What Is Eccentric Hypertrophy of the Heart?

Hypertrophy describes an increase in the size of an organ or tissue because the component cells themselves have grown larger. When this process affects the heart, it is called cardiac hypertrophy, which is the heart’s way of adapting to a consistently high workload. Eccentric hypertrophy (EH) is a specific type of heart enlargement driven by chronic volume overload. It results in a structural change that allows the heart to accommodate a greater volume of blood, distinguishing it from other forms of cardiac remodeling.

Definition and Structural Characteristics

Eccentric hypertrophy develops as an adaptation to chronic volume overload, such as a leaky heart valve or high cardiac output states. This persistent increase in the amount of blood filling the ventricle during the resting phase, known as preload, leads to significant stretching of the heart muscle. The muscle cells, called cardiomyocytes, respond to this sustained stretch by synthesizing new contractile units, sarcomeres, and adding them end-to-end, or “in series.”

The addition of sarcomeres in series causes the individual cardiomyocytes to lengthen, leading to the characteristic structural change of eccentric hypertrophy. The overall size of the ventricular chamber increases dramatically, a process known as dilation. While the wall thickness may also increase, the enlargement of the chamber diameter is proportional or greater than the thickening of the wall.

This remodeling is characterized by an increase in the left ventricular mass with a normal or low relative wall thickness (RWT), defined as the ratio of the wall thickness to the chamber radius. Essentially, the heart takes on a more spherical or enlarged, balloon-like shape. This structural change allows the heart to hold a larger volume of blood, which initially helps maintain the heart’s pumping efficiency against the volume challenge.

Contrasting Eccentric and Concentric Hypertrophy

Cardiac hypertrophy primarily splits into two distinct structural patterns: eccentric and concentric, each resulting from a different type of mechanical stress. Eccentric hypertrophy is a response to volume overload, while concentric hypertrophy (CH) is an adaptation to chronic pressure overload. Pressure overload occurs when the heart must pump against consistently high resistance, such as in cases of uncontrolled high blood pressure or a narrowed aortic valve.

In concentric hypertrophy, the cardiomyocytes add new sarcomeres in a different configuration, specifically adding them side-by-side, or “in parallel.” This parallel arrangement causes the heart muscle cells to increase in width, leading to substantial thickening of the ventricular wall. The chamber volume, however, remains normal or may even decrease.

The key structural difference lies in the relative wall thickness (RWT), the ratio of wall thickness to chamber radius. In concentric hypertrophy, the RWT is increased because the wall is thicker relative to the chamber size. In contrast, eccentric hypertrophy results in a normal or reduced RWT because the chamber has dilated significantly. Therefore, concentric growth produces a smaller, thick-walled ventricle, while eccentric growth creates a larger, dilated chamber with a wall thickness proportional to the increased size.

Triggers: Athlete’s Heart Versus Disease

The underlying cause of the volume overload determines whether eccentric hypertrophy is a beneficial, reversible adaptation or a progressive, harmful condition. The two main triggers are intense, sustained physical training and chronic disease states.

Physiological eccentric hypertrophy is most commonly seen in endurance athletes, often referred to as “athlete’s heart.” Activities like marathon running or competitive cycling cause a repeated, large increase in blood return to the heart (volume load). This adaptation is generally considered beneficial, as the enlarged chambers improve the heart’s stroke volume and overall cardiac output, enhancing athletic performance.

Pathological eccentric hypertrophy is a response to chronic disease, typically conditions like valvular regurgitation, where a leaky valve causes blood to flow backward, increasing the volume the heart must handle. Severe anemia or certain congenital heart defects can also lead to this remodeling. This disease-induced adaptation is initially compensatory, but it is often accompanied by molecular changes and the development of myocardial fibrosis (scarring), which ultimately impairs function and can lead to heart failure.

The crucial distinction between the physiological and pathological forms lies in the cellular environment. Physiological hypertrophy is characterized by an organized growth pattern, normal function, and a lack of fibrosis. Pathological hypertrophy involves abnormal gene expression and the presence of scarring, which stiffens the heart muscle and indicates a worse long-term outcome if the underlying stimulus is not resolved.

Clinical Significance and Management

When eccentric hypertrophy is caused by disease, its presence indicates progressive cardiac dysfunction. The increase in chamber size, while initially compensatory, eventually leads to elevated wall stress, making the heart less efficient and predisposing the patient to heart failure. This remodeling pattern is the most common type seen in patients with established heart failure and a reduced ejection fraction.

Diagnosis typically involves imaging tests, with the echocardiogram being the most common method used to assess the heart’s structure and function. The echocardiogram precisely measures the ventricular wall thickness and chamber diameter, allowing clinicians to calculate the relative wall thickness and classify the geometric pattern of hypertrophy.

Management of pathological eccentric hypertrophy focuses on treating the root cause of the volume overload. For instance, if a leaky heart valve is the trigger, surgical repair or replacement may be necessary to remove the chronic stress on the heart. Medication also plays a role, often involving agents that reduce blood volume or ease the heart’s workload to slow the progression of remodeling.