Clinical Images

An Atypical Case of Acute Myocardial Infarction

Marc Laine, MD, Dominique Grisoli, MD†, Laurent Bonello, MD

Marc Laine, MD, Dominique Grisoli, MD†, Laurent Bonello, MD

ABSTRACT: Most ST-elevation myocardial infarctions are related to atherothrombosis and benefit from emergent percutaneous coronary intervention. On the other hand, type-A aortic dissection is a less frequent but deadly disease requiring emergent surgery. In the present case, we aimed to report the case of a patient who presented with aortic dissection responsible for STEMI and cardiogenic shock related to a compressive hematoma of the left main trunk. This atypical case underlines the need for careful assessment of the aorta in case of left main trunk occlusion in patients without evidence of atheroma in the other coronary segment. Unfortunately, in this case, refractory cardiogenic shock postponed surgical repair and led to the patient’s death.

J INVASIVE CARDIOL 2011;23:305–306

Key words: aortic dissection, percutaneous coronary intervention, ST-elevation myocardial infarction


Case Report

A 75-year-old man was admitted to our department for cardiogenic shock in the setting of anterior ST-elevation myocardial infarction (STEMI). He presented with chest pain of 6-hour duration when he came to the emergency department. The pain came suddenly while the patient was at rest, was constrictive in nature, and occurred for the first time. It was associated with New York Heart Association class-IV dyspnea.

The patient was a heavy smoker (2 packs/day) and had no medical history except for hypertension treated by angiotensin II receptor antagonist. On admission, physical examination showed a low blood pressure (80/64 mmHg in both arms) and sinus tachycardia (112 bpm), Killip IV. There was no pulse deficit. Pulmonary auscultation showed diffused crackles.

On the electrocardiogram, signs of acute myocardial infarction in the anterior territory were present, with ST elevation in leads V1 to V4 and ST depression in leads DII, DIII and VF. Q-waves were noted from leads V1 to V6 (Figure 1A).

Cardiogenic shock related to STEMI in the anterior territory was diagnosed. The patient therefore received pre-treatment with clopidogrel 600 mg per os, intravenous unfractionated heparin and 250 mg intravenous aspirin. The patient was immediately transferred to the catheterization laboratory for coronarography and percutaneous coronary intervention (PCI).1 During the first dye injection into the left main, an atypical lesion was observed in the proximal left main, which could either have been a dissection or a thrombus with TIMI-2 flow in the left coronary artery. No other lesion was noted on angiography (Figure 1B). PCI was immediately performed with direct stenting using a 3.5 x 15 mm bare-metal stent. TIMI-3 flow was restored (Figure 1C). Right coronary showed no sign of atheroma (Figure 1D).

Despite successful revascularization, the patient remained in pain. Because of the atypical lesion in the left main and persistent pain, we decided to perform an aortic angiography. It revealed an aortic dissection (Figure 1E).

Transesophageal echocardiography confirmed the diagnosis of type-A aortic dissection, with a peri-aortic hematoma of the ascending thoracic aorta associated with a mild aortic regurgitation. Transthoracic echocardiography showed a severely depressed left ventricular ejection fraction of 20%, with an anterior and lateral akinesis without pericardial effusion.

Inotropic support using intravenous dobutamine was started. Because of the aortic dissection, an intra-aortic balloon pump was not inserted and the patient was transferred to another hospital to undergo surgery. On arrival, surgery was postponed due to refractory cardiogenic shock.

A computed tomography angiogram of the aorta was performed. This exam showed a non-circulating hematoma of segment I of the aorta extending from the anterior wall to the right wall. The thickness of the hematoma was 14 mm and aortic diameter was 55 mm. The hematoma ran from segment 0 of the aorta to segment I. It crushed the ostium of the left main artery (Figure 2). Segments II and III of the aorta and the supra-aortic arteries were not involved in the dissection.

Unfortunately, because of the refractory cardiogenic shock, despite inotropic support and successful revascularization, the patient died of multi-organ dysfunction related to cardiogenic shock within 48 hours. Peak creatinine, phosphokinase, and troponin IC were 9, 255, and 400, respectively.


Thoracic aortic dissection is related to a breach in the intima responsible for the creation of a neo-channel, which splits media between its third means and its third extern. The spontaneous mortality at 48 hours is 50%.2 The typical patient presents with abrupt onset of chest pain, which is sharp (more often than constrictive) and moves toward the back if there is distal extension. The clinical features can be less common, such as syncope with or without chest pain, renal failure, or as in this case, an acute myocardial infarction related to occlusion of the left main artery. There are two mechanisms of ischemia during aortic dissection: dynamic, in which the intimal flap causes an occasional obstruction of a collateral artery; and static, in which the hematoma narrows the lumen of a branch artery (as in this case).

Type-A aortic dissection may cause STEMI in rare cases. Therefore, particular care should be taken in atypical acute myocardial infarction involving coronary ostia without evidence of atheroma in the other coronary segments and when the pain continues despite revascularization. Systematic angiography and/or transesophageal echocardiogram should be performed.

In a previous report, a patient underwent emergent surgery after PCI of the left main which achieved hemodynamic support and was released alive; thus, the present strategy of emergent PCI followed by aortic surgery may be lifesaving.3

The 2010 ACC/AHA guidelines on thoracic aortic disease4 recommend a bedside pre-test assessment for acute thoracic aortic disease. High-risk conditions, such as Marfan’s syndrome or intra-aortic aortic aneurysm, have to be taken into account. In addition, one must assess high-risk pain features, such as chest or back pain, abrupt onset and high-risk exam features including pulse deficit and systolic blood pressure asymmetry. Following this assessment, the patient should be classified as: low-risk (no high-risk features); intermediate (one high-risk feature); or high-risk (two or more high-risk features). The management of the high-risk patient requires immediate surgical consultation and aortic imaging. In this case, the patient would had been classified as “high-risk” because of the pain description associated with the collapse. However, we decided to first perform a coronarography, as guided by the electrocardiogram, which presented with a typical pattern of STEMI.4


  1. Van de Werf F, Bax J, Betriu A, et al. Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: The task force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology. Eur Heart J 2008;29:2909–2945.
  2. Erbel R, Alfonso F, Boileau C, et al. Diagnosis and management of aortic dissection. Eur Heart J 2001;22:1642–1681. 
  3. Shimamura J, Kubota H, Tonari K, et al. Acute aortic dissection with left main coronary malperfusion treated with precedent stenting followed by a definitive surgery. Kyobu Geka 2010;63:537–541. 
  4. Hiratzka LF, Bakris GL, Beckman JA, et al. Guidelines for the diagnosis and management of patients with thoracic aortic disease: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation 2010;121:E266–E369.


From Hopital Universitaire Nord de Marseille and Hopital de la Timone, Marseille, France.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted December 21, 2010, provisional acceptance given January 24, 2011, final version accepted March 28, 2011.
Address for correspondence: Laurent Bonello, MD, Hopital Universitaire Nord de Marseille, Departement de cardiologie, Chemin des bourrely, Marseille, 13015, France. Email: