Aortic Regurgitation as a Risk Factor for Coronary Embolization from Complex Atheromatous Aortic Plaques: A Clinical Case.

Patients with mobile aortic arch atheroma and severe aortic regurgitation may be at higher risk of systemic embolism. We report the case of a 68-year-old male patient with complex aortic arch plaque with superimposed thrombus, in which an acute inferior ST-elevation myocardial infarction occurred. In the reported case, coronary embolism may have been caused by flaked aortic plaque and/or superimposed thrombus, which was possibly carried by aortic regurgitation flow. It is a very rare mechanism by which a coronary embolism is possible from an aortic complex plaque.

INTRODUCTION

Approximately one in four patients with an embolic event is found to have variable grades of aortic atheromatosis at transesophageal echocardiography (TEE).[12]

Atherosclerotic lesions of the thoracic aorta, especially complex plaques with superimposed thrombi and thickness >4 mm, are thought to be a risk factor for both cerebral and peripheral embolization.[23]

Often, it is difficult to understand the correlation between an embolic event and the presence of a complex aortic plaque.

CASE REPORT

The case is about a 68-year-old male with dyslipidemia, hypertension, and aortic valve bioprosthesis (Mitroflow N.21) implanted 7 years before and complicated by a significant intraprosthetic regurgitation [Figure 1]. The regurgitation was reported as severe because of a jet width/left ventricular outflow tract width of 0.80, and it was due to structural valve deterioration.

Figure 1

Transesophageal echocardiography image of severe aortic bioprosthesis regurgitation demonstrating a large regurgitant jet due to structural valve deterioration

A TEE was performed because fever started 2 weeks before and due to a suspicious of infective endocarditis.

At the time of TEE, the patient was on aspirin, angiotensin-converting enzyme inhibitor (ACEi), statin, beta-blockers, and antibiotics.

TEE demonstrated a large atherosclerotic plaque in the aortic arch with two mobile lesions (debris), the largest one sized 1.2 cm × 0.5 cm [Figure 2].

Figure 2

Aortic debris with two mobile lesions (sized about 1.2 cm × 0.5 cm) in the aortic arch

There was no evidence of vegetations on native or prosthetic valves. Dual antiplatelet therapy (DAPT) with aspirin and clopidogrel was started, and a high-intensity statin was prescribed.

TEE was repeated at 2-month follow-up. It demonstrated a clear increase in sizing of aortic mobile lesions, indicating a superimposed thrombosis [Figure 3]. The patient continued DAPT.

Figure 3

Aortic debris with superimposed thrombus causing an increase in sizing of the mobile lesions

Four weeks after, the patient was taken to the emergency department because of a persistent chest pain with the electrocardiogram demonstrating an acute inferolateral ST-elevation myocardial infarction [Figure 4].

Figure 4

Electrocardiogram demonstrating an inferolateral ST-elevation myocardial infarction

Left circumflex (LCx) coronary thrombectomy with aspiration catheter was performed and solid material (thrombus) was collected. There was no atherosclerotic coronary stenosis on the culprit vessel [Figure 5].

Figure 5

LCx coronary artery obstructed by embolic material at the midsegment

Coronary embolism, in this case, may have been caused by flaked aortic plaque and/or superimposed thrombus, which was possibly carried by aortic regurgitation flow.

Fortunately, embolization of the other parts, including brain, kidney, and peripheral arteries, was not found by computed tomography and ultrasound examinations. There were no previous anterograde embolisms in the patient's history.

After the acute coronary event, the patient started rivaroxaban 15 mg OD together with DAPT (aspirin plus clopidogrel) and continued high-intensity statin, ACEi, and beta-blocker. Follow-up is ongoing, and at 6 months, the outcome is favorable.

DISCUSSION

Coronary artery embolism resulting in acute myocardial infarction is infrequent, but usually correlated with chronic atrial fibrillation, valvular prosthesis, dilated cardiomyopathy, infective endocarditis, intracardiac shunts, cardiac myxoma, mural thrombi, and hypercoagulable state.

We reported a unique case of myocardial infarction likely due to coronary artery embolism from flaked aortic plaque, which was possibly carried by bloodstream of aortic regurgitation flow.

The prevalence of arch/descending aorta complex atheromatous plaques is 6.1% in unselected patients undergoing TEE for various reasons. It is 25% in patients with embolic episodes.[245]

Katsanos et al.[2] found that atherosclerotic lesions of the thoracic aorta, especially complex plaques with superimposed thrombi and/or thickness >4 mm, are thought to be a risk factor for both cerebral and peripheral embolization.

Sharma and Tak[4] said that atheromas with >4 mm in thickness or with plaque rupture and mobile fragments are more likely to be associated with peripheral embolic events.

Retrograde embolization from complex plaques of the proximal descending aorta to all brain territories in early diastole is theoretically possible and could provide an alternative embolic source that should be taken into consideration, especially in patients with cryptogenic stroke.

Retrograde embolism from the descending thoracic aorta is one possible cause of undetermined ischemic stroke, but we do not know the true mechanism by which this phenomenon occurs.

Chhabra et al.[5] stated that the mechanism of retrograde embolization from complex aortic plaques may be a reversal aortic blood flow.

Studies by Harloff et al. and Wehrum et al.[67] using three-dimensional (3D) magnetic resonance imaging (MRI) and 4D MRI data via image fusion demonstrated that retrograde flow from the complex descending aortic plaques reached the left subclavian artery in 67%, common carotid artery in 24.7%, and brachiocephalic trunk in 14.4% of cases.

One of the mechanisms amplifying the reversal aortic flow and leading to a retrograde embolization from complex aortic plaques is related to aortic valve regurgitation.

Kim et al.[8] demonstrated that significant aortic regurgitation can increase the amount of reverse flow in the thoracic aorta and thus it may be associated with an increased incidence of stroke. They found that significant aortic regurgitation was more prevalent in patients with undetermined embolic stroke and complex aortic plaques than in patients without complex aortic plaques. In addition, the authors found that the distribution of complex aortic plaques according to the severity of aortic regurgitation in patients with undetermined embolic stroke had a tendency toward the ascending thoracic aorta and proximal aortic arch.[8]

In the reported case, the patient may have been affected by a coronary embolization from a complex aortic plaque. Then, the brain may not be the only target of a retrograde embolization from a complex aortic plaque.

Recently, Nakamura et al.[9] found that patients with mobile aortic arch atheroma and moderate-to-severe aortic regurgitation may be at higher risk of coronary embolism.

Ozaki et al.[10] reported a case of acute myocardial infarction that was considered to be caused by embolism from a floating mass in the ascending aorta. There was no aortic regurgitation in the pathophysiological pathway of this case.

Eguchi et al.[11] published a case of acute myocardial infarction as a result of multiple coronary embolism caused by thrombosis in the right sinus of Valsalva with a second aortic arch thrombosis, contributed by protein S deficiency. Furthermore, in this case, an aortic regurgitation was not reported.

Then, there may be a correlation between significant aortic regurgitation, complex aortic plaques, and coronary embolism. It is not well known the pathophysiological mechanism at the base of this correlation, even if an amplified reverse flow in the thoracic aorta may play a crucial role.

No indications are reported in the literature about the medical treatment of these cases.

Antiplatelet agents, oral anticoagulants, and statins have been suggested in the management of aortic atheromas, but sufficiently powered, randomized, controlled trials are not available to guide medical management of this pathology.[4] For this reason, in our case, we considered reasonable to start a DAPT with aspirin plus clopidogrel, adding a direct oral anticoagulant when an acute coronary event occurred.

To date, this may be the first case of acute myocardial infarction due to a coronary embolism starting from a complex aortic plaque in a patient with valvular aortic bioprosthesis structural deterioration complicated by severe aortic regurgitation.

CONCLUSION

The reported case describes a new mechanism by which a coronary embolism may occur.

The described mechanism starts from a complex aortic plaque, complicated by superimposed thrombi and associated with aortic reversal flow, amplified by significant aortic regurgitation that finally leads to coronary embolism.

This particular situation should be taken into consideration in patients with a severe aortic regurgitation associated with a complex atheromatous aortic plaque.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.