Coronary heart disease is a disease in which fatty deposits made up of cholesterol and other cellular materials (plaque) accumulate inside the coronary arteries on the surface of the heart, leading to the narrowing of the arteries." (World Health Organization) It is the most common heart disease in the United States of America.
Prolonged tobacco use has a strong correlation with diagnosis of coronary heart disease. This includes smoking and secondhand smoke from tobacco and tobacco products such as vape and cigarettes. High cholesterol, diabetes/insulin resistance, high blood pressure, not getting enough exercise and smoking or tobacco use may be the causes of damage to the coronary arteries.
Healthy coronary arteries (Source)
There are several risk factors that are associated with increasing the likelihood of CHD. Some of the well known risk factors are:
CHD can be prevented up to certain extent by strategies and actions to promote healthy lifestyle and reduce the likelihood of the disease. Some approaches could :
CHD can manifest with a range of symptoms that vary in intensity and presentation. Some of the common symptoms include-
Plaque buildup in the coronary arteries (Source)
Several diagnostic methods are used to assess CHD. These methods help healthcare professionals evaluate the extent of blockages or narrowing in the coronary arteries and determine appropriate treatment. Common diagnostic techniques include:
A decreased flow to the heart of blood containing oxygen, which may result in a heart attack and could cause serious harm to the heart or abrupt death. Typically, this happens slowly over a long period of time, and many individuals with this condition are only made aware after they suffer from a severe heart attack.
According to Chu et al., the levels of pentraxin 3 protein were higher in subjects with coronary artery disease compared to those in the control group. However, it's important to note that correlation does not imply causation. Therefore, there isn't a definitive link to support the notion that the PTX3 protein directly contributes to the development of coronary artery disease.
PCSK9's interactions with other proteins in the body (Source)
Certain proteins have been identified as potentially related to coronary artery disease. One such protein is Apolipoprotein A5 (APOA5), which plays a crucial role in regulating plasma triglyceride levels in the blood—a recognized risk factor for coronary artery disease. APOA5 is a component of high-density lipoprotein (HDL), also known as 'good' cholesterol, responsible for cholesterol absorption and transport to the liver. Mutations in this gene can lead to elevated triglyceride levels, potentially contributing to coronary artery disease. A study published in the Journal of Lipid Research highlighted a connection between APOA5 gene mutations and hypertriglyceridemia—a condition marked by high fat concentrations in the blood, associated with various cardiovascular diseases, including coronary heart disease. This gene is situated on chromosome 11 and consists of 118 amino acids.
Another protein implicated in coronary heart disease is Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9), which plays a pivotal role in regulating plasma cholesterol homeostasis—a state of equilibrium among interdependent elements, maintained by physiological processes. Imbalanced cholesterol levels resulting from disrupted homeostasis can contribute to coronary artery disease. The molecular functions of this gene encompass hydrolase and protease activities, and its expression occurs in kidney, liver, and intestine tissues. PCSK9 facilitates the transport of specific receptors responsible for lysosome degradation and influences fatty acid and cholesterol metabolism. Autosomal dominant familial hypercholesterolemia, characterized by elevated cholesterol levels in the bloodstream, has been associated with PCSK9 gene mutations.
Illustration of the influence of various proteins on the coronary arteries (Source)
Notably, this gene interacts with three distinct proteins: ANXA2, MMP2, and LDLR. Among these interactions, direct associations exist with MMP2 and LDLR. ANXA2, a protein coding gene, enhances tumor development, invasion, and metastasis. MMP2, a protein, contributes to the regulation of inflammatory signaling cascades. The LDLR gene encodes the low-density lipoprotein receptor, the primary transporter of cholesterol in the blood. These interactions provide evidence supporting the link to coronary heart disease—since inflammation in coronary arteries is a contributor to coronary artery disease, and elevated blood cholesterol levels lead to plaque accumulation, obstructing blood flow to the heart.
Individualized treatment plans are based on the severity of CHD, the presence of other medical conditions, and the patient's overall health. Regular communication with healthcare providers and adherence to recommended treatments are key to effective clinical management and improved outcomes for individuals with CHD.
The APOA5 and PCSK9 genes are associated with coronary heart disease and may act as contributing factors to the inflammation and constriction of coronary arteries when mutations in these genes are present. These mutations can be hereditary, potentially leading to future cardiovascular health issues. Individuals with close genetic ties to affected individuals are at a higher risk of developing coronary heart disease. To prevent the onset of this condition, adopting a healthy lifestyle is essential. This includes maintaining a balanced diet, engaging in regular exercise, managing stress, refraining from smoking, and moderating alcohol intake to promote cardiovascular well-being.
Hello! My name is Almari Rheeder and I am an 18 year old from South Africa, but currently in my senior year of high school in Beijing, China. My project is about CHD (coronary heart disease) and how it manifests. I investigated the causes, risk factors, prevention, and molecular insight regarding this disease. During this course, I learned a lot about genetics, genomics, and their importance for study in the medical fields. This program has opened me up to making new friends in other places in the world, and has inspired me to consider a wider range of careers within the medical field.
Chu, Y., Teng, J., Feng, P., Liu, H., Wang, F., & Li, X. (2019). Pentraxin-3 in coronary artery disease: A meta-analysis. Cytokine, 119, 197–201. https://doi.org/10.1016/j.cyto.2019.03.017
Hilfiker-Kleiner, D., Landmesser, U., Drexler, H. (2006). Molecular Mechanisms in Heart Failure: Focus on Cardiac Hypertrophy, Inflammation, Angiogenesis, and Apoptosis.Critical Issues in Cardiovascular Research, 48(9), A56-A66.https://www.sciencedirect.com/science/article/pii/S0735109706018080
Jansen, H., Samani, N. J., & Schunkert, H. (2014). Mendelian randomization studies incoronary artery disease. European heart journal, 35(29), 1917–1924. https://doi.org/10.1093/eurheartj/ehu208
Khera, A. V., & Kathiresan, S. (2017). Genetics of coronary artery disease: discovery, biology and clinical translation. Nature reviews. Genetics, 18(6), 331–344. https://doi.org/10.1038/nrg.2016.160
Korzonek-Szlacheta, I., Danikiewicz, A., Szkodziński, J., Nowak, J., Lekston, A., Gąsior, M.,Zubelewicz-Szkodzińska, B., & Hudzik, B. (2018). Relationship Between Plasma Pentraxin 3 Concentration and Platelet Indices in Patients With Stable Coronary Artery Disease. Angiology, 69(3), 264–269.https://doi.org/10.1177/0003319717732929
Mayo Clinic Staff. (2022, May 25). Coronary Artery Disease. Mayo Clinic. Retrieved August 1, 2023, from www.mayoclinic.org/diseases-conditions/coronary-artery-disease/symptoms-causes/syc-20350613.
Suzuki, S., & Takeishi, Y. (2018). Molecular mechanisms and clinical features of heart failure. Fukushima journal of medical science, 64(3), 116–124.https://doi.org/10.5387/fms.2018-17
Project done at Elio Academy of Biomedical Sciences
The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of Elio Academy.