The aortic valve controls the flow of oxygenated blood from the heart’s main pumping chamber, the left ventricle, into the aorta. Normally, the valve opens fully during contraction and closes tightly to prevent backflow. Aortic Valve Regurgitation (AR), or aortic insufficiency, occurs when the valve leaflets do not close completely, causing a leak. This leakage allows blood to flow backward into the left ventricle. This backward flow forces the heart to handle a greater volume of blood, compelling it to work harder to maintain effective circulation.
Understanding the Mechanics of Aortic Regurgitation
The aortic valve typically consists of three small flaps of tissue, called cusps or leaflets, which open and close with each heartbeat. In aortic regurgitation, these cusps fail to meet properly during diastole, the heart’s relaxation phase. This structural failure creates a gap, forcing blood from the high-pressure aorta back into the low-pressure left ventricle.
This backward flow, known as the regurgitant jet, immediately increases the total volume of blood the chamber must hold before its next contraction. This condition is termed volume overload. To accommodate the increased volume, the left ventricle begins to dilate, or enlarge, in a process known as eccentric hypertrophy.
The increased volume requires the heart to contract with greater force to eject enough blood into the aorta. This cycle of overfilling and forceful contraction increases pressure within the ventricle. A defining characteristic of this process is a widening of the pulse pressure, where the systolic pressure rises and the diastolic pressure drops significantly due to the rapid backflow.
Common Triggers and Risk Factors
The primary causes of aortic regurgitation damage the valve cusps or lead to the dilation of the aortic root, pulling the cusps apart. A common cause is a congenital defect, such as a bicuspid aortic valve, where the valve has only two leaflets instead of three.
Another significant trigger is infective endocarditis, a bacterial infection that rapidly destroys valve tissue, leading to acute, severe regurgitation. Chronic conditions also play a role, including uncontrolled high blood pressure, which stretches the aortic root, and rheumatic heart disease, which causes the valve to become stiff or damaged. Age-related wear and tear and calcification are increasingly frequent causes of chronic aortic regurgitation. Connective tissue disorders, such as Marfan syndrome, can also predispose individuals by causing the aorta to widen and weaken.
How Aortic Regurgitation Affects the Body
The heart’s continuous struggle with volume overload eventually leads to physical symptoms and long-term changes. The constant overfilling causes the left ventricle to remodel, becoming enlarged and dilated. While this initial compensation allows the heart to maintain function for years, the muscular walls can eventually become stretched and weakened, resulting in heart failure.
Patients often experience shortness of breath, particularly during physical activity, as the heart struggles to pump sufficient blood forward. As the condition progresses, fluid backing up into the lungs can cause difficulty breathing when lying flat (orthopnea) or waking up suddenly feeling breathless. Persistent fatigue and generalized weakness, especially with exertion, are also common due to ineffective circulation.
The forceful heartbeat required to compensate for the leak can manifest as heart palpitations, felt as a rapid or fluttering heart rate. Some individuals may also experience chest pain, similar to angina, often noticeable at night. In advanced stages, reduced blood flow to the brain can cause lightheadedness or fainting spells (syncope).
Diagnostic Procedures
The initial step involves a physical examination where a healthcare professional listens to the heart. The characteristic finding is a specific heart murmur—a blowing, high-pitched sound heard during diastole. Physical signs of severe disease, such as a widened pulse pressure, may also be noted.
The definitive diagnostic tool is the transthoracic echocardiogram (TTE). The TTE allows physicians to visualize the aortic valve structure, measure the size and function of the left ventricle, and assess the severity of the backflow using Doppler ultrasound. If TTE images are unclear or more detail is needed, a transesophageal echocardiogram (TEE) or cardiac MRI may be performed.
Further evaluation includes an electrocardiogram (EKG) to check for abnormal heart rhythms or signs of left ventricular enlargement. A chest X-ray can also provide visual evidence if the heart or aorta has become enlarged. These combined tests help determine the overall impact and guide the timing of intervention.
Treatment Pathways
The management of aortic regurgitation is tailored to the severity of the leak, symptoms, and the degree of left ventricular damage. For patients with mild or moderate regurgitation who are asymptomatic, the treatment is active surveillance. This involves regular monitoring with physical exams and periodic echocardiograms to detect progression.
Medication is used primarily to manage associated symptoms and control blood pressure, reducing strain on the heart. Angiotensin-converting enzyme (ACE) inhibitors or calcium channel blockers are often used to reduce the afterload, the resistance the heart must pump against. Medical therapy does not fix the valve itself; its purpose is to delay the need for surgical intervention and manage risk factors.
Surgical intervention is necessary for patients who develop symptoms or show signs of severe left ventricular dysfunction or excessive enlargement. The most common procedure is Aortic Valve Replacement (AVR), where the damaged valve is replaced with a mechanical or tissue valve.
Valve Repair and Replacement Options
In some cases, a valve-sparing repair procedure may be an option if the leaflets are structurally sound. Transcatheter Aortic Valve Replacement (TAVR), a minimally invasive approach primarily used for aortic stenosis, is currently being investigated for pure aortic regurgitation. The decision for surgery is timed precisely to prevent permanent heart damage, guided by measurements of the left ventricle’s size and function.