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Penetrating Atherosclerotic Ulcer and Intramural Hematoma
Acknowledgment
The authors acknowledge the contributions of Dr. Raimund Erbel, Dr. Sofia Churzidse, Dr. Riccardo Gorla, and Dr. Alexander Janosi, who were the authors of this chapter in the previous edition.
Intramural hematoma (IMH) and penetrating atherosclerotic ulcers (PAU), along with acute aortic dissection (AD), are part of the spectrum of acute aortic syndromes, which involve disruption of the medial layer of the aortic wall ( Fig. 134.1 ). Of these, AD is the most common (62%–88%), followed by IMH (10%–30%) and PAU (2%–8%). Noninvasive imaging techniques—including echocardiography, computed tomography (CT), and magnetic resonance imaging (MRI)—play a crucial role in ensuring early and accurate diagnosis of these potentially life-threatening conditions. , This chapter focuses on the clinical presentation, etiology, and noninvasive imaging findings in IMH and PAU, along with guidance for diagnosis and management.
Acute aortic syndromes.
Adapted with permission, from Baliga RR, et al. The role of imaging in aortic dissection and related syndromes, JACC Cardiovasc Imag 7:406–424, 2014.
Intramural Hematoma
IMH is defined as the presence of blood or thrombus within the medial layer of the aortic wall but without evidence of overt communication with the aortic lumen or flow within the wall. Historically, IMH has been believed to result from rupture of the vasa vasorum, the small blood vessels that nourish the aortic media, leading to bleeding directly within the aortic media. However, more recent evidence suggests that many IMHs are caused by very small intimal tears that allow blood to seep into the medial layer and thrombose, preventing ongoing or visible flow within the media. IMHs are considered a variant of classic AD, accounting for approximately 10% to 25% of patients with acute aortic syndrome. In contrast to a classic AD, IMHs do not have a dissection flap, a reentry site, or the presence of a double-channel aorta. Importantly, the prognosis of IMH appears to be similar to that of classic acute dissection. ,
Clinical Presentation
Abrupt onset of severe pain in the chest or back is the typical presenting symptom of IMH, making it indistinguishable from classic AD on clinical grounds alone. Migration of the pain can be similar to AD but rarely reaches the legs. IMH tends to occur more frequently in the descending (Stanford type B) than the ascending thoracic aorta (Stanford type A). , Patients with IMH are less likely to develop aortic regurgitation or pulse deficits than patients with AD but are more likely to develop periaortic hematoma and pericardial effusion and are still prone to rupture. The most common risk factors include arterial hypertension, hypercholesterolemia, and a history of smoking; conversely, IMH is not commonly associated with Marfan syndrome or bicuspid aortic valves. Of note, IMH can also be caused by blunt trauma to the thorax or can be iatrogenic after catheter manipulations.
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