A potential connection between fibrinaloid microclots and the development of atrial fibrillation (AF) has been uncovered by recent research. AF is a common heart arrhythmia that has implications for global health. Clot formation within the atrial chamber is a known consequence of AF and contributes to the risk of strokes and coronary heart disease. Now, researchers are exploring the role of fibrinaloid microclots, which are small clots found in plasma or serum, in the development of AF.
These fibrinaloid microclots have an amyloid nature and are resistant to being dissolved, allowing them to persist in circulation. External stimuli, such as bacterial cell wall substances and the spike protein of SARS-CoV-2, can catalyze the formation of these microclots. The spike proteins produced by mRNA vaccines for COVID-19 could also potentially contribute to their formation. Once formed, these microclots can have cytotoxic effects, including hypoxia/reperfusion.
Understanding the mechanisms behind the development of fibrinaloid microclots is a focus of current research. Soluble fibrinogen, a key component in clot formation, undergoes polymerization to fibrin in the presence of the serine protease thrombin. Abnormal conformations of fibrin fibers, known as “dense matted deposits,” have been identified in chronic, inflammatory conditions. These fibers are resistant to being broken down and have been identified as amyloid.
Identifying risk factors for AF is crucial, and researchers are investigating the potential link between factors like age, gender, BMI, and fibrinaloid microclots. Lifestyle choices, such as alcohol consumption and exposure to particulate matter, may also play a role in AF development. Investigating the relationship between these risk factors and fibrinaloid microclots is essential for a comprehensive understanding of AF.
Chronic, inflammatory diseases share common features such as inflammation, oxidative stress, and iron dysregulation. The presence of fibrinaloid microclots in these diseases suggests a shared underlying cause. Infections, both viral and bacterial, have been implicated in the development of AF. Infections like community-acquired pneumonia and SARS-CoV-2 have been linked to new-onset AF, and long COVID increases the likelihood of AF. This complex relationship between infections, fibrinaloid microclots, and AF requires further investigation.
The emerging evidence suggests a significant role for fibrinaloid microclots in the development of AF. Understanding this connection has important implications for AF management and the development of new treatment approaches. Further research should focus on investigating the independent role of fibrinaloid microclots as a risk factor for AF, which could potentially reshape our approach to managing this prevalent heart arrhythmia.