Cardiac fibrosis is a condition characterized by the formation of scar tissue within the heart muscle. While this scarring is the heart’s attempt to repair damage, it can ultimately lead to impaired heart function. Excessive scar tissue makes the heart stiffer and less able to pump blood effectively throughout the body.
Understanding Cardiac Fibrosis
Cardiac fibrosis involves the excessive buildup of extracellular matrix (ECM) proteins, primarily collagen, within the heart tissue. This process is a response to various forms of cardiac injury or stress. Normally, cardiac fibroblasts, a type of cell in the heart, produce collagen for structural support.
However, when the heart is injured, these fibroblasts can become overactive and transform into myofibroblasts. Myofibroblasts produce elevated levels of ECM proteins, leading to an overabundance of collagen. This excessive deposition results in the formation of stiff, non-functional scar tissue. While the heart’s attempt at repair is initially adaptive, this persistent scarring distorts the heart’s architecture and increases its stiffness, becoming detrimental if prolonged or exaggerated.
Common Causes and Risk Factors
Cardiac fibrosis often arises from chronic or sudden damage to the heart. High blood pressure (hypertension) is a significant cause, placing increased strain on the heart over time. This chronic pressure overload stimulates collagen production and structural changes in the heart muscle. The renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure, also promotes fibroblast proliferation and collagen synthesis.
Heart attacks (myocardial infarctions) are another common trigger. When a heart attack occurs, damaged heart muscle is replaced with non-functional fibrotic scar tissue. Chronic heart failure can also lead to widespread fibrosis as the heart tries to remodel and compensate for its reduced pumping ability.
Other factors contributing to cardiac fibrosis include certain genetic conditions, inflammation (e.g., viral infections like myocarditis), and toxin exposure. Aging also plays a role, as cumulative stress can lead to a gradual increase in fibrosis over time. Diabetes and obesity are also associated with increased risk.
Impact on Heart Function
The accumulation of scar tissue from cardiac fibrosis significantly impacts the heart’s ability to function. Fibrotic tissue is less flexible and cannot contract or relax efficiently like healthy heart muscle. This increased stiffness, particularly in the ventricles, impairs the heart’s filling capacity, known as diastolic dysfunction. As a result, the heart struggles to fill with enough blood.
Fibrosis also reduces the heart’s ability to pump blood out to the body, affecting its systolic function. Excessive scar tissue disrupts heart muscle cells, leading to reduced contractility and overall pumping efficiency. Over time, this diminished capacity can progress to heart failure.
Cardiac fibrosis can also interfere with the heart’s electrical signaling. Scar tissue creates abnormal pathways for electrical impulses, increasing the risk of irregular heart rhythms (arrhythmias). These electrical disturbances can range from mild to life-threatening.
The combination of reduced pumping ability and electrical instability makes cardiac fibrosis a significant contributor to cardiovascular disease progression.
Approaches to Management
Managing cardiac fibrosis primarily focuses on addressing the underlying conditions that cause the scarring. Controlling high blood pressure through lifestyle changes and medication is a primary strategy. Medications that inhibit the renin-angiotensin-aldosterone system (RAAS), such as ACE inhibitors and angiotensin receptor blockers (ARBs), are commonly used to reduce collagen production and improve cardiac function.
Lifestyle modifications, including a balanced diet and regular physical activity, are important approaches to support heart health and manage conditions that contribute to fibrosis. For individuals with heart failure, treatments aimed at improving heart function, such as beta-blockers and mineralocorticoid receptor antagonists, can also have beneficial effects on fibrosis. These interventions do not directly remove existing scar tissue but work to prevent further scarring and mitigate its effects.
While no specific medication directly reverses cardiac fibrosis, research continues into novel therapies. Scientists are exploring targets to develop more direct anti-fibrotic treatments, aiming to reduce excessive scarring while preserving the heart’s necessary repair mechanisms.