Cardiac scar tissue, medically known as myocardial fibrosis, is the replacement of healthy heart muscle with dense, stiff, non-functional tissue. This process is the body’s natural response to injury, aiming to rapidly repair structural damage and prevent the heart wall from rupturing. Composed primarily of collagen, the resulting scar lacks the ability to contract and conduct electrical signals. The most frequent trigger for this damage is a heart attack, where a blockage starves a region of the heart of oxygen, causing cell death.
Chronic conditions, such as high blood pressure or certain cardiomyopathies, can also lead to a diffuse pattern of scarring. The presence of this tissue forces the heart to work harder, ultimately leading to a decline in function. Solutions involve managing the effects of the scar and research focused on reversing the tissue damage itself.
Understanding Why Scar Tissue Forms
The formation of cardiac scar tissue is a fundamental part of the healing process following acute injury, such as a myocardial infarction. When heart muscle cells (cardiomyocytes) die due to lack of blood flow, the body cannot regenerate them because adult cardiomyocytes have limited capacity to divide. Specialized connective tissue cells called fibroblasts rapidly migrate to the damaged area and transform into myofibroblasts. These activated cells secrete large amounts of extracellular matrix proteins, predominantly Type I and Type III collagen, forming a patch that structurally stabilizes the injured wall.
While this process prevents immediate catastrophic failure of the heart wall, it introduces a permanent defect in function. The scar tissue disrupts the synchronized contraction of the ventricle, leading to inefficient pumping and chamber dilation, known as adverse remodeling. The border zone between the healthy muscle and the dense scar becomes a source of dangerous electrical instability, setting the stage for life-threatening arrhythmias. Scarring also impairs the left ventricle’s ability to relax and fill with blood, contributing to heart failure symptoms.
Managing the Effects of Cardiac Scarring
Current medical management focuses on mitigating the consequences of the scar, primarily heart failure and electrical instability, rather than eliminating the scar itself. Pharmacological therapies are designed to reduce the workload on the remaining healthy muscle and prevent progressive enlargement and damage of the heart chamber. Medications targeting the body’s neurohormonal systems are the foundation of this treatment strategy.
Pharmacological Management
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) prevent the signaling cascade that promotes maladaptive ventricular remodeling and fibrosis in non-scarred tissue. Beta-blockers dampen the effects of stress hormones on the heart, slowing the heart rate and allowing more time for filling. Certain beta-blockers can also promote a modest reversal of ventricular remodeling by improving pumping efficiency.
Mineralocorticoid Receptor Antagonists (MRAs), such as spironolactone, directly target the profibrotic effects of aldosterone. Aldosterone promotes the formation of reactive fibrosis in viable myocardium, independent of blood pressure effects. MRAs block this process, protecting healthy heart tissue from further stiffening and helping to improve the heart’s overall ejection fraction.
Device Therapy
Device therapy is frequently required to address the electrical instability introduced by the scar tissue. An Implantable Cardioverter-Defibrillator (ICD) monitors the heart rhythm and delivers an electrical shock to stop dangerous, rapid rhythms like ventricular tachycardia (VT). The size and heterogeneity of the scar are strong predictors of a patient’s risk for sudden cardiac death, guiding the decision for ICD implantation.
Cardiac Resynchronization Therapy (CRT) is used when the scar has led to electrical dyssynchrony, causing the ventricles to contract out of step. A CRT device uses precisely timed electrical impulses to pace both sides of the heart simultaneously, restoring coordinated contraction. This resynchronization can lead to reverse remodeling, improving the heart’s overall pumping function and reducing heart failure symptoms.
Structural Interventions and Ablation Procedures
When medical management is insufficient, structural and electrical interventions can physically alter the heart or the scar tissue to improve function and stability.
Surgical Ventricular Restoration (SVR)
SVR, often called the Dor procedure, is an open-heart surgery designed to reshape an enlarged left ventricle. This procedure removes or excludes the large, thin, scarred segment of the heart wall that cannot contract and bulges outward during systole. By isolating the non-moving scarred area and reducing the chamber volume, SVR decreases wall tension. This increases the mechanical efficiency of the remaining healthy muscle, improving the heart’s pumping capacity. This intervention is typically reserved for patients with a large, well-defined scar following a heart attack.
Catheter Ablation
Catheter ablation is a minimally invasive procedure that targets the electrical pathways within the scar that cause dangerous arrhythmias, particularly ventricular tachycardia (VT). The scar tissue creates a circuit of slow, chaotic conduction that sustains rapid heart rhythms. During the procedure, an electrophysiologist uses a catheter threaded through blood vessels to reach the heart chamber. Using a 3D mapping system, the physician identifies the specific channels within the scar critical to the VT circuit. Radiofrequency energy or cryoablation is then applied to destroy these abnormal electrical pathways, creating a new, non-conductive micro-scar. This targeted substrate modification stabilizes the heart’s electrical system, significantly reducing the frequency of VT episodes and the need for ICD shocks.
Regenerative and Emerging Therapies
The most promising area of research focuses on therapies that aim to heal or replace the scar tissue.
Cellular Therapies
Cellular therapies, often involving various types of stem cells, are at the forefront of this emerging field. Researchers are investigating cells like mesenchymal stem cells (MSCs) and cardiac progenitor cells, which are injected directly into the heart muscle or coronary arteries. These cells are thought to work primarily by secreting beneficial factors that reduce inflammation and modulate the scar environment, rather than directly turning into new heart muscle. While clinical trials have shown slight improvement in ventricular function and scar size, results remain inconsistent. The primary challenge is ensuring transplanted cells survive and properly integrate into the complex heart tissue.
Gene Therapy and Molecular Approaches
Gene therapy and molecular approaches seek to manipulate the heart’s cellular environment to block the scarring process or encourage regeneration. One strategy involves blocking signaling molecules, such as Transforming Growth Factor-beta (TGF-beta), a powerful driver of fibroblast activation and collagen production. Another approach is direct cardiac reprogramming, which uses gene delivery to instruct non-muscle cells within the scar to transform directly into functional, beating cardiomyocytes. Preclinical studies show this can reduce scar tissue and improve contractile function, but human safety and efficiency are still under investigation.
Biomaterials and Tissue Engineering
Biomaterials and cardiac tissue engineering offer a mechanical and biological scaffold to support the weakened ventricular wall. These materials, such as injectable hydrogels or bio-absorbable patches, are designed to stiffen the scarred area, preventing it from bulging outward under pressure. The scaffolds can also serve as a delivery system for growth factors or stem cells, providing a supportive microenvironment to promote muscle regeneration.