Atrioventricular Valves: Anatomy, Structure, and Imaging

The atrioventricular (AV) valves ensure unidirectional blood flow through the heart, preventing backflow and maintaining efficient circulation. Understanding their structure and imaging is essential for diagnosing and managing heart conditions.

Anatomy And Function

The AV valves, consisting of the tricuspid and mitral valves, regulate blood flow between the atria and ventricles. The tricuspid valve, on the right, separates the right atrium from the right ventricle, while the mitral valve, on the left, connects the left atrium to the left ventricle. These valves open and close in response to pressure changes, ensuring forward blood flow without regurgitation.

Each valve is composed of leaflets, chordae tendineae, and papillary muscles, which maintain structural integrity during the cardiac cycle. The tricuspid valve typically has three leaflets—anterior, posterior, and septal—while the mitral valve has two—anterior and posterior. Chordae tendineae, fibrous strands, anchor the leaflets to the papillary muscles in the ventricles. During ventricular contraction, the papillary muscles contract, preventing leaflet prolapse into the atria and ensuring a secure closure.

The opening and closing of the AV valves are governed by pressure differentials. During diastole, when the ventricles relax, atrial pressure exceeds ventricular pressure, causing the valves to open. As the ventricles contract during systole, rising pressure forces the valves shut, preventing backflow. This process is synchronized with the heart’s electrical conduction system, particularly the atrioventricular node, which delays ventricular contraction to allow complete atrial emptying before closure.

Structural Features

The AV valves are specialized to withstand the significant forces of the cardiac cycle. Their leaflets, made of dense connective tissue with collagen and elastin, provide durability and flexibility. The fibrous skeleton of the heart anchors the valve annuli, maintaining structural integrity and electrically insulating the atria from the ventricles.

Beneath the leaflets, the extracellular matrix (ECM) consists of three layers: the fibrosa, spongiosa, and ventricularis. The fibrosa, on the atrial side, contains collagen for tensile strength. The spongiosa, a middle layer of proteoglycans and glycosaminoglycans, absorbs mechanical stress. The ventricularis, adjacent to the ventricular side, has elastin fibers that enhance flexibility. This multilayered organization ensures durability and responsiveness.

The chordae tendineae, extending from the leaflets to the papillary muscles, prevent prolapse. Primary chordae bear most of the load, while secondary and tertiary chordae provide additional support. The papillary muscles, embedded in the ventricular walls, contract with ventricular systole, maintaining tension on the chordae tendineae to ensure proper valve closure.

Coordination With Blood Flow

The AV valves regulate intracardiac blood movement, responding to pressure fluctuations. As the atria fill with blood, the pressure differential dictates valve behavior. When ventricular pressure falls below atrial pressure during diastole, the valves open, allowing blood to flow into the ventricles. Atrial contraction provides an additional boost before systole.

As the ventricles contract, rising pressure forces the AV valves to close, preventing retrograde blood flow. This process is synchronized by the heart’s electrical conduction system to optimize efficiency. Any delay in closure can lead to hemodynamic inefficiencies, increasing cardiac workload and predisposing individuals to conditions like atrial dilation or pulmonary congestion.

The papillary muscles contract with ventricular systole, maintaining tension on the chordae tendineae and preventing leaflet prolapse. This coordination ensures the valves form a complete seal, minimizing regurgitation and allowing the heart to sustain high cardiac output under varying physiological demands.

Advanced Imaging Techniques

Modern imaging provides detailed visualization of AV valve morphology and function. Echocardiography is the primary diagnostic tool, with transthoracic echocardiography (TTE) offering real-time images of valve motion. Doppler echocardiography measures blood flow velocities to assess regurgitation or stenosis. Transesophageal echocardiography (TEE) provides higher resolution for posterior structures and subtle abnormalities.

Cardiac magnetic resonance imaging (CMR) offers high soft tissue contrast and quantitative analysis of valve dynamics. Using phase-contrast sequences, CMR measures blood flow across the AV valves, assessing regurgitant volume and orifice area. This is particularly useful when echocardiographic findings are inconclusive.

Multidetector computed tomography (MDCT) is valuable for assessing valvular anatomy, particularly in preoperative planning. Its high spatial resolution allows precise measurement of annular dimensions, leaflet thickness, and calcification, aiding surgical and transcatheter interventions.

Common Abnormalities

AV valve dysfunction can impair cardiac efficiency, leading to conditions ranging from mild insufficiency to severe heart failure. Structural abnormalities may arise from congenital defects, degenerative changes, or increased cardiac stress. These dysfunctions often manifest as regurgitation, where the valve fails to close properly, or stenosis, where leaflet thickening or calcification obstructs blood flow. Left untreated, these conditions can contribute to atrial enlargement, pulmonary hypertension, and reduced cardiac output, requiring medical or surgical intervention.

Mitral valve prolapse (MVP) affects approximately 2-3% of the population and results from myxomatous degeneration. Excess connective tissue weakens the valve leaflets, causing them to bulge into the left atrium during systole. While often asymptomatic, severe prolapse can lead to mitral regurgitation, increasing the risk of atrial fibrillation and heart failure.

Tricuspid regurgitation frequently develops due to right ventricular dilatation from pulmonary hypertension or left-sided heart disease. Tricuspid stenosis, though less common, typically results from rheumatic heart disease, restricting valve opening and impairing venous return.