Interventricular Septum

The interventricular septum, also known as the ventricular septum, refers to the triangular wall of cardiac tissue that separates the left and right ventricles (i.e., the lower chambers) of the heart. The entire interventricular septum can be further divided into two parts: a muscular portion and a membranous portion.   

At the apex of the heart, or the lowest tip of the heart that points downwards, the interventricular septum is composed of muscular tissue and receives its blood supply from the left coronary artery. This muscular tissue at the apex can be divided into three components: the inlet septum, trabecular septum, and infundibular septum.   

The portion of the interventricular septum located near the base, or upper portion of the heart containing the aorta, consists mainly of membranous tissue and is where most defects of the septum can occur. The blood supply to this region is provided by a branch of the right coronary artery.  

The interventricular septum separates the ventricles and allows for proper blood flow through the heart. Venous blood from the vena cava flows from the right atrium through the tricuspid valve to the right ventricle and then to the lungs. From the pulmonary circulation, it goes to the left atrium, through the mitral valve and into the left ventricle, and out to the aorta. As the heart is pumping blood out during systole, the interventricular septum shortens longitudinally and becomes thicker. Additionally, the septum moves towards the left side of the heart and acts as a support structure for the right ventricle during systole. Conversely, as the ventricles fill during the diastolic phase, the septum lengthens and moves towards the right ventricle. Correct placement of the interventricular septum is required for proper function.  

In addition to facilitating proper blood flow, the septum is a conduit for a part of the conduction system of the heart. The atrioventricular bundle of His transmits electrical impulses from the atrioventricular (AV) node to the Purkinje fibers in the ventricles, allowing for coordinated contraction of the heart. These fibers run through the interventricular septum in order to reach their respective target.  

Disorders of the interventricular septum may be congenital or acquired over an individual’s lifetime (i.e., due to blunt trauma to the chest or weakening of the septal wall after a myocardial infarction).   

Most commonly, disorders affecting the ventricular septum are congenital, as seen in ventricular septal defects (VSD), where there is a hole in the ventricular septum at birth. In fact, ventricular septal defects are the most common congenital heart defect, accounting for 20-30% of children seen in pediatric cardiology clinics.   

There are several types of ventricular defects, including conoventricular VSD (a hole where portions of the ventricular septum should meet below the pulmonic and aortic valves); perimembranous VSD (a hole in the upper ventricular septum); inlet VSD (a hole in the septum where blood enters the ventricles via the tricuspid and mitral valves); and muscular VSD (a hole in the lower, muscular ventricular septum), which is the most common of the four.  

Congenital ventricular septal defects can arise as a result of developmental disorders (e.g., Down syndrome, Turner syndrome), maternal diabetes or congenital infections, as well as  due to maternal intake of certain medications during pregnancy. Common medications that potentially cause VSD include antiepileptic agents like valproic acid, sulfasalazine (i.e., used to treat ulcerative colitis, rheumatoid arthritis, and other rheumatologic diseases), lithium, ACE inhibitors (e.g., enalapril, lisinopril), isotretinoin, and warfarin. Certain studies have also linked a higher risk of congenital anomalies, including ventricular septal defects, in infants born to mothers who used cannabis during pregnancy.  

A VSD can occur on its own or in association with other heart defects, such as Tetralogy of Fallot, which is a rare heart condition present at birth, or transposition of the great vessels, where the two main arteries leaving the heart are reversed. When a VSD occurs along with tetralogy of Fallot or transposition of the great vessels, there is mixing of oxygenated blood with deoxygenated blood that is then sent out to the body in the systemic circulation, resulting in hypoxia, or low oxygen concentration in the tissues. This typically does not occur when a VSD is present in isolation since the higher pressures of the left heart pushes oxygenated blood to the right heart and to the lungs.    

Myocardial infarction, commonly known as a heart attack, can also predispose the walls of the heart to rupture. As the heart tissue, or myocardium, repairs itself after a myocardial infarction, dead muscle cells are replaced with fibrous tissue that is less adaptive to changes in blood flow pressure, allowing for increased risk of rupture. Lastly, ventricular hypertrophy, or thickening of the ventricular walls and septum, can affect the interventricular septum. This may occur as a result of atherosclerosis, or a build-up of plaque in the arterial walls, as a result of genetic and lifestyle factors, such as diet. As the blood vessels narrow, higher pressures are needed to maintain blood flow and the left ventricle can thicken to compensate. As a result, there is reduced efficiency in blood pumping, which can lead to left heart failure.