Abstract
A 49-year-old woman was transferred to our hospital with acute-onset chest pain. Her electrocardiogram showed complete atrioventricular block and bradycardia with ST-segment elevation in the inferior leads, and she presented with cardiogenic shock. She was diagnosed with inferior acute myocardial infarction (AMI), and subsequent emergency cardiac catheterization was performed. Selective coronary angiography showed neither stenosis nor obstruction in any of the coronary arteries. Left ventriculography showed a large floating object located on the ascending aortic wall above the ostium of the right coronary artery (RCA). Chest enhanced computed tomography confirmed the floating object in the ascending aorta. These findings suggested that the floating object was associated with the RCA occlusion.
To remove the floating object, emergency surgery was performed. The floating object was a large thrombus derived from the localized atheromatous plaque in the ascending aorta. Specialized immunostaining for surface antigen CD34 revealed that regenerated endothelial cells were present on the erosion, along the stalk, and on the floating thrombus. These findings indicate that the CD34-positive endothelial precursor cells strayed into the surface and/or inside of the thrombus, and consequently the floating thrombus supported by these regenerated endothelial cells occluded the RCA, causing AMI.
<Learning objective: A free floating thrombus formed in the ascending aorta can cause obstruction of the coronary artery ostium, leading to AMI. This unusual cause of AMI mostly occurs in females, and shows high mortality rates. Although the risk factors are known to be current smoking, oral hormone therapy, and hypercoagulable state such as pregnancy, the underlying mechanism of thrombus formation is still unclear. This report describes a possible role of CD-34 positive regenerated endothelial cells in thrombus formation.>
Keywords: Acute myocardial infarction, Floating thrombus, CD34-positive endothelial cells
Introduction
Acute myocardial infarction (AMI) is usually a consequence of complicated coronary atherosclerosis with thrombotic occlusion of the arterial lumen [1].
On the other hand, AMI caused by free floating thrombus in the ascending aorta is uncommon and its mechanisms are still unclear 2, 3, 4, 5. This report presents a case of AMI caused by free floating thrombus in the ascending aorta, and shows possible mechanisms of thrombus formation.
Case report
A 49-year-old woman was transferred to our hospital with acute-onset chest pain. Her electrocardiogram showed complete atrioventricular block and bradycardia (heart rate 50 beats per minute) with ST-segment elevation in the inferior leads (Supplemental Fig. 1), and she presented with cardiogenic shock (immeasurable blood pressure). The echocardiography showed hypokinesis of the inferior wall. The troponin T test was negative and none of the other cardiac enzymes was elevated. She had dyslipidemia and was a current smoker, and did not have any previous history of thrombotic events. She had a history of taking oral contraceptive twenty years previously.
The patient was diagnosed with inferior AMI, and subsequent emergency cardiac catheterization was performed. Selective coronary angiography showed neither stenosis nor obstruction in any of the coronary arteries (Fig. 1A and B). Left ventriculography showed a large floating object located on the ascending aortic wall approximately 1 cm above the ostium of the right coronary artery (RCA) (Fig. 1C, Supplemental Videos). Chest enhanced computed tomography (CT) performed immediately after cardiac catheterization confirmed the floating object in the ascending aorta (Fig. 1D). These findings suggested that the floating object was associated with the RCA occlusion. Notably, immediately after the coronary angiography of the RCA, atrioventricular block returned to sinus rhythm, and elevated ST segment resolved gradually, possibly suggesting that occluded RCA by the floating object was recanalized at this time. Abdominal enhanced CT showed the presence of right renal infarction, likely due to thromboembolism (Supplemental Fig. 2).
Fig. 1.
(A and B) The coronary angiography showed neither significant stenosis nor obstruction in the right coronary artery (A), and in the left coronary artery (B). (C) Left ventriculography showing hypokinesis of the inferior and basal posterior segments and a large floating object located on the ascending aortic wall approximately 1 cm above the ostium of the right coronary artery (arrow). (D) Chest enhanced computed tomography performed immediately after cardiac catheterization showing the floating object in the ascending aorta.
To remove the floating object, ascending aorta–aortic arch replacement was performed as an emergency surgery. The floating object was a large thrombus derived from the localized atheromatous plaque in the ascending aorta (Fig. 2A). A detailed histological assessment showed that the thrombus connected with stalk was attached to the endothelial erosion on the aortic plaque (Fig. 2B and C). Importantly, specialized immunostaining for surface antigen CD34 revealed that regenerated endothelial cells were present on the erosion, along the stalk, and on the floating thrombus (arrows, Fig. 2D). The patient was discharged one month after the surgery without any aftereffect of the disease.
Fig. 2.
(A) The floating object attached to the ascending aorta. (B) Hematoxylin–eosin staining of the floating object, which shows a thrombus formed on the atherosclerotic plaque in the aortic wall. Scale bar, 1 mm. (C) A detailed histological assessment showing the thrombus attached to the endothelial erosion on the intimal layer. Scale bar, 500 μm. (D) Specialized immunostaining for surface antigen CD34 showing the regenerated endothelial cells on the erosion, along the stalk, and on the floating thrombus (arrows). Scale bar, 500 μm.
Discussion
AMI is usually caused by a rupture of unstable plaque formed in the coronary artery [6]. Although infrequent, a free floating thrombus formed in the ascending aorta can cause obstruction of the coronary artery ostium, leading to AMI [1]. AMI caused by a mobile thrombus mostly occurs in females, especially young women from 30 through 50 years of age, and shows high mortality rates. The common risk factors are a current smoking, oral hormone therapy, and hypercoagulable states such as pregnancy and collagen disease [2]. The present case did not have any coagulation disorders such as abnormal platelet aggregation, impaired protein C and protein S activity, and lupus anticoagulant. However, her risk factors including current smoking, dyslipidemia, and previous oral contraceptive therapy could partly contribute to the progression of the thrombus formation.
The possible mechanism by which a large thrombus was formed even in a high blood flow area such as the ascending aorta is of great interest. The main factors promoting thrombus formation are damage to the vessel wall, slowing of the blood flow, and changes in the blood composition, which are known as Virchow's triad. Studies have further revealed that thrombus may form on a denuded endothelial plaque surface 1, 7. Wolfsohn et al. reported that the ascending aorta in a patient with AMI caused by floating thrombus had an atherosclerotic plaque with superficial erosion, and that an endothelial erosion presumably becomes a thrombogenic substrate allowing thrombus formation and propagation [8]. Moreover, Knoess et al. described in their report that thrombus formation without plaque disruption in the ascending aorta may depend on an endothelial erosion which seems to be more common in younger women and is promoted by a hyperthrombogenic state [2]. The present case also supports their findings based on an endothelial erosion leading to thrombus formation in the ascending aorta.
The most important issue to be discussed is the role of CD-34 positive regenerated endothelial cells in thrombus formation. CD34-positive circulating endothelial precursor cells (EPCs) are first recruited to the erosion in order to repair the injured endothelium [9]. In the present case, since the thrombus was also growing on the erosion at the same time, it is suggested that the CD34-positive EPCs strayed onto the surface and/or inside of the thrombus, and consequently the floating thrombus supported by these regenerated endothelial cells was formed. Further, the presence of regenerated endothelial cells covering both the plaque and thrombus would indicate that this structure had existed there for a relatively long time. Thus, CD34-positive regenerated endothelial cells may play a possible role in thrombus formation in the ascending aorta.
Conclusions
This is the first report showing that repaired erosion and stalk supported by CD34-positive regenerated endothelial cells are tightly connected to a floating thrombus in the ascending aorta. The anchored thrombus formed on the localized atherosclerotic plaque in a female patient with risk factors was considered to be floating in the ascending aorta and occluding the RCA, thereby causing AMI.
Conflict of interest
Authors have no conflict of interest that should be disclosed.
Footnotes
Supplementary data associated with this article can be found, in the online version, at http://dx.doi.org/10.1016/j.jccase.2013.04.003.
Appendix A. Supplementary data
The following are the supplementary data to this article:
Supplemental Fig. 1.
The electrocardiogram recorded at the emergency room showing complete atrioventricular block and bradycardia (heart rate 50 beats per minute) with ST-segment elevation in leads II, III, and aVF, and reciprocal ST-segment changes in leads I and aVL.
Supplemental Fig. 2.
Abdominal enhanced computed tomography showing the right renal infarction (arrow).
The left ventriculography with the right anterior oblique view (video 1) and the left anterior oblique view (video 2) showing a large floating object located in the ascending aorta. Mitral regurgitation is also observed. Best viewed with Windows Media Player.
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Associated Data
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Supplementary Materials
The left ventriculography with the right anterior oblique view (video 1) and the left anterior oblique view (video 2) showing a large floating object located in the ascending aorta. Mitral regurgitation is also observed. Best viewed with Windows Media Player.