In aortic dissection, a tear in the tunica intima permits blood to enter the tunica media, leading to vessel wall dilation resembling an aneurysm and the creation of true and false lumens. The most critical risk factor for this condition is chronic hypertension, although acute elevations in blood pressure, as with cocaine or amphetamine use, can also precipitate it. The condition predominantly occurs in older males, typically > 60. Genetic syndromes like Marfan syndrome, characterized by a mutation in fibrillin leading to defective elastic tissue, and Ehlers-Danlos, involving disorders of Type III collagen production, predispose younger individuals to aortic dissection.
Iatrogenic factors, such as cardiac catheterization, can also damage the intimal layer, leading to aortic dissection. The condition is frequently associated with intimal damage and vessel wall weakening, often seen in aortic aneurysms. Cystic medial degeneration, a process leading to mucoid degeneration of the medial smooth muscle layer, further weakens the vessel walls, making them more prone to aortic dissection. Anatomically, dissections most commonly occur in the aortic arch, with up to 30% of thoracic aortic dissections taking place at the takeoff of the left subclavian artery, an area subjected to high hemodynamic stress.
Classification of aortic dissections utilizes the Stanford and DeBakey systems. In the Stanford system, those involving the ascending aorta are classified as type A, including those that extend to the descending aorta. Dissections involving only the descending aorta are classified as type B. In the DeBakey system, aneurysms involving both the ascending and descending aorta are type I, those in the ascending aorta alone are type II, and those in the descending aorta, distal to the left subclavian artery, are type III. Clinically, descending thoracic aortic dissections (type B or III) often present with tearing back or posterior chest pain, most commonly between the scapulae. In contrast, ascending thoracic aortic dissections (type I, II, or A) frequently manifest as tearing anterior chest pain radiating to the back.
Clinical presentation varies based on the type of aortic dissection and the vessels involved. Ascending thoracic aortic dissections often manifest as anterior chest pain radiating to the back and can result in complications such as myocardial ischemia leading to MI. They may also expand proximally, causing dilation of the aortic annulus and acute aortic regurgitation, which manifests as a new onset decrescendo diastolic murmur and can lead to acute heart failure and cardiogenic shock. In extreme cases, ascending dissections may rupture into the pericardium, resulting in cardiac tamponade.
On the other hand, descending thoracic dissections usually present with posterior chest pain and can extend to occlude carotid arteries, leading to reduced cerebral blood flow, syncope, ischemia, and ischemic stroke. Aortic dissections can even extend to the aortic bifurcation and occlude the iliac arteries, causing pulselessness and ischemia in the lower extremities.
Both types can result in end-organ dysfunction, such as renal failure, mesenteric ischemia, and spinal cord ischemia, depending on the vessels occluded. Additionally, they may present with signs and symptoms of cardiogenic shock, which could be secondary to myocardial infarction, severe aortic regurgitation, or cardiac tamponade. Furthermore, large amounts of blood can be diverted from the systemic circulation to the false lumen, leading to hypotension or even hypovolemic shock. Progressive vessel wall weakening may result in aortic rupture.
Imaging studies, including chest x-ray, often reveal a widened mediastinum due to aortic dilation. CT angiography typically shows a widened aorta with a 'double lumen' separated by a dark band of tissue, representing the flap of dissected intimal tissue. Management often involves strict blood pressure control to mitigate the spread of the dissection and to decrease the risk of further complications.
An aortic dissection is precipitated by a tear in the tunica intima, the innermost layer of the aorta. This allows blood to enter and expand the tunica media, the middle layer consisting of smooth muscle. The leading risk factor is chronic hypertension, although acute spikes in blood pressure due to substances like cocaine can also be culprits. Age, particularly in males over 60, and genetic conditions such as Ehlers-Danlos and Marfan syndromes further contribute to the risk. Iatrogenic causes like cardiac catheterization and pre-existing aortic aneurysms can also weaken the aortic wall.
The classification of thoracic aortic dissections depends on whether the ascending or descending aorta is involved. Dissections involving the ascending aorta are classified as Type A in the Stanford system, even if they spread to the descending aorta. On the other hand, thoracic aortic dissections involving only the descending aorta are classified as Type B. The DeBakey system, however, classifies thoracic aortic aneurysms involving both the ascending and descending aorta as Type I, those involving only the ascending aorta as Type II, and those involving only the descending aorta as Type III.
Symptoms of aortic dissection may vary depending on the location. Descending thoracic dissections typically cause tearing pain in the back or chest, whereas ascending dissections present with anterior chest pain radiating to the back. Potential complications include ischemia and stroke due to occlusion of carotid arteries, and ischemia in the lower extremities from iliac artery involvement. Aortic dissection can expand and occlude any vessel branching from the aorta, leading to end organ dysfunction such as renal failure and mesenteric ischemia.
An ascending aortic dissection can block the coronary ostia, which arise from the proximal ascending aorta, leading to myocardial ischemia or MI. The dissection can expand proximally and involve the aortic root, resulting in dilation of the aortic annulus and acute aortic regurgitation. This can consequently lead to acute heart failure and cardiogenic shock. Ascending aortic dissection may disrupt the pericardium, leading to cardiac tamponade.
Initial suspicion of aortic dissection may arise from a chest X-ray showing a widened mediastinum, indicative of aortic dilation. For a more definitive diagnosis, CT angiography is often employed, revealing characteristic features such as a "double lumen" in the aorta separated by a dark band. This dark band represents the dissected flap of the tunica intima. Throughout the diagnostic process, meticulous blood pressure management is crucial to minimize further propagation of the dissection.