Aortic Dissection

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.