Biochemical Basis Clinical Implications Atherosclerosis

Atherosclerosis is one of the major causes of premature disability and death in developed nations. It is estimated that this condition will become the leading cause of total disease burden in the near future because its development is fueled by multiple generalized or systemic risk factors. Rao & Kiranmayi1 note that the condition is a dynamic and progressive disease that is brought about by an injury to endothelium and its associated inflammatory response. Since atherosclerosis is likely to become the leading cause of disease burden in developed countries, an understanding of the condition is essential to enhance prevention. Insights into the biochemical basis and clinical implications of atherosclerosis are essential to promote a better understanding and management of the condition.

Atherosclerosis is a disease brought by various causes and is regarded as the primary underlying cause of cardiovascular diseases and cerebrovascular accidents. The biochemical mechanisms underlying this condition involve lipid accumulation and immune activation that take place in the vascular wall. Alfarisi, Mohamed & Ibrahim2 state that inflammation, genetic predisposition, and oxidation are the major factors contributing to the development of this condition. Immune activation and lipid accumulation are processes that are highly regulated by several specialized lipid and protein mediators. These mediators either promote the development of atherosclerosis by stimulating inflammation or inducing resolution of inflammation, which makes them anti-atherosclerosis. Blood vessels play an important role in the development of atherosclerosis as they are generally exposed to several mechanical forces exerted on the vessel wall. Some of these mechanical forces include circumferential, radial, and longitudinal forces or shear stress on the endothelial surface.

The initiation of atherosclerotic lesions is influenced by the stresses and strains on the arteries. Atherosclerotic lesions are initiated at the regions of arteries that are exposed to multifaceted blood flow3. Biological and mechanical factors associated with these processes play a critical role in atherosclerotic development through their complex interactions. Mechanical factors are primarily mechanical forces that regulate the molecular and cellular composition of plaques. On the other hand, the composition of plaques influences the ability of molecules and cells to withstand mechanical load. The complex interaction between biological and mechanical factors influences lesion development and plaque stabilization. The initiation of atherosclerotic lesions occurs when the complex interaction between biological and mechanical factors results in plaque progression and eventual plaque rapture. Plaque progression and rapture occur due to inflammatory response to endothelial injury, which is influenced by the interactions between biological and mechanical forces.

The major goal of understanding the biochemical basis of atherosclerosis is to develop markers of the condition and design therapeutic modalities to prevent and regress the initiation of atherosclerotic lesions. New therapeutic strategies for atherosclerosis should focus on preventing lesion development and promoting plaque stabilization. In addition, current clinical imaging techniques should be combined with modeling techniques to enhance the comprehensive assessment of biomechanical and morphological attributes of atherosclerotic lesions3. Efforts to enhance therapeutic strategies for this condition based on an understanding of its biochemical basis align with the biblical concept of health promotion. Spirituality influences everyday decisions and promotes virtues like self-discipline, which is an important health behavior. The therapeutic strategies for atherosclerosis should be supported by suitable health behaviors as reflected in 3 John 1:2 and 1 Corinthians 10:31.