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Clinical Letter

Near-fatal acute dissection of the thoracic aorta involving the right coronary artery

Chevalley, C*; Montessuit, M; Murith, N; Licker, M*

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European Journal of Anaesthesiology (EJA): November 2000 - Volume 17 - Issue 11 - p 709-711
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Aortic dissection is the most common acute disease involving the ascending aorta and carries a high mortality rate if surgical therapy is not initiated rapidly after the onset of symptoms [1]. Therefore, timely recognition of this situation coupled with urgent and appropriate management is the key to a successful outcome [2].


A 47-year-old Caucasian male (weight 95 kg, body surface area 2.1 m2) with hypertension treated by diuretics was urgently referred to our hospital because of an excruciating thoracic pain that radiated into the lumbar area and the lower limbs. His mental status was normal, initial arterial pressure (110/70 mmHg in the left arm and 120/75 mmHg in the right arm) and heart rate (HR, 80 beats per min) were stable and chest auscultation revealed soft heart sounds with a 2/6 systolic-diastolic murmur over the aortic area. Arterial and intravenous (i.v.) cannulae were rapidly inserted for direct arterial pressure monitoring and eventual fluid resuscitation. An electrocardiogram (ECG) showed sinus rhythm with a normal conduction time and repolarization phase. Clear lung fields and an enlarged aortic knob were observed on radiography. An ascending aortic dissection was diagnosed by transoesophageal echocardiography (TOE) as evidenced by a double-lumen aorta divided by a moving intimal flap.

During the transfer to the operating room, the patient suffered a cardiac arrest from ventricular fibrillation. Cardiopulmonary resuscitation including closed chest massage, mask ventilation, epinephrine (150 μg i.v.), an i.v. fluid challenge (500 mL of lactated-Ringer's solution) and an external electrical shock (300 J) allowed the resumption of a spontaneous circulation (BP 100/60 mmHg, HR 120 beats per min) and consciousness was regained. A two-lead ECG showed sinus rhythm without evidence of myocardial ischaemia. After induction of anaesthesia with etomidate 20 mg and succinylcholine 100 mg, the trachea was intubated and the surgeon rapidly cannulated the femoral vessels to initiate cardiopulmonary bypass (CPB). A second TOE examination showed a type A acute dissection of the aorta extending to the right coronary artery, the descending aorta and the arch arteries; left ventricular function appeared normal with no segmental wall motion abnormalities; importantly, aortic regurgitation was associated with enlargement of the ascending aorta and diastolic prolapse of the dissecting flap through the aortic valve orifice into the left ventricular outflow tract (Fig. 1). CPB was established with systemic cooling at 24°C. After aortic cross-clamping, cold blood cardioplegia was administered through both coronary ostia. The surgeon identified an intimal tear 2 cm above the aortic valve and confirmed the aortic dissection extending into the right coronary artery. A combined mechanical valve-Dacron graft was used, the left coronary ostium was reimplanted and an aortovenous graft was anastomozed to the vertical part of the right coronary artery. Thereafter, the patient was rewarmed and weaned from CPB with a low-dose infusion of epinephrine. Postoperatively, recovery was uneventful, except for increased serum troponin concentration (29 μg ml−1 at 24 h) unaccompanied by ST segment abnormalities or Q waves in the ECG; furthermore, transthoracic echocardiography showed normal left ventricular function without regional dyskinesia. The patient was discharged from the hospital on the 10th postoperative day and has fully resumed his previous professional activity.

Fig. 1
Fig. 1:
Longitudinal view through the ascending aorta (AA), originating near the sinus of Valsalva. (a) Image taken in systole shows the opening of the aortic valve (AV) and the 'true' and 'false' lumens (TL, FL) separated by the intimal flap (arrows). (b) In diastole, the intimal flap prolapses into the left ventricular outflow tract (LVOT), resulting in aortic regurgitation.


In addition to immediate mortality, about 10% of patients admitted to hospital with acute aortic dissection die before surgery can be attempted and this may be due to the aortic rupture, cardiac tamponade, myocardial infarction or heart failure [3]. In patients with acute chest pain, non-invasive diagnostic techniques such as TOE and magnetic nuclear resonance may identify pathological aortic lesions and abnormal heart function: therefore they contribute to improved survival after surgical therapy. Although aortic dissection should be considered in any patient with sudden and severe chest pain, other causes such as myocardial infarction should be excluded in order to prevent inappropriate institution of thrombolytic therapy. TOE is a reliable and fast non-invasive method for the diagnosis of aortic dissection and its possible sequelae, e.g. aortic valve regurgitation, pericardial or pleural effusion and ventricular wall motion abnormalities [4]. Correct and rapid identification of the origin and extent of aortic dissection as well as associated coronary artery disease has a significant impact on surgical management. Angiography is a risky procedure and it delays life-saving surgery in patients with unstable haemodynamic conditions. Nevertheless, in stable patients with cardiovascular risk factors, some surgeons might advocate angiography before surgery to exclude significant coronary artery disease [5].

Extension of the dissection into the coronary arteries is considered as an indication for urgent myocardial revascularization [6]. In patients with type A aortic dissection, involvement of the right coronary artery or both coronary arteries has been reported in as much as 21% or 9% respectively [7]. In these patients with ongoing myocardial ischaemia/infarction, ST segment changes are not always seen because of the presence of pericardial effusion, intermittent coronary obstruction or inadequate placement of the ECG leads [8].

Several reasons could explain the occurrence of ventricular fibrillation as a result of a temporary deficit in coronary perfusion. First, during transfer to the operating room, transient arterial hypotension could induce myocardial ischaemia particularly in a patient with coronary artery stenosis. Second, retrograde extension of the aortic dissection into the right coronary artery, or haematoma formation, or both, in the anterolateral wall of the aorta could progressively obstruct the right coronary artery. Third, dynamic diastolic backward motion of the intimal flap could lead to obstruction of the right ostium, seen during TOE examination. Diastolic obstruction of the right ostium by the intimal flap and the collapse of the true aortic lumen could be aggravated by hypovolaemia and/or arterial vasodilation induced by nitroglycerin [9].

In our patient, the haemodynamic conditions rapidly improved after electrical defibrillation, i.v. fluid resuscitation and low-dose epinephrine, hence dynamic obstruction of the right ostium by the aortocoronary intimal flap was the most likely mechanism. Furthermore, the surgeon confirmed the dissection of the right coronary artery and excluded haematoma formation.

This is an unusual case of successful resuscitation after cardiac arrest due to transient myocardial ischaemia resulting from aortic and right coronary artery dissection. Cardiac function fully recovered after surgery and transient elevation of serum troponin clearly indicated the occurrence of myocardial ischaemia/reperfusion injury. In contrast to aortic rupture that invariably leads to death, aortocoronary dissection with diastolic inward motion of the intimal flap is amenable to life-saving medical and surgical management.


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ANEURYSM, DISSECTING, aortic dissection; ARTERIES, aorta, thoracic; ECHOCARDIOGRAPHY, transoesophageal

© 2000 European Academy of Anaesthesiology