16 respirations per minute with an oxygen saturation of 97% on room air, and a temperature of 36.6 °C. Cardiopulmonary examination was unrevealing. Initial electrocardiogram showed sinus rhythm with ST elevation in V2-V5 consistent with an anterior ST elevation MI. Her initial troponin was elevated to 31.286 μg/L. She underwent emergent coronary angiography that showed an abrupt, complete occlusion in the mid to distal left anterior descending artery (Fig. 1A). The lesion was aspirated with an Export Advance™ catheter (Medtronic Inc., Minneapolis, MN, USA) and flow was restored with balloon angioplasty (Fig. 1B). No stent was placed. Specimens obtained from the aspirate were sent to the pathology department for further analysis. Grossly, the specimens were hard in consistency and ivory colored (Fig. 1C). Microscopic evaluation showed mostly calcified tissue suggestive of embolic etiology (Fig. 1D). Transthoracic echocardiogram showed anterior and distal septum wall motion abnormalities, an akinetic apex, a reduced ejection fraction of 45%, left atrial enlargement, and severe MAC with significant posterior annular involvement (Fig. 1E). Transesophageal echocardiography was not obtained. She remained vitally stable after the procedure, had no recurrence of chest pain, and was without clinical signs of heart failure. She was discharged home two days after presentation on aspirin and clopidogrel.

Fig. 1.

(A) Angiogram demonstrating complete occlusion of the left anterior descending artery (arrow). (B) Angiogram post embolectomy with evident revascularization. (C) Ivory calcific embolic material aspirated from the left anterior descending artery. The two large pieces shown measure 3–4 mm in length. (D) Pathologic evaluation of aspirated tissue containing mostly calcification (dark purple) and fibrin tissue (light pink). Stains were negative for bacterial and fungal organisms. (E) Transthoracic echocardiogram, apical 4-chamber view, demonstrating severe mitral annular calcification with posterior annular involvement (arrow).

Discussion

Embolic phenomena resulting in coronary artery occlusion and MI are rare in comparison to atherosclerotic plaque rupture. Precise diagnosis in the acute setting remains challenging for the interventional cardiologist. Thrombus aspiration for anterior MI is not a standard practice based on mixed results from various studies [4], [5], and the prevalence of non-atherosclerotic processes is not known. About 4–7% of patients diagnosed with anterior MIs do not have atherosclerotic coronary artery disease on coronary angiography or at autopsy [6]. One autopsy study suggests that as many as 13% of infarctions occur from coronary artery embolization [7]. The reported sources of embolization in such cases are variable, the most common of which is thrombi in the setting of non-valvular atrial fibrillation [1]. Although calcific emboli have been a known cause of myocardial infarction in the setting of calcified amorphous tumors [8], to our knowledge this is the first reported case of an ST elevation MI involving MAC alone. The significance of fibrocalcific disease and embolic events has been debated in the literature, particularly regarding its presence in correlation with embolic cerebral infracts [2], [3], [9]. It is unclear which factors influence whether calcium around the mitral annulus is likely to embolize, and we can only provide conjecture regarding the risk factors in relation to our patient’s case.

In considering alternative embolic sources, it is important to note that our patient carried a diagnosis of paroxysmal atrial fibrillation (without receiving anticoagulation) and transesophageal echocardiography was not performed to assess for a left atrial appendage thrombus. However, the pathologic components of the coronary aspirate were less consistent with a blood clot given the high degree of calcification on gross and microscopic examination; it would be more typical for a left atrial appendage thrombus to be more fibrin-rich with minimal calcification. The patient was in sinus rhythm on admission and throughout her hospitalization, which may suggest an overall lower burden of atrial fibrillation, although this cannot be confirmed given the lack of longer-term rhythm monitoring data. Another source to be considered includes calcific debris from an aortic atheroma. Although no prior imaging demonstrated atheromatous plaque in the patient’s aorta, it cannot be excluded as a possible etiology. Nevertheless, we postulate that the severity of the mass-like calcification of the mitral annulus makes it the most plausible origin of the aspirated calcific fragments. In addition, while MAC has been correlated with severity of coronary artery disease [10], in our patient there was no microscopic evidence of platelet-rich thrombin or fibrin typical of plaque rapture. The pathologic findings in the setting of severe MAC, without a clear alternative source of calcific embolic material, make a strong argument for calcific emboli derived from the mitral annulus. This is a significant addition to the differential diagnosis of embolic coronary phenomena that interventional cardiologists should consider to inform their clinical decisions.

Conclusion

We present the first known case of MAC resulting in an acute ST elevation MI as the result of calcific emboli. Although a case such as this has not been reported previously, we suspect that some patients with MAC may be at increased risk of embolic phenomena. What determines the risk for calcific embolism in patients with fibrocalcific disease has yet to elucidated. The role of aspiration during percutaneous coronary intervention in such patients is also unknown.

Conflicts of interest

The authors declare that there is no conflict of interest.