Interventricular Septal diastolic thickness (IVSd) measures the thickness of the muscular wall separating the heart’s two main pumping chambers. The measurement is taken specifically during the heart’s relaxation phase (diastole), making it a reliable indicator of long-term structural changes. An increased IVSd reading is a significant finding that suggests the heart has undergone remodeling, often in response to chronic stress or a genetic condition.
The Interventricular Septum and Diastole
The Interventricular Septum (IVS) is the thick, muscular wall that divides the left ventricle from the right ventricle. The primary function of the IVS is to ensure that oxygenated blood on the left side of the heart remains separate from deoxygenated blood on the right side. During the heart’s pumping cycle, the IVS also plays a mechanical role, contributing significantly to the left ventricle’s ability to contract and eject blood.
The measurement of IVSd is specifically concerned with the phase called diastole, which is the period when the heart muscle relaxes. Diastole is the time when the ventricles fill with blood returning from the atria. By measuring the septum’s thickness at the end of this relaxation period, medical imaging captures the wall’s maximal dimension without the temporary thickening that occurs during contraction (systole). The integrity and proper motion of the IVS are necessary for maintaining efficient blood flow and pressure throughout the body.
Standard Values and Diagnostic Purpose
The IVSd measurement is obtained most commonly through an echocardiogram, an imaging test that uses sound waves to create a moving image of the heart. In a typical adult, the reference range for IVSd is generally considered to be between 0.6 and 1.1 centimeters, or 5 to 11 millimeters.
A reading above this range signals a condition known as left ventricular hypertrophy (LVH), which is an abnormal thickening of the muscle tissue. The purpose of measuring IVSd is to track this structural change, which often serves as an early indicator of cardiovascular risk.
Increased IVSd is used to calculate the left ventricular mass index (LVMI), a value that helps determine the severity of heart enlargement. Observing a thickened septum can serve as a sensitive predictor for the future development of hypertension. A finding of thickened IVS is also associated with an elevated risk of all-cause death in patients with existing coronary artery disease.
Conditions Causing Increased Thickness
The most frequent cause of an increased IVSd is hypertension, which is chronic high blood pressure. High pressure in the arteries forces the left ventricle to pump with greater effort to push blood out to the body. Over time, this constant, strenuous workload causes the heart muscle, including the interventricular septum, to grow thicker.
Another significant cause of septal thickening is aortic stenosis, a condition where the aortic valve narrows. The narrowing creates an obstruction to blood flow leaving the left ventricle, which also increases the pressure the heart must generate. The resulting thickening is a remodeling process where new muscle fibers are added to overcome the obstruction.
In some cases, the thickening is due to Hypertrophic Cardiomyopathy (HCM), a genetic disorder. This condition causes unexplained, often asymmetrical, thickening of the heart muscle, which frequently affects the interventricular septum. The thickening in HCM is caused by mutations in the genes that encode for cardiac muscle proteins rather than a simple response to pressure.
Significant athletic training can lead to a physiological change called “athlete’s heart,” which may also show mild thickening of the IVS. This type of hypertrophy is considered a healthy adaptation to intense aerobic exercise. Unlike disease-related thickening, the athlete’s heart typically maintains normal heart function and does not lead to adverse consequences.
Impact on Heart Function
When the interventricular septum becomes abnormally thick, the primary functional consequence is the development of diastolic dysfunction. A thickened muscle wall is inherently stiffer and less compliant, meaning it cannot relax efficiently during diastole. This impaired relaxation reduces the ventricle’s ability to stretch and fill completely with blood from the atrium.
The decreased filling volume means that less blood is available to be pumped out with each beat, which can eventually lead to a reduction in cardiac output. This inefficiency often manifests as symptoms such as fatigue and shortness of breath, particularly during physical exertion.
In a specific form of the condition, particularly associated with severe septal thickening in HCM, the increased muscle mass can obstruct the flow of blood. This is known as left ventricular outflow tract (LVOT) obstruction, where the thickened septum physically blocks the path blood must take to leave the heart. This obstruction can lead to a dangerous pressure gradient and significantly impair the heart’s ability to pump effectively.
The presence of increased IVSd is also associated with an elevated risk of coronary heart disease and myocardial infarction. The thickened muscle requires a greater blood supply, but the coronary arteries supplying the heart muscle may not be able to keep up with the increased demand.