A 68-year-old male with a 15-year history of poorly controlled hypertension presents to the emergency department with acute-onset, severe "tearing" chest pain radiating to the back. On examination, blood pressure is 165/95 mmHg in the right arm and 135/80 mmHg in the left arm. A new early diastolic decrescendo murmur is heard at the left sternal border. Chest X-ray shows widened mediastinum. CT angiography confirms acute aortic dissection involving the ascending aorta with an intimal flap. The structure marked **A** in the diagram represents the primary intimal tear. Which of the following pathophysiological mechanisms best explains the formation of this tear in the setting of chronic hypertension?

Explanation

## Why cystic medial degeneration is correct The clinical anchor directly states that **pathogenesis of aortic dissection involves cystic medial degeneration (CMD) — loss of elastin and smooth muscle with mucoid pooling — which weakens the aortic wall and predisposes to intimal tear under pulsatile pressure**. Chronic hypertension is the most important risk factor (~70% of cases), and it drives progressive CMD through sustained hemodynamic stress. The intimal tear at **A** occurs when the weakened media can no longer withstand the pulsatile forces transmitted through the aortic wall. This is the foundational pathophysiological mechanism taught in Sabiston and is essential to understanding why hypertensive patients are at highest risk for Type A dissection. ## Why each distractor is wrong - **Atherosclerotic plaque rupture**: While atherosclerosis is listed as a risk factor, it is NOT the primary pathophysiological mechanism of dissection. Atherosclerotic disease causes intimal ulceration and thrombosis, not the medial degeneration that creates the dissection plane. Atherosclerosis is a secondary risk factor, not the fundamental mechanism of intimal tear formation. - **Fibrillin-1 gene mutation**: This is the genetic basis of Marfan syndrome, which is a connective tissue disorder that predisposes to dissection. However, this patient has hypertension as the primary risk factor, not a genetic syndrome. Fibrillin mutations cause dissection through a different mechanism (abnormal TGF-β signaling and elastic fiber defects) and are not the explanation in this hypertensive patient. - **Syphilitic aortitis**: This is a historical cause of aortic disease (tertiary syphilis) but is now rare in developed countries and is NOT the mechanism in this hypertensive patient. Syphilitic aortitis causes inflammation of the vasa vasorum, not cystic medial degeneration. **High-Yield:** Cystic medial degeneration (loss of elastin/smooth muscle) + chronic hypertension = weakened media → intimal tear under pulsatile stress. This is the dominant pathophysiology of Type A dissection. [cite: Sabiston Textbook of Surgery 21e, Ch 60 — Diseases of the Thoracic Aorta]