Coronary Intramural Hematoma: Challenges in Diagnosis and Management.

Coronary intramural hematoma (CIH) after percutaneous coronary intervention (PCI) is a rare cause of acute coronary syndrome. As the diagnosis is really challenging, its incidence is really under estimated. The optimal management of post-PCI CIH has not been well defined. Conventional coronary angiography alone is often insufficient to identify a CIH. Intravascular ultrasound and optical coherence tomography (OCT) are helpful modalities for diagnosis and evaluation of its extension. We present a case of CIH after PCI, highlighting our experience in the diagnostic accuracy of OCT and our strategy in the management of this case.

INTRODUCTION

Coronary intramural hematoma (CIH) is defined as an accumulation of blood within the media that may displace the internal elastic membrane inward and the external elastic membrane outward, with or without identifiable entry or exit points. Its occurrence can be a diagnostic dilemma to an interventionist and might lead to unnecessary intervention. Ischemia and hemodynamic compromises are possible complications if not managed promptly. We present a case in which coronary occlusion developed due to an intramural hematoma after percutaneous coronary intervention (PCI) to the mid-left circumflex artery (LCX). We used optical coherence tomography (OCT) in this case. OCT is a high-resolution real-time intravascular imaging modality that offers microscopic visualization of the biological tissues.

CASE PRESENTATION

A 45-year-old Asian gentleman, with a history of hypertension and epilepsy on regular treatment, presented to the hospital with typical retrosternal chest pain for 2 hours duration. A 12 lead electrocardiogram (ECG) revealed ST elevation in lead II III, and avF and was labeled as acute inferior wall myocardial infarction. He was successfully thrombolysed. A transthoracic echocardiogram showed normal global systolic function of the left ventricle with an ejection fraction of 56%. There were wall motion abnormalities at the basal inferior, basal inferolateral, mid-inferior, and mid-inferolateral wall segments. The right ventricle function was normal.

The patient was then transferred to tertiary hospital for coronary angiogram. His coronary angiogram showed 90% mid-LCX stenosis and 100% mid-right coronary artery (RCA) chronic total occlusion with collaterals from proximal RCA supplying the distal RCA and collaterals from the distal left anterior descending artery (LAD) supplying the right posterior descending artery [Figure 1]. The mid-LCX was directly stented successfully with 3.5 mm × 12 mm drug-eluting stent (DES) [Figure 2] and then postdilated with noncompliant balloon at a pressure of 12 atm for 20 s. He had mild chest pain for a short period after the procedure without any new ECG changes and then became asymptomatic for the rest of the day. He slept at night with no symptoms.

Figure 1

Angiography of the left coronary artery demonstrating the original stenosis in the mid-left circumflex artery (arrow)

Figure 2

Angiography of the left coronary artery demonstrating successful stent implantation in the mid-left circumflex artery (arrow)

Next day morning, he was found to have elevated high-sensitive troponin T of 1572. His baseline troponin T before the procedure was only 29.8. No new ECG changes were found. Telemetry review showed two short runs of ventricular tachycardia the same day morning. Hence, he was taken for a relook coronary angiogram. It showed new 80% long and hazy stenosis with TIMI flow 3 at the proximal obtuse marginal artery (OM2) extending from the distal end of the LCX stent which was deployed a day before [Figure 3]. OCT showed edge dissection at the distal end of the stent that created a big intramural hematoma compressing the true lumen of the LCX [Figure 4].

Figure 3

Relook angiography of the left coronary artery showing a new long and hazy luminal narrowing just distal to the stent (arrow)

Figure 4

(a) Optical coherence tomography of the left circumflex artery showing edge dissection distal to the stent. (b) Optical coherence tomography of the left circumflex artery showing intramural hematoma secondary to edge dissection distal to the stent

We decided to perform angioplasty as the patient had two short runs of ventricular tachycardia and high-sensitive troponin T was highly elevated. Direct stenting was performed in the proximal OM2 using DES (Xience PRO × 3.0 mm × 23 mm) overlapped with previous stent in the mid-LCX covering the edge dissection [Figure 5]. The inflation pressure was kept low at 10 atm for 17 seconds. Postdilation was performed only at the stent-overlapped area using a Quantum 3.5 mm × 8 mm noncompliant balloon at a pressure of 16 atm for 16 seconds.

Figure 5

Relook angiography of the left coronary artery showed successful stent implantation in the proximal obtuse marginal artery (arrow)

Following the intervention, there was no stenosis. Poststenting OCT showed complete resolution of the intramural hematoma and edge dissection, with well-apposed stents [Figure 6]. The patient was discharged after few days in a very good condition, and his clinical outcomes were excellent at 1 month after intervention.

Figure 6

Poststenting optical coherence tomography of the left circumflex artery showing complete resolution of intramural hematoma and edge dissection, with well-apposed stent

DISCUSSION

Intramural coronary hematoma is a rare, challenging cause of acute coronary syndrome. It is defined as an accumulation of blood within the media that may displace the internal elastic membrane inward and the external elastic membrane outward, with or without identifiable entry or exit points. Further expansion of this hematoma may lead to compression of the true lumen of the coronary artery and result in myocardial ischemia or infarction.

Intramural hematoma after PCI occurs in up to 6.7% of cases.[1] The clinical presentations of intramural hematoma depend on the degree of pressure-driven enlargement of the hematoma space, with progressive true lumen compression, resulting in myocardial ischemia or infarction. Several factors such as the pre- and post-partum periods, trauma, hypertension, vasculitis, and the use of contraceptives or illicit medications are potential risk factors that relate to this phenomenon. Our patient was hypertensive.[2]

Coronary angiography (CAG) has limited diagnostic value in the absence of intimal dissections, and lesions are often angiographically ambiguous.[3] Intravascular ultrasound (IVUS) and OCT can be valuable in establishing the correct diagnosis and in planning the management procedure.[234]

In this case, we decided to use OCT to identify the etiology of this new lesion as OCT offers clear, high-resolution images, compared to grainy, lower resolution IVUS images.[25]

OCT provides a complete vessel wall assessment and can reveal more insight into the mechanisms of intramural hematomas such as entry point of the dissection, propagation direction, underlying arterial plaque, severity of the intramural hematoma, and luminal compromise.

Due to the rarity of this clinical scenario, no randomized controlled trials exist to guide treatment, and no consensus regarding management is available.[6] Currently, treatment strategies are based on a case by case clinical assessment and experiences.[1] Treatment options for intramural hematomas include conservative medical therapy, close angiographic follow-up, and PCI.

Revascularization remains challenging and therefore should be restricted to patients with ongoing/recurrent ischemia and suitable anatomy.[5] However, the optimal treatment approach remains controversial. It has already been reported that stenting to restore distal flow in a narrowed vessel is an effective management approach. However, there are some concerns that stenting may cause longitudinal hematoma extension and is associated with an increased rate of restenosis and stent thrombosis.[2] Importantly, a hematoma's healing process is absorption of the hemorrhage, which is quite different from those of plaque rupture or erosion.

In this case, we decided to stent the lesion as the patient had two short runs of ventricular tachycardia and high-sensitive troponin T was highly elevated. To avoid longitudinal extension of the hematoma, direct stenting was performed, overlapped with previous stent covering the edge dissection. We used low inflation pressure of 10 atm for 17 seconds and postdilation pressure was kept at 16 atm for 16 seconds. Poststenting OCT showed complete resolution of the hematoma with well-apposed stents.

A similar case was published in Circulation[7] where Coronary Angiography (CAG) and IVUS demonstrated intramural hematoma in the proximal LAD in a patient who presented with ST elevation myocardial infarction. Furthermore, the vessel wall around the hematoma segments seemed to be less atherosclerotic and nearly healthy in structure. As both ischemic symptoms and signs completely disappeared during catheterization, no additional interventional treatments were performed for this patient. CAG and IVUS performed 35 days later showed complete resolution of intramural hematoma. Another similar case was published in JACC[8] where a 51-year-old man with a positive stress echocardiogram underwent coronary angiogram. The LAD stenosis was predilated with a 3.0 mm × 9 mm balloon, and a 3.5 mm × 16 mm DES was placed, with a maximal inflation pressure of 16 atm. After stent placement, there appeared to be a “new lesion” at the distal end of the stent that was not relieved by intracoronary nitroglycerin or verapamil. An IVUS was performed which revealed an intramural hematoma originating at the distal end of the stent with no identifiable entry point. This was treated with an overlapping 3.0 mm × 20 mm DES deployed at a maximal pressure of 12 atm. The stent length was chosen to cover beyond the distal extent of the intramural hematoma. Final IVUS showed resolution of the intramural hematoma. Angiography demonstrated no residual stenosis.

CONCLUSION

Coronary intramural hematoma (CIH) after PCI has to be suspected as a cause of elevated troponin and short runs of ventricular tachycardia even if the patient is otherwise clinically asymptomatic. Only a few number of cases have been reported, and optimal management has not been well defined. Therefore, treatment should be individualized based on patient characteristics and the clinical scenario.

From our experience, we highlight the importance of OCT in guiding treatment strategy when angiographic assessment is ambiguous. OCT offers clear, high-resolution images. Moreover, direct stenting with low inflation pressure will decrease post-PCI complications such as longitudinal hematoma extension, restenosis, and stent thrombosis. Poststenting OCT is very important to evaluate the resolution of intramural hematoma and to ensure the stent is well apposed despite the low inflation pressure used.

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.