Introduction For many years, scientists and other researchers have sought to undertake tones of research experiments with the aim of discovering the structure of reliable ways of diagnosing and subsequently curing human diseases. Without a doubt, their efforts paid off with the discovery of many medicinal drugs and injections such as the deoxyribonucleic acid discovered by Watson and Crick fifty years ago (Teng, 2009). Years down the line, things have changed, and the future looks promising as far as heart disease treatment is concerned. With the help of genomic tools and an array of leukemia, important mechanistic insights have come into being. According to the Academic Search Premier that discuses missense mutations that are relevant to human cardiac disease, illnesses resulting from cardiovascular problems are the number one cause of deaths in America and other countries. This paper will seek to discuss the role played by mitochondrial dysfunction in cardiovascular disease. Aim of the study The article “Serial Review” by Victor Darley paints a clear picture of how cardiovascular disease endangers the future of adults, as it is the leading cause of morbidity and mortality worldwide since 1900. This indicates that the leading cause of cardiovascular disease is atherosclerosis, which accounts for three-fourths of the total deaths related to heart diseases (Darley, 2004). The process is rigid as injured atherosclerosis develops. Consequently, this development causes the accumulation of lumps of lipids in the area with the injured artery. According to facts laid upon by mitochondria susceptibility and its role in mediating for damages due to increased nitro oxidative stress, it is true to say that very few people understand this behavior. Given the explanation, the article is aimed to discuss the aspects of relating mitochondrial function and damage to the development of cardiovascular disease and the risk factors involved. Genes involved Because mitochondria are responsible for the reaction of nitrogen and oxygen species that mediate alterations and functions, they are very sensitive. Additionally, since they are the main producers of oxidative energy required by the cell, they act as cell power plants (Teng, 2009). Sources that maintain mitochondrial DNA mutations have close links with many reported cases of human diseases. Furthermore, marked clinical heterogeneity shows that deficits of endocrine, renal, cardiovascular, and neuromuscular functions are also related to missense mutations. This indicates that the gene involved in this missense mutation in relation to cardiac diseases is the mitochondrial gene. When the cardiac cells experience abnormal functions, they begin to face cardiac complications commonly referred to as cardiomyopathy and cardiac arrhythmias (Darley, 2004). The biological role of this gene is to distribute tissues. In simple terms, it rearranges and deletes or inserts mutations. This means that single-base mutations result in missense mutations or simply alter the protein function. In addition, this gene (mtDNA) mutates or synthesizes the rNA and tRNA proteins. This happens because the rearrangement of mutations normally leads to the deletion of a n