Scarring on the heart, medically termed myocardial fibrosis, is a serious structural change where healthy heart muscle tissue is permanently replaced by inert, non-contractile material. This process is the body’s attempt to heal damage, but the resulting scar tissue lacks the functional properties of the original muscle. The presence of this scar indicates prior injury and fundamentally alters the heart’s architecture. The extent and location of this scarring dictate the heart’s ability to pump blood effectively and maintain a steady electrical rhythm.
Defining Myocardial Scarring
Heart muscle cells (cardiomyocytes) have a very limited ability to regenerate after injury. When a part of the heart muscle dies, the body initiates a healing response involving specialized cells called fibroblasts. These fibroblasts deposit an excessive amount of the protein collagen to form a dense, fibrous patch.
This collagenous patch is the scar tissue, or fibrosis, which mechanically stabilizes the heart wall and prevents rupture. Unlike healthy muscle tissue, which contracts and conducts electrical impulses, scar tissue is electrically and mechanically inert. The pattern of scarring provides important clues about the underlying cause of the damage.
Myocardial fibrosis is broadly categorized into two types based on its distribution. Focal or reparative scarring is a dense, localized patch that replaces a large area of dead muscle, often seen after a heart attack. In contrast, diffuse or reactive fibrosis involves a scattered, microscopic accumulation of collagen throughout the muscle, which increases the stiffness of the entire heart wall.
Primary Causes of Heart Scarring
The most common cause of myocardial scarring is an ischemic injury, such as a heart attack (myocardial infarction). When a coronary artery is blocked, the deprived heart muscle dies from lack of oxygen. The body replaces this necrotic tissue with a dense, focal scar over several weeks to maintain the wall’s structural integrity.
Chronic conditions that place a constant burden on the heart often lead to the diffuse form of scarring. Chronic pressure overload, typically from long-standing, uncontrolled high blood pressure (hypertension) or severe aortic valve disease, strains the heart muscle. The heart responds to this stress by remodeling and developing microscopic collagen deposits between the muscle cells, which increases the heart wall’s rigidity.
Inflammatory conditions, such as myocarditis, can also trigger scarring. Myocarditis is inflammation of the heart muscle, often caused by a viral infection or an autoimmune response, which directly damages the cardiomyocytes. As the inflammation subsides, the damaged muscle is replaced by scar tissue, resulting in patchy or diffuse fibrosis.
Finally, genetic or inherited conditions, collectively known as cardiomyopathies, predispose individuals to heart scarring. Hypertrophic cardiomyopathy, for instance, involves abnormal thickening of the heart muscle, often including significant replacement fibrosis. Certain genetic mutations cause structural defects that lead to chronic stress and remodeling, resulting in ongoing scar formation even without a massive acute event.
How Scar Tissue Impairs Heart Function
Scar tissue impairs the heart’s performance mechanically and electrically. Mechanically, the inability of scar tissue to contract directly reduces the heart’s overall pumping strength. Since a portion of the muscle is permanently inactive, the amount of blood the heart can eject with each beat (ejection fraction) is lowered.
This loss of contractile function can lead to Heart Failure, where the heart cannot pump enough blood to meet the body’s metabolic demands. Diffuse scarring increases the stiffness of the heart wall, impeding the ventricle’s ability to fully relax and fill with blood between beats. This rigidity compromises the heart’s compliance, reducing its efficiency as a pump.
Electrically, scar tissue acts as an insulator, disrupting the heart’s highly organized electrical conduction system. The electrical signal coordinating the heartbeat must navigate around the inert scar tissue, creating slow, circuitous pathways. These detours can become the substrate for dangerous, irregular heart rhythms, known as arrhythmias, such as ventricular tachycardia.
The surviving heart muscle immediately adjacent to the scar, called the border zone, is particularly vulnerable to these electrical disturbances. Slow conduction velocity in this area can promote a re-entry circuit, where the electrical signal loops back on itself, causing rapid and chaotic contractions. The risk of sudden cardiac death is significantly elevated in patients with substantial scarring due to the potential for these life-threatening arrhythmias.
Diagnosis and Management Approaches
Doctors rely on specialized imaging techniques to accurately identify and quantify heart scarring. Cardiac Magnetic Resonance Imaging (cMRI), particularly with Late Gadolinium Enhancement (LGE), is the gold standard for visualizing fibrosis. The gadolinium contrast agent pools in the expanded extracellular space of the scar tissue, causing it to “light up” on the scan, which precisely maps the scar’s size and location.
Other diagnostic tools assess the functional consequences of the scar. An Echocardiogram evaluates the heart’s pumping efficiency and overall wall motion. An Electrocardiogram (ECG or EKG) detects electrical abnormalities and irregular rhythms caused by scar-related disruption of conduction pathways.
Since established scar tissue is permanent, management focuses on treating the underlying condition, mitigating symptoms, and preventing complications. Medications are prescribed to reduce the heart’s workload and manage heart failure symptoms. Common examples include ACE inhibitors or ARBs, which relax blood vessels, and beta-blockers, which slow the heart rate and decrease the force of contraction.
For patients at high risk of life-threatening arrhythmias due to electrical instability, an Implantable Cardioverter-Defibrillator (ICD) may be necessary. This device continuously monitors the heart rhythm and delivers an electrical shock if a dangerous arrhythmia is detected. In severe cases leading to advanced heart failure, procedures like valve repair or a heart transplant may be required.