Scar tissue in the heart, known as myocardial fibrosis, is the body’s attempt to repair damage, most often following a heart attack (myocardial infarction). This process replaces dead or injured functional muscle cells (myocytes) with dense, non-functional connective tissue primarily composed of collagen. While scarring is a survival mechanism in other organs, it is uniquely detrimental in the heart because it fundamentally changes the organ’s structure and impairs its two primary jobs: pumping blood and maintaining a steady electrical rhythm.
Scar Tissue Does Not Contract
The most immediate consequence of myocardial fibrosis is the permanent loss of the heart’s pumping capability in the scarred region. Scar tissue is inert and rigid, lacking the necessary contractile proteins to participate in the pumping action.
Every myocyte replaced by collagen tissue represents a permanent subtraction from the total muscle mass capable of contracting. This reduction in viable muscle mass directly translates to a decrease in the heart’s mechanical efficiency. The primary measure of this efficiency is the ejection fraction, the percentage of blood pumped out of the ventricle with each beat.
When a significant portion of the ventricular wall is scarred, the ejection fraction drops, meaning the heart cannot meet the body’s demand for blood flow. This reduced ability to pump blood effectively is the fundamental cause of ischemic heart failure. Furthermore, the rigid scar tissue may paradoxically bulge outward under the high internal pressure, which wastes energy and diminishes the forward stroke volume.
Disruption of the Heart’s Electrical System
Beyond the mechanical failure, cardiac scar tissue poses an electrical hazard. Healthy heart muscle is designed for rapid and uniform electrical signal conduction, allowing all muscle cells to contract in a coordinated fashion. Scar tissue acts as a dense, non-conductive barrier and electrical insulator that fragments the normal pathways.
This electrical discontinuity forces signals to navigate around the scar in circuitous paths through surviving muscle bundles. These tortuous routes significantly slow the conduction velocity of the electrical impulse. The combination of a fixed anatomical obstacle—the scar—and slow conduction creates the ideal conditions for a phenomenon known as a re-entry circuit.
In a re-entry circuit, the electrical impulse loops back around the scar to re-excite the tissue it just activated, creating an abnormal, self-sustaining electrical spiral. This runaway electrical activity is the mechanism behind dangerous ventricular arrhythmias, such as ventricular tachycardia and ventricular fibrillation. These chaotic rhythms can prevent the heart from pumping any blood at all, leading directly to sudden cardiac death.
Long-Term Structural Weakening and Remodeling
The presence of scar tissue initiates a process known as adverse ventricular remodeling, which structurally weakens the heart over time. Scar tissue lacks the tensile strength and elasticity of the original muscle fibers. This means the scarred area is structurally compromised and unable to withstand the pressure generated inside the ventricle during each heartbeat.
Under the constant mechanical stress, the ventricular wall begins to stretch and thin out, a process called infarct expansion. This stretching causes the entire ventricle chamber to dilate, moving from its efficient, elongated shape to a more spherical and less effective geometry. The increased diameter forces the remaining healthy muscle to work harder, which perpetuates the cycle of damage and dilation.
In severe cases, the extreme thinning and outward bulging of the scar tissue can result in the formation of a ventricular aneurysm. This permanent pouch in the heart wall does not contract and can become a stagnant pocket for blood. This significantly increases the risk of forming blood clots, which can subsequently travel to the brain or other organs. This progressive structural deterioration is a major determinant of long-term morbidity and mortality following a heart injury.