Left Circumflex Artery Rupture with Left Atrial Tamponade and Functional Mitral Stenosis

The growth in percutaneous transluminal devices has enabled operators to tackle more complex, native, and post-bypass surgery anatomy. However, complications such as coronary artery dissection, coronary perforation, retrograde aortic dissection, arrhythmias, and acute coronary syndrome still occur with resulting mortality rates of up to 4.2% in complex interventions. Perforation of the circumflex artery is of particular interest in view of its position and relation to the surrounding cardiac structures. This is a site of potential fluid collection, and as the left atrium is fixed to the parietal pericardium at the entry of the pulmonary veins, fluid in the oblique sinus can accumulate enough pressure to compress the left atrium and the coronary sinus. We present a case of left circumflex artery perforation which demonstrates the physiologic complications of coronary sinus and left atrial compression and the resultant functional mitral stenosis.


Case
A 70-year-old gentleman was admitted to the emergency room for unstable angina. He underwent coronary artery bypass grafting 6 years prior to current admission and also had persistent atrial brillation on rate control and anticoagulation. His ejection fraction was 65%. Coronary angiogram showed occlusion of all vein grafts but patent left internal mammary graft to left anterior descending artery with severe native multivessel disease. ere was severe stenosis of the native left circum ex artery (Figure 1(a)); the proximal right coronary artery was completely occluded, and it was supplied distally by bridging collaterals and collaterals from the left circum ex artery. After extensive discussion with the patient, decision was made for percutaneous coronary intervention (PCI) of the native left circum ex artery. Serial balloon dilation to the mid circum ex artery was performed: rst with a 2.5 mm × 15 mm balloon but a waist was noted (Figure 1(b)), followed by a noncompliant 2.5 mm × 12 mm balloon but a residual waist was still observed, and nally with a 2.5 mm × 10 mm scoring balloon (AngioSculpt, Spectranetics, Milwaukee, Wisconsin, USA) in ating up to 20 atmospheres (Figure 1(c)). e stenosis gave way, and repeat angiogram noted Ellis Class III perforation (Figure 1(d)). e operators immediately in ated a 3.0 mm balloon to 8 atmospheres at the site of perforation followed by deployment of a 2.5 × 24 mm covered stent. However, repeat angiography still showed extravasation from perforation site and a second 2.5 × 12 mm covered stent was deployed, but there was continued extravasation. Protamine sulfate was given, and prolonged balloon in ation was then performed. Subsequent angiography showed that the circum ex artery was thrombosed.
Immediate bedside transthoracic echocardiogram showed very small 4 mm pericardial e usion. Pericardiocentesis was attempted but was unsuccessful. e ejection fraction was normal, and there were no other echocardiographic features of cardiac tamponade. e patient remained hemodynamically stable for about 20 minutes before developing progressive hypotension. e ECG showed fast atrial brillation with acute ST elevation in II, III and aVF ( Figure 2). He was supported with inotropes but developed pulseless ventricular tachycardia requiring cardioversion and 10 minutes of cardiopulmonary resuscitation. Venoarterial extracorporeal membrane oxygenation (VA ECMO) was inserted for hemodynamic stabilization. Repeat assessment by echocardiogram showed no increase in pericardial e usion, but there was a new collection of uid at the atrioventricular groove (Figure 3(a)), compressing on the left atrium. ere was neither pulsus paradoxus on hemodynamic monitoring nor other echocardiographic features of cardiac tamponade. Doppler echocardiography showed an increased mitral in ow gradient of 8 mmHg, suggesting functional mitral stenosis (Figure 3(b)).
Coronary sinus cannulation was attempted (Figure 4(a)), and the venogram showed no ow in coronary sinus (Figure 4(b)), suggesting extrinsic compression of the coronary sinus. Repeat pericardiocentesis was not attempted, as the uid collection was posterior and there were no accessible windows.
An urgent computed tomography scan was performed con rming the presence of the large 7.6 cm × 3.9 cm collection in the posterior aspect of the mediastinum extrinsically compressing and displacing the left atrium superiorly and to the right ( Figure 5). e coronary sinus could not be visualized due to extrinsic compression by the hematoma. e patient was sent for emergent surgical evacuation of the hematoma with ndings of large amounts of subepicardial hematoma, which had dissected the epicardium from the myocardium with left atrial compression. ere were also multiple adhesions noted intraoperatively, likely from his previous cardiac bypass surgery. Hemodynamics improved after hemostasis and evacuation of clots compressing the left atrium and coronary sinus.
However, the patient deteriorated multiple times during the hospital stay due to reaccumulation of hematoma and had to undergo repeat sternotomies and evacuation of hematoma. His course was complicated by oliguric acute kidney injury requiring continuous renal replacement therapy, sepsis, and ischemic stroke. He was supported by VA ECMO throughout and died seven weeks after his procedure due to multiorgan failure.

Discussion
e incidence of coronary perforation is reported to be 0.3-0.6% of all PCI procedures in combined reviews of approximately 50,000 cases [1,2]. e incidence is usually higher with the use of newer devices such as rotational artherectomy, direction artherectomy, cutting balloon, and excimer laser, and when PCI is performed in postcardiac bypass patients. Most lesions can be treated by temporizing with balloon in ation at the site of perforation for up to 15 minutes to stop the blood ow into the pericardium, emergency pericardiocentesis if there are signs of hemodynamic instability, followed by placement of embolization coils for distal perforations or polytetra uoroethylene membranecovered stents to seal o further ow through the perforation [3,4]. However, if there is continued bleeding or hemodynamic instability, emergency referral must be made to cardiothoracic surgery for surgical repair.
Coronary sinus compression as a sign of cardiac tamponade secondary to increase pericardial pressure [5] and tamponade phenomena secondary to left atrial compression are rare and di cult to detect, with few case reports in literature [1,3]. ese cases mostly occur during intervention to the circum ex artery due to its position in relation to its surrounding structures. e circum ex artery, which branches o from the left main artery, runs along the atrioventricular groove around the left atrium, giving rise to left marginal branches in the process. It continues around the left atrium and terminates in the posterior inferior aspect of the heart. e coronary sinus, which receives drainage from the great, middle, and posterior left ventricular veins, is a low-pressure venous conduit that runs along the atrioventricular groove, which is  in close proximity to the left circum ex artery [5]. Posterior to the left atrium lays the oblique pericardial sinus, bounded by the inferior vena cava, right pulmonary veins, and the left pulmonary veins. is case illustrates the anatomic and physiologic consequences during circum ex artery perforation. Blood collects in the oblique sinus, and as the left atrium is xed to the parietal pericardium by the entry of the pulmonary veins, uid in this xed space accumulates pressure [6]. As the blood volume increases, pressure accumulates until it compresses on the low-pressure coronary sinus, obstructing the ow. Previous cardiac bypass surgery could have formed adhesions around the pericardium, preventing redistribution of blood around the pericardial space. As the coronary sinus provides the primary drainage of the myocardial venous system, abrupt occlusion is likely to result in signi cant elevation of the transcapillary pressure. is in turn is likely to result in reduced myocardial perfusion pressure, aggravating myocardial ischemia [7], explaining the patient's ischemic ECG changes and arrhythmic collapse. Further blood collection in the oblique sinus will tamponade the left atrium and obstruct left atrial lling. e stroke volume consequently decreases and cardiac output drops, causing hypotension.
ere are few possible theories for the gradient across the mitral valve and functional mitral stenosis. Firstly, the hematoma externally compresses against the mitral annulus; this reduces the size of the mitral valve ori ce and limits the movement of the annulus, a ecting ow across the mitral valve. Secondly, the high external pressure from the hematoma obstructs lling of the atrium from the pulmonary veins; if the left ventricle function is relatively intact, this creates a suction force and gradient across the mitral valve.
Although extremely rare, it is important to recognize such subtle signs of tamponade following perforation during coronary angioplasty, especially in the circum ex artery and post-bypass surgery patients. is life-threatening complication requires clinical awareness for rapid diagnosis, and emergent referral needs to be made to cardiothoracic surgery for surgical treatment.

Conflicts of Interest
e authors declare that they have no con icts of interest.