How does aortic regurgitation affect blood pressure?

How Aortic Regurgitation Affects Blood Pressure

Aortic regurgitation causes systolic hypertension with widened pulse pressure due to increased total stroke volume, while diastolic blood pressure decreases as blood regurgitates back into the left ventricle during diastole. 1, 2

Hemodynamic Changes in Chronic Aortic Regurgitation

Systolic Blood Pressure Effects

• Volume overload from significant AR leads to increased total stroke volume, resulting in systolic hypertension and afterload mismatch. 1
• The left ventricle ejects a larger total stroke volume to compensate for the regurgitant volume, which elevates systolic arterial pressure. 1, 2
• This systolic hypertension creates characteristic peripheral physical findings such as bounding pulses (water-hammer pulse). 2

Diastolic Blood Pressure Effects

• Diastolic blood pressure falls because blood regurgitates from the aorta back into the left ventricle throughout diastole, reducing aortic diastolic pressure. 1
• The aortic diastolic pressure equilibrates with the elevated LV diastolic pressure, particularly in acute severe AR. 1
• Lower diastolic blood pressure (DBP) is independently associated with increased mortality in chronic AR—each 10 mmHg decrease in DBP increases mortality risk (adjusted HR: 0.79, meaning lower DBP = higher mortality). 3
• Excess mortality rises steeply when DBP falls below 70 mmHg, peaking at 55 mmHg. 3

Pulse Pressure Widening

• The combination of elevated systolic pressure and reduced diastolic pressure creates a characteristically wide pulse pressure. 1, 2
• This widened pulse pressure accounts for many of the classic peripheral signs of chronic AR (Corrigan pulse, de Musset sign, Quincke pulse). 2

Acute vs. Chronic AR: Different Blood Pressure Patterns

Acute Severe AR

• Pulse pressure may NOT be increased in acute AR because systolic pressure is reduced and diastolic pressure equilibrates rapidly with elevated LV diastolic pressure. 1
• The sudden volume overload on a normal-sized, non-compliant ventricle causes dramatic increases in LV end-diastolic pressure, leading to pulmonary edema and cardiogenic shock. 1
• Patients frequently present with hypotension rather than hypertension. 1

Chronic Severe AR

• Compensatory eccentric LV remodeling initially normalizes wall stress and maintains forward stroke volume. 1
• The afterload excess from systolic hypertension leads to progressive LV dilation and eventual systolic dysfunction. 2

Clinical Implications for Blood Pressure Management

Hypertension Treatment in AR

• Systolic hypertension triples the average annual risk of cardiac events in chronic severe AR (8.47% vs 2.85% without hypertension). 4
• Blood pressure control with antihypertensive treatment is recommended for patients with AR and systolic BP >140 mmHg. 1, 5
• Use vasodilators that do NOT slow heart rate—specifically ACE inhibitors or dihydropyridine calcium channel blockers (e.g., nifedipine). 1, 5
• Beta blockers should be avoided because they prolong diastole and increase regurgitant volume, potentially worsening AR. 1, 5

Important Caveats

• While blood pressure control is recommended, antihypertensive therapy as a group has not been shown to improve outcomes in AR, and some agents may be deleterious. 4
• The goal of vasodilator therapy is to achieve significant decrease in systolic arterial pressure to reduce afterload and delay need for surgery. 2
• Marked reduction in DBP may lower coronary perfusion pressure in severe AR, though outcomes data supporting this theoretical concern are lacking. 1

Heart Rate Considerations

• Resting heart rate is independently associated with mortality in AR—each 10 bpm increase raises mortality risk (adjusted HR: 1.23). 3
• Excess mortality rises in direct proportion to heart rate starting at 60 bpm. 3
• AR severity is reduced at high heart rates as diastole shortens, even if systemic pressure rises. 1
• This explains why beta blockers are contraindicated—slowing heart rate prolongs diastolic filling time and increases regurgitant volume. 1, 5