Acute Myocardial Infarction Due to Left Main Compression Aortic Dissection Treated By Direct Stenting

ABSTRACT: We describe a case of acute myocardial infarction (AMI) due to compression of the left main coronary artery (LMCA) by a false channel created by an acute aortic dissection (AAD). The dynamic pattern of artery obstruction is detailed as a key element to the diagnosis of extrinsic coronary compression throughout the angiography. Treatment by direct stenting restored complete anterograde coronary flow and improved myocardial perfusion.

Key words: aortic diseases, coronary vessels, stents

The goal of acute myocardial infarction (AMI) treatment is reperfusion,¹ which can be achieved either by percutaneous transluminal coronary angioplasty (PTCA)^2,3 or thrombolytic therapy.^4–6 In most cases, the cause of acute coronary artery occlusion is the presence of thrombus superimposed on a more or less severe atheromatous plaque.⁷ We describe a patient with AMI in whom the etiology was not thrombotic, but rather compression of the left main coronary artery (LMCA) by a false channel created by an acute aortic dissection (AAD). Case Report. A 68-year-old man was admitted to our institution for evolving anterior myocardial infarction. Initially, he was evaluated by the emergency medical team, and diagnosed with an anterior AMI. Pre-hospital thrombolysis was contraindicated because of recent hemoptysis in this patient with an inoperable pulmonary neoplasm treated by radiotherapy two years prior. The patient was then considered for primary angioplasty. Upon admission, he had retrosternal chest discomfort with irradiation to the jaws and left arm. Physical examination showed blood pressure of 80/50 mmHg, heart rate of 80 beats/minute, no cardiac murmur and Killip III status. The peripheral pulses were symmetrically present. The electrocardiogram (ECG) showed ST elevation in the antero-lateral leads (Figure 1). Before transfer to the cath lab, a transthoracic echocardiogram (TTE) showed major left ventricular dysfunction with severe hypokinesia of the septal, apical and anterior walls. Ejection fraction was 25%. There was no valvular regurgitation. The pericardium was normal. At the cath lab, the procedure was carried out as usual through a right radial approach. Right coronary angiography showed a moderately diseased artery without significant stenosis. There was some retrograde filling of the left anterior descending (LAD) and circumflex (CX) arteries. A 6 French, extra-backup (XB), 3.5 catheter was then introduced in order to cannulate the left coronary ostium. The initial injection revealed a very tight stenosis of the LMCA (Figure 2) with persistence of contrast medium at the LAD and CX levels, despite a very normal pressure curve at the tip of the catheter (Figure 3). This suggested to us that the main stem was undergoing extrinsic compression. The guiding catheter was then withdrawn through the ascending aorta, where a more powerful injection demonstrated an acute coronary dissection with a false lumen compressing the LMCA (Figure 4). Subsequently, the left coronary ostium was engaged again and a more vigorous injection showed a typical image of coronary artery compression, i.e., complete resolution of the tight stenosis resulting in a wide open LMCA with intermittent diastolic collapse of the lumen (Figure 5). At this point, we diagnosed AMI secondary to LMCA compression by AAD. Consequently, we performed direct left main stenting in order to bridge for possible aortic surgery (Figure 6). After deployment of a 4 mm (diameter) x 13.0 mm (length) stent (Figure 7), the patient became free of pain and the ECG normalized. We completed the procedure by a supravalvular aortography, which showed a Stanford type A aortic dissection. Subsequently, a transesophageal echocardiogram (TEE) was performed to evaluate the extension of the aortic dissection. TEE revealed that the dissection extended from the sinotubular junction to the abdominal aorta. The cardiac surgeon judged that major aortic surgery was contraindicated in this patient because of his pulmonary neoplasm treated by palliative radiotherapy. The patient was then admitted to the intensive coronary unit where, several hours later, he presented with acute ischemia of the left leg followed by cataclysmic hemoptysis, probably due to aortic rupture, leading to death. Discussion. Ascending AAD is associated with a 7–13% incidence of retrograde dissection of either one or both coronary ostia.^8,9 About 4–12% of patients with this condition will develop clinical and electrocardiographic findings compatible with AMI^10,11 and may receive inappropriate thrombolytic therapy. Mortality in these circumstances ranges from 69–100%, with most deaths occurring within the first two days after treatment as a consequence of cardiac tamponade or aortic rupture.^10–15 AMI is a critical condition requiring early treatment.¹⁶ Time- consuming diagnostic tests (TEE, computer tomography scan or aortography) are generally not indicated before thrombolytic therapy.¹⁷ In patients with AMI and contraindications for thrombolytic therapy, primary PTCA is the treatment of choice.¹⁷ Since recent studies have demonstrated the superiority of interventional reperfusion therapy in the early phase of AMI, PTCA is becoming a preferred strategy.^18–20 Careful reading of images during coronarography is essential in order to establish the diagnosis and mechanism of coronary narrowing, especially in cases where the etiology of the AMI is unusual, such as coronary artery dissection, embolism or compression. In a setting of AAD, intimal rupture permits the progression of blood through the false channel, forming a large obstructive intramedial hematoma, which can extend to the coronary ostium and compress the lumen. The dynamic pattern of the artery obstruction is the key to diagnose LMCA compression by vascular structure as dilated pulmonary artery or AAD.²¹ Lumen size varies according to diastolic and systolic flow, producing an image of “swinging lumen.” In cases where this phenomenon reaches maximum amplitude, diastolic interruption of coronary flow, as in our patient, will produce a persistent contrast-filling image despite perfectly normal pressure curves at the aortic level. A definitive diagnosis can be achieved at the cath lab with aortography. Treating patients of this kind is always a challenge. The goals of therapy are early reperfusion of the injured muscle and definitive etiological management. In the past decade, perfusion balloons allowed moderate anterograde flow restoration.^22,23 At present, the development of coronary stents permits appropriate management of coronary compression, restoring complete anterograde coronary flow and improving myocardial perfusion.²⁴ Following this, prompt aortography or computer tomography scan should be carried out in order to prepare for surgical management, which remains essential. Conclusion. AAD is a rare but real cause of AMI. Because of the growing use of PTCA in the setting of AMI, the interventional cardiologist must be aware of the angiographic characteristics of coronary artery compression, especially in the case of AAD, since this condition requires prompt reperfusion by stenting in order to stabilize the patient and allow the necessary surgical management.