Great cardiac vein injury after circumflex artery intervention: a case report

Abstract

Background

Injury of the great cardiac vein (GCV) during circumflex coronary artery intervention is not discussed enough in the literature. In addition, relationship between the GCV and circumflex artery is highly variable and practically unpredictable in 30% of cases. This report describes a rare case of GCV injury during circumflex artery intervention.

Case summary

An 80-year-old man with known ischaemic heart disease was admitted with unstable anginal pain for urgent coronary angiography. Circumflex (Cx) percutaneous coronary intervention (PCI) of proximal-to-medial high-grade calcified stenosis was performed. Two hours later, the patient developed pericardial tamponade. Pericardiocentesis revealed a venous bloody effusion. Due to continuous bleeding, an urgent exploratory thoracotomy was performed. Intraoperatively, a large pericardial haematoma in the Cx region was evacuated. The perforation site was sought and identified as a tear at the GCV. Further hospitalization was uneventful, and the patient was discharged after one week. Clinical and echocardiographic outcomes were favourable at the 3-month follow-up.

Discussion

A GCV injury during PCI is a diagnosis of exclusion if there is a venous pericardial effusion directly after PCI and no injury of the right ventricle or surrounding structures, and thoracic computed tomography demonstrates a pericardial haematoma in the PCI region, especially the Cx region. A haematoma can deteriorate the haemodynamic status without effusion ‘dry tamponade’. Treatment should be addressed according to haemodynamics. A conservative therapy, pericardiocentesis, catheter-based bailout intervention or even an explorative pericardiotomy could be imperative to evacuate the haematoma and seal the injured vein.

Learning Points

• Injury of the great cardiac vein (GCV) is not a preventable complication but could be predicted by severely calcific circumflex artery intervention.

• The relations between the vein and circumflex artery are highly variable and practically unpredictable in 30% of the cases. The anterior interventricular vein is superficial to the artery in 60–70% of the population and passes under the artery in 30%.

• This is a peculiarity and uniqueness of the left circumflex coronary compared with other coronary arteries.

• A GCV injury during percutaneous coronary intervention (PCI) is a diagnosis of exclusion if there is a venous pericardial effusion

  • directly after PCI, particularly in the Cx region, and no injury on the right side of the heart or surrounding structures and

  • thoracic computed tomography demonstrates a haematoma in the PCI region.

• A haematoma can deteriorate the haemodynamic status without effusion ‘dry tamponade’.

• First, consider conservative therapy; if the patient is haemodynamically unstable or bleeds progressively, an explorative pericardiotomy could be imperative to evacuate the haematoma and seal the injured vein. Other interventional techniques could be helpful as a bailout technique in high-risk patients.

Introduction

Coronary artery perforation is a potentially life-threatening complication in 0.2–0.6% of all patients undergoing percutaneous coronary intervention (PCI).¹

However, injury of the great cardiac vein (GCV) after circumflex artery intervention is not discussed enough in the literature. It could be predicted by severely calcific circumflex artery intervention, as the relations between the vein and circumflex artery are highly variable and practically unpredictable in 30% of the cases.²

The GCV is the longest venous vessel of the heart. On reaching the area of the coronary sulcus, the GCV crosses the anterior interventricular branch and the circumflex branch of the left coronary artery, forming the triangle of Brocq.² The anterior interventricular vein (arrows) courses superficial to the arteries in 60–70% of the population (Figure 1A) and passes under both arteries in 30% of the population (Figure 1B). This is a peculiarity and uniqueness of the left circumflex coronary compared with other coronary arteries.³

Figure 1.

(A and B) Imaging of the cardiac venous system (CVS) by computed tomographic (CT) mapping of the coronary veins and its relations to coronary artery. Great cardiac vein crossing the left anterior descending (LAD) and left circumflex (LCx) arteries, forming a triangle. The relations of the vein and these arteries are highly variable. The anterior interventricular vein (arrows) courses superficial to the arteries in 60–70% of the population (A) and passes under both arteries in 20% of the population (B).³

If perforation leaks blood into the myocardium, causing large septal, intramural haematomas or into the pericardium causing pericardial haematoma ‘dry tamponade’, it could mask the situation with false impressions that there is no source of bleeding or obvious pathology and may require emergency explorative surgery or bailout intervention.

This report presents a rare case of GCV injury after percutaneous circumflex coronary artery intervention.

Summary figure

Case presentation

An 80-year-old man presented with known hyperlipoproteinaemia, arterial hypertension, and known ischaemic heart disease with Ramus intermedius coronary artery-drug-eluting stent due to ST elevation myocardial infarction of the lateral wall. He was admitted with unstable anginal pain (new, worsening chest tightness, get worse with little physical exertion and radiate to the left shoulder and arm) for urgent coronary angiography. Electrocardiogram revealed sinus rhythm with incomplete right bundle branch block. Transthoracic echocardiography (TTE) revealed low normal left ventricular function with an ejection fraction of 50%, and troponin value of 31 ng/L.

Diagnostic angiography using the right femoral artery approach showed that the proximal-to-medial circumflex artery had a high-grade calcified stenosis (see Supplementary material online, Figure S1). With a 6 French extra backup guider, attempts were initially made using an Hi-Torque hydrophilic coating guide wire (Abbott BMW 0.014), followed by an Hi-Torque polymer-covered hydrophilic guide wire (Abbott Whisper MS 0.014) as a buddy wire. The lesion was successfully crossed with a wire tip placed in the distal left circumflex, and multiple balloon inflations at stenosis sites using a non-compliant 3.0 × 15 balloon (20 atmosphere) were undertaken. This was followed by proximal-to-medial placement of a 3.0 × 20 and 2.75 × 24 mm drug-eluting stent (Boston Scientific Promus Premier). Angiography post-stent deployment showed thrombolysis in myocardial infarction (TIMI)-Flow III (see Supplementary material online, Figure S2). Two hours later, the patient developed dyspnoea according to New York Heart Association grade IV and cardiogenic shock and became haemodynamically unstable with 15 mm pericardial effusion visualized on bedside TTE without any signs of compression on the right side of the heart. Pericardiocentesis was performed with an aspiration of 600 mL haemorrhagic venous effusion confirmed in blood gas analysis: Hb 11 g/dL, SO₂ 45%. This was the first clue that the source of bleeding had not been understood.

A second coronary angiography was performed, which showed no signs of coronary artery perforation with TIMI-Flow III in all of the coronary arteries. We further conducted aortography (see Supplementary material online, Figure S3) and left (see Supplementary material online, Figure S4) and right ventricular angiography (see Supplementary material online, Figure S5), which showed no signs of perforation or extravasation. As the patient’s haemodynamic deteriorated again with a second pericardial drainage of 600 mL of haemorrhagic venous effusion, three units of packed red blood cells were given, and we performed thoracic computed tomography (CT). It revealed circumferential haemorrhagic pericardial effusion with delineation of the contrast medium in the area of the Cx that exceeds the myocardial contour (Figure 2A, B). After cardiothoracic consultation, we transferred the patient to a tertiary heart centre. As the patient’s haemodynamic deteriorated for the third time with pericardial drainage of 600 mL of haemorrhagic venous effusion, the decision for emergency exploratory thoracotomy was made. Intraoperatively, a large myocardial haematoma in the circumflex region was evacuated. The perforation site was sought and identified as a tear at the GCV (see Supplementary material online, Figure S6A, B). The whole area was sealed with Tachosil.

Figure 2.

(A and B) Thoracic computed tomography revealed haemorrhagic pericardial effusion with delineation of a contrast medium in the area of the left circumflex (LCx) that exceeds the myocardial contour (haematoma).

The patient recovered post-surgery with no deficits and was discharged 7 days later. The discharge medications were acetylsalicylic acid, clopidogrel, statin, angiotensin-converting enzyme inhibitor, and B-blocker. Three months after the procedure, follow-up did not show quality of life limitations.

Discussion

We present a very rare complication of GCV injury after severe calcific Cx artery intervention. Retrospectively, we tried to understand the mechanism of bleeding in this rare case. As demonstrated in Figures 3 and 4, the calcific lesion in the Cx artery protruded outside and injured the underlying neighbouring GCV.

Figure 3.

Mechanism of great cardiac vein injury after circumflex artery intervention. (A) Severely calcific Circumflex (Cx) lesion. (B) Cx percutaneous coronary intervention lead to protrusion of calcific plaque outside the Cx artery and injured the great cardiac vein. (C) Possible Cx stenting and prolonged balloon inflation as bailout interventional technique.

Figure 4.

(A) Course and (B) mechanism of great cardiac vein injury after circumflex artery intervention.

A GCV injury during PCI is a diagnosis of exclusion if the patient has:

1. a venous pericardial effusion;

2. directly after PCI, particularly in the Cx region;

3. no injury of the right ventricle or other surrounding structures;

4. a haematoma in the PCI region confirmed by thoracic CT.

A haematoma can deteriorate the haemodynamic status without effusion ‘dry tamponade’.

First, consider conservative therapy; if the patient is haemodynamically unstable or bleeds progressively, do a pericardial drainage and contact a heart surgeon as soon as possible for explorative pericardiotomy, to evacuate the haematoma, and to seal the injured vein.

Catheter-based intervention could be helpful as a bailout technique in high-risk patients as follows. First, intubate the coronary sinus and try to wire the GCV, then use a bailout prolonged balloon or covered stent implantation to stop the bleeding (Figure 5). However, it is difficult to say that it is reproducible for use in daily coronary intervention.

Figure 5.

(A) Illustration of great cardiac vein drainage into coronary sinus and (B) possible bailout intervention technique of great cardiac vein injury through coronary sinus with prolonged balloon inflation.

In this case, a successful explorative pericardiotomy to seal the injured vein and evacuate the haematoma was an attempt to save a difficult and rare complication.

Conclusion

A GCV injury during PCI is a rare complication. It is a diagnosis of exclusion if there is a venous pericardial effusion directly after PCI, particularly in the Cx region, and no injury on the right side of the heart or surrounding structures, and thoracic CT demonstrates a haematoma in the PCI region. A haematoma can deteriorate the haemodynamic status without effusion ‘dry tamponade’. First, consider conservative therapy. If the patient is haemodynamically unstable or bleeds progressively, perform a pericardial drainage. Explorative pericardiotomy could be imperative to evacuate the haematoma and seal the injured vein. Other catheter-based interventions could be helpful bailout techniques in high-risk patients.

Lead author biography

Abdelrahman Elhakim is an interventional cardiologist and head of the catheter laboratory at Schoen Hospital Neustadt in Holstein, Germany. He completed his cardiovascular medicine residency and interventional cardiology fellowship in several hospitals in Germany. He also sub-specialized in coronary artery intervention, intensive care, and emergency medicine in Germany. He has led pulmonary embolism workshops and completed a medical doctoral study on pulmonary embolism at Schleswig-Holstein University Hospital in Luebeck. He also holds a Master’s degree in cardiovascular medicine from Al-Azhar University, Egypt, and a second Master’s degree in business and health administration from Nuernberg University, Germany.

Supplementary material

Supplementary material is available at European Heart Journal – Case Reports online.

Data availability

The data underlying this article are available in the article and in its online Supplementary material.