Coronary Artery Disease

The cardiovascular system is vital to the optimal performance of the body. We are constantly reminded the importance of looking after our bodies in a heart healthy way. These reminders come from patient encounters, family or self-experience, and/or multiple sources of advertisement. One would be hard pressed to say “I didn’t know”. The Centers for Disease Control and Prevention provide us with riveting statistics of heart disease and its effects on the American population. Every 60 seconds, a death occurs secondary to a heart disease-related event. Heart disease is the leading cause of death for both men and women, and ethnicity or race bring little to no advantage. Key risk factors include hypertension (HTN), high cholesterol, smoking, and obesity. Other risk factors include diabetes, poor diet, inactivity, and excessive alcohol abuse. Many of these risk factors are controllable. Coronary heart disease is the most common type of heart disease causing 370,000 deaths per year (CDC, 2014).

Coronary Artery Disease

Coronary Artery Disease (CAD) starts with Atherosclerosis. When arteries are healthy they are elastic and have flexibility. Atherosclerosis occurs when the blood vessels carrying nutrients and oxygen throughout the body become stiff and thick (hardened). This build up (plaque) on the arteries is a result of fat, cholesterol, and other substances. The plaque can restrict blood flow by narrowing the vessel or it may break off (clot) and block the blood flow. Atherosclerosis can effect arteries everywhere in the body causing problem to any organ that blood cannot properly flow to. The coronary arteries are the main supply of blood, oxygen, and nutrients to the heart. CAD is when these main blood vessels around the heart become damaged or diseased (Mayo Clinic, 2015).

“The pathophysiology of Atherosclerosis begins with injury to the endothelial cells that line artery walls” (Huether & McCance, 2012, p. 594). Major risk factors causing injury to the endothelial cells include smoking, HTN, diabetes, increased levels of low-density lipoprotein (LDL) and decreased level of high-density lipoproteins (HDL) (Huether & McCance, 2012). Huether and McCance explain that the injured endothelial cells on the vessel walls become inflamed. These inflamed endothelial cells cannot protect the vessels by adequately producing anti-thrombic and vasodilating cytokines as they are supposed to. Instead these inflamed cells encourage macrophage adherence which release inflammatory cytokines and enzymes that continue to injure the vessel wall. LDL oxidation caused by the inflammation process mixed with any number of risk factors listed result in lipid laden macrophages (foam cells) that build lesions (fatty streaks) on the walls of the vessel. Macrophages release growth factors that cause cell proliferation with the injured cell producing collagen forming a fibrous plaque covering the fatty streaks. This plaque is unstable on the wall of the vessel and is prone to rupture without any warning signs. If rupture occurs exposure of the underlying tissue results in platelet adhesion, initiation of the clotting cascade and from there thrombus formation is rapid bringing potential occlusion which can results in ischemia and infarction (2012).

Huether and McCance continue to inform us that CAD leads us on a pathophysiologic continuum that interferes with the pumping ability of the heart, as the heart muscle is deprived of essential oxygen and nutrients necessary to function at its full potential (2012). A resting heart requires 7% of our body’s consumption of oxygen just to work properly. Coronary blood flow brings oxygen and removes waste products such as carbon dioxide, lactic acid, and hydrogen ions (McPhee & Hammer, 2012). It is important for blood to flow adequately through the coronary arteries. When damage or disease is present in the coronary arteries the optimal function of the heart it is at risk. Even though atherosclerosis is typically the cause of CAD, spasms, emboli, or congenital abnormalities must also be considered (McPhee & Hammer, 2012). One of clinical manifestations that is most common is chest pain (angina) Chest pain often presents itself as a result of increased demand of oxygen or a decreased supply of oxygen to the heart. The cause must be determined rapidly. We have all heard the phrase “time is muscle”.

Impact of Genetics (Family History) on the Pathophysiology of CAD

Nonmodifiable risk factors for CAD include 1) age, 2) male gender or women after menopause, and 3) family history. Family history/genetics play a large role in the susceptibility to CAD. Many studies provided over the years indicate a familial inheritance of 40%-60% for CAD (Roberts, 2014). “Many gene polymorphisms have been associated with CAD and its risk factors” (Huether & McCance, 2012, p. 598). Roberts tells us that plasma lipids are highly regulated by genetic variants. 70%-80% of cholesterol is synthesized endogenously under the control of many genetic variants (2014). High cholesterol, diabetes, and HTN all have genetic dispositions and are risk factors for CAD. While I agree that there are some individuals that are likely predisposed and susceptible CAD, I believe utilizing control of the modifiable risk factors can greatly influence the susceptibility or potentially the prevention of CAD.

Dyslipidemia, Genetics, and CAD

Huether and McCance explain lipoproteins are lipids, phospholipids, cholesterol, and triglycerides that are bound to protein. Chemical reactions in the liver produces lipoproteins that are utilized in various ways to help organ and system functions. When these level are increased beyond usefulness to the body it is referred to a dyslipidemia (dyslipoproteinemia). “Primary or familial dyslipoproteinemias are a results of genetic defects causing abnormalities in lipid metabolizing enzymes and abnormal cellular lipid receptors” (2012, p. 599). Cholesterol, lipids, and triglycerides each have significant roles in supporting various cell functions, fat disposition, energy sources, or necessary functions. Dietary intake provides us with much of our intake, however, cholesterol is also produced by some cells. Monitoring levels of cholesterol is important. Increased LDL plays a large role in the injury to the endothelial cells, thus the higher the level the more damage. HDL is responsible for sending excess cholesterol to the liver to be eliminated in the bile. Therefore when HDL is too low this is not done adequately.

Monitoring lab values is the only indicator as high cholesterol has no symptoms. Optimal Lab values include: Total Cholesterol <200, LDL <100, HDL >60, Triglycerides <150 (Huether & McCance, 2012, p. 598).

Summary

CAD is one of the leading health concerns not only for the United States but worldwide, as 17.5 million people die every year worldwide from cardiovascular diseases (WHO, 2014). It is imperative that as health care providers we are aware down to the cellular level the ways to diagnose, the causes, the treatments, and what the risk factors are. We must help to educate the population on these diseases. For a great portion of our population heart disease can be prevented.

References

Centers for Disease Control and Prevention. (2015). Heart disease fact sheet. Retrieved September 21, 2015, from http://www.cdc.gov/heartdisease/facts.htm
Huether, S., & McCance, K. (2012). Understanding pathophysiology (Fifth ed.). St. Louis, MO: Mosby.
Mayo Clinic. (2015). Diseases and conditions. Retrieved September 9, 2015, from http://www.mayoclinic.org/diseases-conditions
McPhee, S. J., & Hammer, G. D. (2012). Pathophysiology of disease: An introduction to clinical medicine (Sixth ed.). New York, NY: McGraw-Hill Medical.
Roberts, R. (2014). Genetics of Coronary Artery Disease. Circulation Research, , 1890-1903. doi:DOI: 10.1161/CIRCRESAHA.114.302692
World Health Organization. (2014). Cardiovascular Disease. Retrieved September 21, 2015, from http://www.who.int/cardiovascular_diseases/en/

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