Editorial Comment: What really matters in aortic dissection?

Abstract

Aortic dissection affects between 5 and 30 people per million population per year, while the incidence of acute myocardial infarction exceeds 4400 per million per year [1]. More than 70% of dissection patients are hypertensive before the event and 30% have pre-existing aneurysmal dilatation of the ascending aorta [2]. Many are misdiagnosed on initial evaluation, and around 30% are discovered at autopsy [3]. It can be difficult to differentiate between dissection and myocardial infarction on clinical history or initial findings and this delays surgical repair. Seventy percent of dissection patients have electrocardiographic changes and around 25% manifest troponin elevation [4]. For those with troponin elevation, 14% have ST segment elevation, 14% ST depression and 36% T-wave inversion. Though dissection commonly involves the coronary ostia, an additional mechanism for troponin release is haemodynamic stress through acute aortic regurgitation. Those with troponin elevation have a four times elevated risk of early death [3]. Information from the International Registry of Acute Aortic Dissection (IRAD) shows that 15% of patients suffer acute myocardial ischaemia through coronary malperfusion and 3% present with myocardial infarction [1]. As for primary myocardial infarction, these patients are likely to experience myocardial stunning with cardiogenic shock or prehospital cardiac arrest. The overall number with combined dissection plus acute myocardial infarction is probably underestimated, because they die before reaching the hospital. While no one disputes the value of protocol-driven antiplatelet therapy or thrombolysis for myocardial infarction, this has become a frequent and unnecessary risk factor in aortic dissection surgery. Inhibition of coagulation promotes bleeding during surgical repair and, intuitively, it facilities the propagation of dissection by preventing thrombosis in the false lumen [5]. It provides the surgeon with a further taxing problem in an already difficult condition. Some prefer to postpone surgery until the coagulation profile is improved. So far, there is little evidence to support or refute this approach, but an interim death may raise concerns. During aortic root repair, it is common to find periostial dissection around the right coronary ostium, because the primary tear begins in the convexity with propagation of the false lumen proximally and distally. Periostial dissection is found less frequently in the left coronary sinus. Autopsy findings show the dissection to extend down the coronary artery through the outer one-third of the media in a circumferential or spiral passage. Haematoma within the vessel wall alters the tolerance of the coronary endothelium to shear stress, which may result in a secondary intimal tear. Narrowing of the true lumen by the false lumen or flap may interrupt flow. The process is similar to that of spontaneous coronary dissection, so lessons may be learnt from the treatment of that disorder [6]. Selective coronary angiography may worsen ischaemia if contrast injection increases pressure in the false lumen or the guide wire tears the delicate dissected membranes [7]. If extensive mural thrombus is present with no luminal flap, stenting may simply displace haematoma proximal or distal to the stent. Long segments of stent may be needed to completely exclude the false lumen. In spontaneous coronary dissection, intravascular ultrasound is recommended to guide stent deployment, but if the lumen remains adequate, conservative management is advisable [7]. Coronary bypass surgery is an option, but because of branch occlusion by dissection, this may not revascularize the ischaemic territory. Surgical revascularization is also rarely achieved soon enough to abort the infarction process. In this issue, Imoto et al .[ 8] retrospectively review 516 acute Type A dissection patients, 15% of whom had coronary artery involvement documented variously by direct intraoperative inspection, coronary angiography or echocardiographic detection of wall motion abnormality. Of those with coronary dissection, 64% had myocardial ischaemia. The right coronary was most frequently affected, with the left coronary involved in only 32 (6%) of the 516 patients. Left coronary artery involvement was associated with widespread anterolateral ischaemia, ST segment elevation, extensive hypokinesia and low cardiac output state. While the overall mortality for coronary dissection patients was 24%, it was 7.4% in those without ischaemia vs 33% for those with. Relative mortalities were 15% for right coronary involvement, 47% for left main dissection and 100% when both coronaries were involved. Specific risk factors for mortality were myocardial ischaemia, left main coronary involvement and preoperative cardiac arrest. Patients with widespread anterolateral ischaemia, low cardiac output state and preoperative cardiopulmonary resuscitation had universally poor outcome. This led the authors to suggest that preoperative stenting of the left main stem is advisable before surgical repair when left coronary involvement is suspected. This occurred in only 7 (1.35% of all)