Aortic Regurgitation¶
Chapter 273 | Part 6: Disorders of the Cardiovascular System
KEY CLINICAL POINTS¶
- Aortic regurgitation (AR) is caused by valvular disease, aortic root dilation, or trauma, with bicuspid aortic valve and infective endocarditis being common etiologies.
- Chronic AR leads to left ventricular (LV) dilation and hypertrophy, with hemodynamic compensation through increased preload and afterload.
- Clinical features include a holodiastolic murmur, widened pulse pressure, and signs of heart failure, with acute AR presenting as severe LV dysfunction and cardiogenic shock.
- Echocardiography is the cornerstone of diagnosis, with key parameters including regurgitant volume (RVol ≥ 60 mL), regurgitant fraction (RF ≥ 50%), and vena contracta (VC >0.6 cm).
- Surgical aortic valve replacement (AVR) is indicated for severe symptomatic AR or LV dysfunction, with valve-sparing techniques (e.g., David procedure) preferred when feasible.
1. DEFINITION & OVERVIEW¶
Aortic regurgitation (AR) is the abnormal retrograde flow of blood from the aorta into the left ventricle during diastole, resulting from structural abnormalities of the aortic valve or root. It may be acute or chronic, with distinct hemodynamic and clinical manifestations.
Table 273-1 Major Causes of Aortic Regurgitation¶
| VALVE LESION | ETIOLOGIES |
|---|---|
| Aortic regurgitation | Valvular |
| Congenital (bicuspid) | |
| Endocarditis | |
| Rheumatic fever | |
| Myxomatous (prolapse) | |
| Radiation | |
| Trauma | |
| Syphilis | |
| Ankylosing spondylitis | |
| Aortic root disease | |
| Aortic dissection | |
| Medial degeneration | |
| Marfan syndrome |
| VALVE LESION | ETIOLOGIES |
|---|---|
| Bicuspid aortic valve | |
| Nonsyndromic familial aneurysm | |
| Aortitis | |
| Hypertension |
1.1 Classification¶
AR is classified based on severity (mild, moderate, severe) and etiology (valvular, root, or traumatic). Severe AR is defined by RVol ≥ 60 mL, RF ≥ 50%, or VC >0.6 cm.
1.2 Hemodynamics¶
AR increases LV preload and afterload, leading to LV dilation and hypertrophy. Chronic AR is associated with preserved LV ejection fraction (LVEF) until late stages, while acute AR causes rapid LV dysfunction.
2. EPIDEMIOLOGY¶
AR is more common in men (75% of cases). Risk factors include Marfan syndrome, bicuspid aortic valve, chronic hypertension, and aortic dissection. Prevalence increases with age, and severe AR is associated with a 5–10% annual mortality risk.
2.1 Demographics¶
Approximately 3/4 of patients with pure valvular AR are men. Women predominate in cases of primary aortic root disease. Chronic AR may remain asymptomatic for 10–15 years.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
AR arises from valvular pathology (e.g., bicuspid valve, endocarditis) or aortic root dilation. Pathophysiology involves increased LV preload, compensatory hypertrophy, and eventual decompensation with heart failure.
3.1 Valvular Causes¶
Rheumatic fever, congenital bicuspid valve, infective endocarditis, and myxomatous degeneration are common valvular causes. Syphilis and ankylosing spondylitis may cause aortic media inflammation.
3.2 Aortic Root Disease¶
Marfan syndrome, medial degeneration, and aortic dissection cause root dilation. Aortic annular widening leads to regurgitation without primary valve involvement.
4. CLINICAL FEATURES¶
Chronic AR presents with dyspnea, orthopnea, and a holodiastolic murmur. Acute AR causes sudden LV dysfunction, pulmonary edema, and cardiogenic shock. Physical findings include Corrigan’s pulse and Duroziez’s sign.
4.1 Symptoms¶
Exertional dyspnea, anginal chest pain, and fatigue are common. Acute AR may present with syncope, hypotension, and pulmonary edema.
4.2 Physical Findings¶
A high-pitched, decrescendo diastolic murmur is heard best at the left sternal border. Corrigan’s pulse (water-hammer pulse) and Duroziez’s sign (to-and-fro murmur) are characteristic.
5. DIFFERENTIAL DIAGNOSIS¶
Differential diagnoses include mitral regurgitation, aortic stenosis, and hypertrophic cardiomyopathy. The Austin Flint murmur (mid-to-late diastolic murmur) may mimic mitral regurgitation.
5.1 Key Differentiators¶
AR is distinguished by a holodiastolic murmur, widened pulse pressure, and LV dilation. Mitral regurgitation presents with a pansystolic murmur and left atrial enlargement.
6. INVESTIGATIONS & DIAGNOSIS¶
Echocardiography is the primary diagnostic tool. Key findings include LV dilation, regurgitant jet width, and Doppler-derived parameters. Chest X-ray and cardiac catheterization may confirm severity.
6.1 Echocardiography¶
Echocardiography assesses LV size, regurgitant volume (RVol ≥ 60 mL), regurgitant fraction (RF ≥ 50%), and vena contracta (VC >0.6 cm). Color flow Doppler identifies jet width and flow reversal.
6.2 Imaging¶
Chest X-ray shows left ventricular enlargement and aortic dilation. Cardiac MRI and CT provide detailed anatomical assessment of the aortic root and valve.
7. MANAGEMENT & TREATMENT¶
Medical management includes vasodilators and diuretics for chronic AR. Acute AR requires urgent surgical intervention. Long-term management focuses on preventing LV decompensation and aortic aneurysm progression.
7.1 Medical Therapy¶
Vasodilators (e.g., ACE inhibitors, ARBs) reduce afterload. Diuretics manage fluid overload. Beta-blockers may be used cautiously in chronic AR to reduce LV workload.
7.2 Surgical Treatment¶
Aortic valve replacement (AVR) is indicated for severe symptomatic AR or LV dysfunction. Valve-sparing techniques (e.g., David procedure) are preferred when feasible.
7.3 Algorithm¶
- Assess severity via echocardiography (RVol, RF, VC). 2. Monitor asymptomatic patients with LV function ≥ 55% and LVESD ≤ 25 mm/m². 3. Operate for severe AR with symptoms, LV dysfunction, or aortic aneurysm. 4. Consider TAVI in high-risk patients.
8. PROGNOSIS & COMPLICATIONS¶
Chronic AR has a 5–10% annual mortality risk with LV dysfunction. Complications include heart failure, arrhythmias, and aortic dissection. Early intervention improves outcomes.
8.1 Prognostic Factors¶
Prognosis is worse with advanced LV dysfunction (EF ≤ 55%), LVESD >50 mm, or aortic root dilation. Early surgical intervention reduces mortality.
9. SPECIAL CONSIDERATIONS¶
Pregnancy requires close monitoring due to increased cardiac workload. Pediatric patients with BAV may need early intervention. Elderly patients with comorbidities face higher surgical risks.
9.1 Pregnancy¶
Pregnancy in AR patients increases risk of heart failure and aortic dissection. Close monitoring and antihypertensive therapy are essential.
10. KEY POINTS & CLINICAL PEARLS¶
- Chronic AR is managed with echocardiographic monitoring and medical therapy. 2. Acute AR requires urgent surgical intervention. 3. Valve-sparing techniques are preferred for bicuspid valve disease. 4. Early detection of LV dysfunction improves outcomes. 5. Long-term follow-up is critical for asymptomatic patients with mild AR.