Myocardial Infarction Caused by Ostial Right Coronary Artery Thrombus in the Absence of Atheromatosis

ABSTRACT: Myocardial infarction in patients with normal coronary vessels is a relatively rare entity that is observed in up to 2.8% of patients with myocardial infarction. In this case, we present a patient in whom presence of thrombus was suspected by pressure damping during engagement of the right coronary ostium despite the normal angiographic morphology. Further contrast injections with the catheter resting outside the ostium and intravascular imaging with optical coherence tomography helped confirm the suspicion of ostial thrombosis, as well as the presence of non-atheromatic vascular wall. The patient was consequently treated with thrombus aspiration and stenting of the vessel ostium.

J INVASIVE CARDIOL 2012;24(9):E188-E189

Key words: acute coronary syndrome, coronary angiography, thrombosis, optical coherence
tomography, stent

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Myocardial infarction (MI) in patients with normal coronary vessels is a relatively rare entity that is observed in up to 2.8% of patients with MI, and is associated with better prognosis than that of patients with MI and obstructive coronary lesions.¹ In this case report, we present the case of a patient with ST-elevation MI, in whom, despite the normal angiographic morphology, presence of thrombus was suspected by pressure damping during engagement of the right coronary ostium.

Case Report. A 65-year-old female patient presented at the emergency department with typical anginal pain of 30 minutes duration. The patient had no prior medical history, denied any use of alcohol or drugs, and had no coronary disease risk factors, except for smoking (20 pack/year). ST-segment elevation (2 mm) was present in leads II, III, and aVF at the electrocardiogram. The patient was hemodynamically stable (blood pressure: 130/80, 70 bpm) and received at admission standard therapy with chewed aspirin 300 mg, 600 mg loading dose of clopidogrel, nitrates, and 2 boluses of morphine 2 mg with resolution of chest pain. The patient was transferred to the cath lab in order to perform primary percutaneous coronary intervention (pain-to-needle time: 45 minutes). Before catheterization, the patient developed third degree atrioventricular block with 50 bpm ventricular rate and blood pressure 100/60.

Coronary angiography revealed a normal left coronary artery (Figure 1A). The right coronary artery (RCA) was catheterized using a JR4 6 Fr guiding catheter. However, during attempts to engage the catheter into the ostium of the RCA, significant pressure damping was observed, subsiding with catheter withdrawal. Following a trial contrast injection in the RCA, haziness was temporarily observed in the right posterior lateral branch. Subsequently, the patient was spontaneously restored to sinus rhythm with simultaneous resolution of the ST-segment elevation. Angiography of the RCA did not reveal any obstructive lesions or haziness (Figures 1B and 1C), despite the fact that pressure damping was still present during engagement of the ostium. This raised suspicion of thrombus at the ostium of the vessel. Contrast injection was performed with the catheter resting outside the ostium of the RCA, and a focal contrast deficit was then observed (Figure 2A).

A decision was made to proceed with manual aspiration of the thrombus. A guidewire was inserted into the RCA and manual aspiration with a 10 mm syringe was performed using the guiding catheter, resulting in extraction of small amounts of thrombus. Optical coherence tomography (OCT) was then performed in the proximal 25 mm of the RCA using the C7 LightLab system (LightLab Imaging) and the corresponding intravascular OCT catheter (C7 DragonflyTM). OCT examination revealed the existence of small fragments of thrombus near the ostium of the vessel and the absence of any atheromatic changes of the vascular wall, or any evidence of spontaneous dissection (Figures 2B and 2C). Then, we proceeded with stenting of the RCA ostium using a 4 mm/16 mm Promus stent (Boston Scientific), with a good angiographic result (Figure 1D).

The patient recovery was uneventful. Peak troponin levels were 65.8 ng/mL and peak creatine kinase-MB levels were 193 IU/L. Echocardiography revealed no segmental hypokinesia or existence of left ventricular thrombus that could have led to a coronary embolus. Screening for hypercoagulation disorders and systemic autoimmune diseases was also negative. The patient was discharged 6 days later on dual antiplatelet therapy (aspirin, clopidogrel).

Discussion. MI in patients with normal coronary vessels is a relatively rare entity that is observed in up to 2.8% of patients with MI.¹ The prognosis of these patients is better than the prognosis of patients with occlusive coronary disease.¹ A variety of pathogenetic mechanisms has been suggested, including hypercoagulation disorders,² autoimmune disorders,³ substance abuse,⁴ and coronary spasm.⁵ Rare causes of intracoronary thrombus also include embolism from intracardiac sites⁶ or a thrombus originating from a deep venous thrombosis site, crossing via a patent foramen ovale.⁷ In such cases, a transesophageal echocardiogram can assist in the diagnosis.

In our case, we detected that thrombus formation was the culprit for the clinical syndrome, after observing unexpected alterations of the pressure waveform. By coronary angiography and OCT examination, we confirmed the suspicion of ostial thrombosis. Furthermore, by OCT, a high-resolution method with the potential to image the majority of morphological characteristics of complicated plaques,^8,9 we demonstrated the integrity of vascular endothelium and the absence of atheromatosis. Interestingly, screening for hypercoagulation disorders or inflammatory disorders was negative, while there was no history of substance abuse or evidence of coronary spasm during catheterization. Transthoracic echocardiogram was also negative for intracardiac thrombus, although a transesophageal echocardiogram that could exclude this diagnosis with higher sensitivity or exclude the presence of a patent foramen ovale was not performed. Thus, the cause of thrombosis in our patient was not identified.

Conclusions. In this case report, we presented a patient in whom, despite the normal angiographic morphology, presence of thrombus was suspected by pressure damping. Use of a guiding catheter with side holes, instead of the catheter used, would have probably led to misdiagnosis. Further contrast injections and intravascular imaging helped to confirm the existence of thrombus and decide on subsequent treatment.

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From the First Department of Cardiology, Athens Medical School, Hippokration Hospital, Athens, Greece.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted February 27, 2012, provisional acceptance given April 23, 2012, final version accepted April 26, 2012.
Address for correspondence: Antonios Karanasos, MD, 19 Omirou str., 15344 Gerakas, Athens, Greece. E-mail: akaranasos@hotmail.com