Aortic Dissection – Symptoms, Types & Pathophysiology

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Aortic dissection is relatively uncommon, but it often presents acutely as a catastrophic illness with severe chest pain and acute hemodynamic compromise. Early and accurate diagnosis and treatment are crucial for survival.
Death from aortic dissection can be related to rupture of the dissection into the pericardium precipitating cardiac tamponade, acute dissection into the aortic valvular annulus leading to severe aortic regurgitation, obstruction of the coronary artery ostia leading to myocardial infarction, and end-organ failure due to abdominal aortic branch vessel obstruction.
The primary event in aortic dissection is a tear in the aortic intima. Degeneration of the aortic media, or cystic medial necrosis, is felt to be a prerequisite for the development of nontraumatic aortic dissection. Blood passes into the aortic media through the tear, separating the intima from the surrounding media and/or adventitia, and creating a false lumen. It is uncertain whether the initiating event is a primary rupture of the intima with secondary dissection of the media, or hemorrhage within the media and subsequent rupture of the overlying intima.
Fifty to 65 percent of aortic intimal tears originate in the ascending aorta within the sinotubular junction and extend to involve remaining portions of the thoracoabdominal aorta. Approximately 20 to 30 percent of intimal tears will originate in the vicinity of the left subclavian artery and extend into the descending thoracic and thoracoabdominal aorta. The commonality of these two predominant locales for development of the aortic tear is hypothesized to be related to shear forces (dP/dT) being highest in these regions.
The dissection can propagate proximally or distally to involve the aortic valve and enter the pericardial space, or branch vessels. Such propagation is responsible for many of the ischemic clinical manifestations, including aortic regurgitation, cardiac tamponade, or ischemia (coronary, cerebral, spinal, or visceral). Patients with involvement of the ascending aorta have imminent risk for aortic rupture. The intimal tear with type B dissection can spiral into a cleavage plane within the media of the aorta along the posterolateral descending thoracic aorta, leaving the celiac artery, superior mesenteric artery, and right renal artery, typically originating in the true lumen, with the left renal artery deriving false lumen flow. Variations in anatomy of the dissection are typical and underscore the critical need for proper axial imaging. In addition, multiple communications may form between the true lumen and the false lumen.
Immediately following dissection, there is “intrinsic true lumen collapse” to a variable degree, and false lumen dilation, thus increasing the aortic cross-sectional area. The increase of the false lumen area correlates with blood pressure, the size of the entry tear into the false lumen, the depth of the dissection plane within the media, and the percentage of aortic circumference involved. Because the outer wall of the false lumen is thinned, it expands to generate the necessary wall tension to accommodate aortic pressure. The true lumen collapses as a result of the pressure differential between the true and false lumens, and may be exacerbated by the intrinsic recoil of the muscular elements within the dissection flap.
Malperfusion of aortic branch vessels may occur due to the extension of the dissection throughout the thoracoabdominal aorta. Malperfusion of a vascular bed can occur in one or more branch territories simultaneously. The standard nomenclature of the mechanisms of malperfusion of aortic branch vessels is termed “dynamic obstruction” and “static obstruction”. Malperfusion syndromes may occur in 30 to 45 percent of descending dissections and correlate with early mortality.

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