 Introduction/Background Acute aortic syndrome (AAS) includes the entities of acute aortic dissection (AD), intramural hematoma (IMH), and penetrating atherosclerotic ulcer (PAU). AAS typically presents with sudden onset of severe, tearing, anterior, or interscapular back pain [1]. Symptoms may be dominated by malperfusion syndrome due to obstruction of the lumen of the aorta and/or a side branch when the intimal and medial layers are separated. Risk factors include hypertension, family history, and underlying collagen vascular disorders [2]. Timely diagnosis of AAS is crucial to permit prompt management; early mortality rates are reported to be 1% to 2% per hour after the onset of symptoms for untreated ascending AD [3]. Medical management of acute ascending AD is associated with a mortality rate of nearly 20% by 24 hours after presentation, 30% by 48 hours, 40% to 70% by day 7 [4], and 50% by 1 month [3,5]. The major cause of early death with AAS is aortic rupture [6]. AAS limited to the descending aorta may be managed medically and/or with open surgical or endovascular treatment based on extent of disease, aortic size, malperfusion of end organs, and clinical parameters; medical management is usually undertaken unless the aorta is dilated and/or there is mesenteric or limb ischemia [6]. IMH occurs with approximately 10% of the frequency of AD [7], and can be seen in isolation or in conjunction with AD and PAU. Imaging findings of AAS include any disruption of the intimal and medial layers, either with an IMH within the media (with or without the presence of a penetrating ulcer) or with an intimal flap. The prevalence of isolated IMHs in patients with suspected AAS is reported to be 21% to 30% [3]. Over time, 28% to 47% of patients may progress to a classic AD, and in other patients, the IMH will resolve with or without aneurysmal enlargement of the aorta [6]. PAUs that disrupt the intima most commonly occur in the mid and distal descending aorta [8].
Suspected Acute Aortic Syndrome.  Introduction/Background Acute aortic syndrome (AAS) includes the entities of acute aortic dissection (AD), intramural hematoma (IMH), and penetrating atherosclerotic ulcer (PAU). AAS typically presents with sudden onset of severe, tearing, anterior, or interscapular back pain [1]. Symptoms may be dominated by malperfusion syndrome due to obstruction of the lumen of the aorta and/or a side branch when the intimal and medial layers are separated. Risk factors include hypertension, family history, and underlying collagen vascular disorders [2]. Timely diagnosis of AAS is crucial to permit prompt management; early mortality rates are reported to be 1% to 2% per hour after the onset of symptoms for untreated ascending AD [3]. Medical management of acute ascending AD is associated with a mortality rate of nearly 20% by 24 hours after presentation, 30% by 48 hours, 40% to 70% by day 7 [4], and 50% by 1 month [3,5]. The major cause of early death with AAS is aortic rupture [6]. AAS limited to the descending aorta may be managed medically and/or with open surgical or endovascular treatment based on extent of disease, aortic size, malperfusion of end organs, and clinical parameters; medical management is usually undertaken unless the aorta is dilated and/or there is mesenteric or limb ischemia [6]. IMH occurs with approximately 10% of the frequency of AD [7], and can be seen in isolation or in conjunction with AD and PAU. Imaging findings of AAS include any disruption of the intimal and medial layers, either with an IMH within the media (with or without the presence of a penetrating ulcer) or with an intimal flap. The prevalence of isolated IMHs in patients with suspected AAS is reported to be 21% to 30% [3]. Over time, 28% to 47% of patients may progress to a classic AD, and in other patients, the IMH will resolve with or without aneurysmal enlargement of the aorta [6]. PAUs that disrupt the intima most commonly occur in the mid and distal descending aorta [8].