Case Report

Acute myocardial infarction with cardiogenic shock in a patient with acute aortic dissection

Abstract

Diagnosing acute Stanford type A aortic dissection with the uncommon involvement of the left main coronary artery (LMCA) remains challenging for the emergency physician because it can resemble acute myocardial infarction with cardiogenic shock. The following case report illustrate this infrequent but critical situation. A 52-year-old woman with a history of hypertension awakened with acute Retrosternal chest pain accompanied by nausea and vomiting. She was referred to our hospital for primary coronary intervention because of acute myocardial infarction with cardiogenic shock. Coronary angiography indeed revealed LMCA occlusion. Subsequently successful percutaneous coronary intervention with stent implantation was performed, fol- lowed by immediate clinical improvement of the patient. Soon after admission at the coronary care unit, severe chest pain, hypotension, and electrocardiographic signs of diffuse myocardial ischemia relapsed. Control coronary angiogra- phy, however, showed no in-Stent thrombosis. Review of clinical examination revealed an aortic regurgitation mur- mur. Because of this dynamic pattern of (1) signs of acute myocardial ischemia, (2) relapse of Hemodynamic collapse, and (3) unaltered control coronary angiography together with the confirmed aortic regurgitation at transthoracic echocardiography, the patient was suspected of having aortic dissection. Transesophageal echocardiography revealed Stanford type A aortic dissection with severe eccentric aortic regurgitation and no pericardial effusion. Emergent valve-sparing aortic replacement was performed. The patient recovered completely. In this case, the lifesaving element was primary coronary intervention with stenting of the LMCA preventing extensive myocardial damage followed by a surgical correction of the aorta.

A 52-year-old woman with a history of hypertension awakened with acute chest pain accompanied by nausea and vomiting. Emergency personnel considered the diagnosis acute myocardial infarction, and she was referred directly to our catheterization laboratory for primary percutaneous

coronary intervention (PCI). She was treated with 600 mg of clopidogrel, 500 mg of aspirin, and 5000 U of heparin. At arrival, she was in cardiogenic shock with an invasive blood pressure of 40/20 mm Hg. The 12-lead electrocardiogram showed Sinus bradycardia with diffuse ST-segment depression and elevation in Lead aVR (Fig. 1). She was suspected of acute anterior myocardial infarction with cardiogenic shock by occlusion of the left main coronary artery (LMCA). Indeed, at coronary angiography, the left coronary artery showed occlusion of the LMCA (Fig. 2A) with thrombolysis in myocardial infarction (TMI) 1 flow to the proximal ramus descendens anterior and proximal ramus circumflexus. The right coronary artery showed no abnorm- alities. PCI with stent implantation was performed, which resulted in recovery of coronary flow (Fig. 2B). The clinical condition improved immediately with resolution of chest pain and normalization of the blood pressure.

Soon after admission at the coronary care unit, severe chest discomfort returned with hypotension. The ECG showed a similar pattern of diffuse myocardial ischemia as was seen at admission. Because of relapse acute myocardial ischemia (ie, severe chest discomfort and ECG abnormal- ities) and hemodynamic collapse, an intra-aortic balloon pump was inserted and control coronary angiography was performed. This revealed no abnormalities. The patient became hemodynamic stable and pain free, and she returned to the coronary care unit for further observation. A review of the clinical examination revealed a diastolic murmur at the third intercostal space on the left. There was an aortic regurgitation confirmed by transthoracic echocardiography. The left ventricular function was normal without pericardial effusion. Because of the trias (1) dynamic pattern of acute myocardial ischemia, (2) unaltered control angiography, and

(3) aortic regurgitation, there was high suspicion of an aortic dissection involving the LMCA. Transesophageal echocardiography revealed an intimal flap directly above the aortic valve with severe eccentric aortic regurgitation (Fig. 3A and B). The patient was sent for emergency cardiothoracic surgery, which confirmed the dissection of the Ascending aorta with involvement of the left coronary artery. A valve-sparing aortic root replacement (Yacoub procedure) was done followed by replacement of the partial ascending aorta and aortic arcus. Postsurgery, the patient did

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Fig. 1 Electrocardiography showing signs of diffuse myocardial ischemia.

well and was shortly admitted to the intensive care unit. After 5 days, she was in a good clinical condition and transported back to our hospital for further rehabilitation.

The diagnosis of an acute Stanford type A aortic dissection remains a challenge for the emergency physi-

cian. This case illustrates the difficulty in the diagnosis of an aortic dissection, where the clinical symptoms resemble acute myocardial infarction complicated by cardiogenic shock. There are several case reports of acute myocardial infarction due to acute thoracic

Fig. 2 A, Coronary angiography of the left coronary artery before PCI. Right anterior oblique with cranial angulation. B, Coronary angiography of the left coronary artery after PCI and stenting of the LMCA. Left anterior oblique with cranial angulation.

Fig. 3 A, Transesophageal echocardiography with visualization of an intimal flap. B, Transesophageal echocardiography with visualization of an intimal flap with an eccentric aortic regurgitation.

dissection, all associated with high hospital mortality rates due to left ventricular dysfunction or death [1-9]. Myocardial infarction or ischemia complicating aortic dissection represents a critical situation with reported incidence of 3% and 5%, respectively [10]. It is well known that cardiogenic shock can be due to other factors than the infarction itself. The differential diagnosis of an acute aortic dissection should always be considered because more delay will result in a higher mortality rate. However, when confronted with a patient presenting with cardiogenic shock with the suspicion of an occluded LMCA based on the ECG, no time has to be wasted, and urgent transport with intent to Primary PCI is crucial [11,12]. Eventually, the interventional procedure in this patient was the right choice, allowing for survival of the patient and retrospectively subsequent correction of the diseased thoracic aorta. In addition, 3 case reports describe a similar and successful approach [7-9]. There are 3 main types of coronary lesion due to aortic dissection. Type A is a disruption of the inner layer limited to the area of the coronary ostium (ostial dissection), type B is a dissection extending to the inner layer, and type C is a coronary disruption (intimal detachment) [4]. In our case, the intermittently obstructing intimal aortic flap was the main etiology of the dynamic pattern of chest pain, ECG abnormalities, hypotension, and unaltered control coronary angiography.

Diagnosing acute Stanford type A aortic dissection with the uncommon involvement of the LMCA is difficult because it can resemble acute myocardial infarction with cardiogenic shock. Eventually, the dynamic pattern of (1) signs of acute myocardial ischemia, (2) relapse of hemodynamic collapse, and (3) unaltered control coronary angiography should immediately point to the probability of extrinsic coronary compression. In this case, the lifesaving element was primary coronary intervention

with stenting of the LMCA preventing extensive myo- cardial damage followed by a surgical correction of the aorta.

Cyril Camaro MD Department of Cardiology Rijnstate Hospital, PO Box 9555 6800 TA Arnhem, The Netherlands

E-mail addressess: [email protected],

[email protected]

Noemi T.A.E. Wouters MD

Department of Cardiology Radboud University Medical Centre 6500 HB Nijmegen, The Netherlands

Melvyn Tjon Joe Gin MD

Department of Cardiology Rijnstate Hospital, 6800 TA Arnhem

The Netherlands

Hans A. Bosker MD, PhD

Department of Cardiology Rijnstate Hospital, 6800 TA Arnhem

The Netherlands

doi:10.1016/j.ajem.2008.11.007

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