September 2012

Suggested Citation: Garko, M.G. (2012, September). Coronary heart disease – Part I: The prevalence, incidence, mortality and pathogenesis of the leading cause of death in the United States. Health and Wellness Monthly. Retrieved (insert month, day, year), from www.letstalknutrition.com.

 

Coronary Heart Disease – Part I: The Prevalence, Incidence, Mortality and Pathogenesis of the Leading Cause of Death in the United States

 Michael Garko, Ph.D.

Host of Let’s Talk Nutrition

Introduction 

Although it is only a bit larger than a fist, each day the human heart on average expands and contracts about 100,000 times and pumps approximately 2,000 gallons of blood throughout the vast circulatory system of the body. If the network of blood vessels of the circulatory system were laid out end-to-end, it would extend for a distance approximately equivalent to 60,000 miles or more than twice around the earth. Over a 70 year period the heart beats more than 2.5 billion times (Thomas et al., 2006).

These facts about the heart underscore the extent to which it must work over a person’s lifetime. They also point to the importance of keeping the heart healthy and free from disease, if it is expected to satisfy a workload that few mechanical pumps could meet.

Yet, coronary heart disease (CHD) is the most prevalent form of cardiovascular disease (CVD) in the United States and takes more American lives annually than any other degenerative disease. More than likely someone in your immediate family, circle of friends or coworkers has died from CHD. Make no mistake about it. Either directly or indirectly, CHD looms as a health threat to potentially each and every person reading this article.

Given its lethal prominence over all other diseases, the September, 2012, issues of Health and Wellness Monthly focuses on what CHD is and its prevalence, incidence, mortality and deadly pathogenic nature. Particular attention will be given to atherosclerosis, the underlying cause of CHD, and the role of inflammation in the origination and development of CHD.

 

Definition of Coronary Heart Disease

 

Coronary heart disease (CHD)[1] is a disease of the heart in which the inner endothelial lining or walls of one or more of its coronary arteries[2] become partially or completely narrowed by a long-term accumulation of atheromatous plaque[3] which reduces the flow of nutrient rich, oxygenated blood from the lungs to the heart muscle, undermines the structure and function of the heart and increases the risk of such cardiac events as chest pain (i.e., angina pectoris) and heart attack (myocardial infarction).

 

Prevalence, Incidence and Mortality of Coronary Heart Disease

 

The prevalence, incidence and mortality statistics related to coronary heart disease (CHD) reveal that far too many Americans are failing to practice good heart health.[4] This is evidenced by the fact that CHD is the most common type of cardiovascular disease (CVD) in the United States.[5]

 

Prevalence

 It is estimated that 16,300,000 people or 7% of American adults 20 years of age and older have CHD. Out of the total population of people diagnosed with CHD, 8.3% are males and 6.1% are females. It is predicted that by 2030 another 8,000,000 American adults could be diagnosed with CHD, representing a 16.6% increase in its prevalence from 2010 (see Roger et al., 2011).

 

Incidence

 Typically, the incidence of CHD is discussed and presented in the literature as the number of new cases of a coronary/heart attack (i.e., myocardial infarction – MI). According to Roger et al. (2011), in 2011 approximately 785,000 American adults will have a new coronary attack, while 470,000 American adults will experience a recurrent heart attack. It is estimated that the annual incidence of new cases of coronary attack is 610,000, with 325,000 recurrent attacks. The average age of experiencing a first heart attack is 64.5 years for men and 70.3 years for women.

 When it comes to gender and the incidence of CHD, there are some important differences between men and women. According to Roger et al. (2011), CHD comprises more than half of all cardiovascular events in men and women under age 75, with the lifetime risk of developing CHD after age 40 being 49% for men and 32% for women. The incidence of CHD itself is also different for men and women. The incidence of CHD in women falls behind men by 10 years for total CHD and lags behind by 20 years for more catastrophic clinical events such as MI and sudden death (see Roger et al., 2011).

 

Mortality

 When compared to other deadly degenerative diseases that plague Americans (including cancer), CHD ranks as the single leading cause of death of American males and females. It is responsible for one out of six deaths in the United States. In 2008 (most recent year reported), death from CHD was 405,309 (see Roger et al., 2011).

About every 25 seconds an American will experience a coronary related event and about every minute a person will experience a fatal cardiac event, usually a heart attack. About 34% of the people who experience a coronary attack in a given year will die from it. Approximately 15% of those who have a heart attack (MI) will from it and approximately every 34 seconds an American adult will have a heart attack (see Roger et al., 2011).

 

Pathogenesis of CHD: Atherosclerosis and Inflammation  

Understanding the underlying disease process of CHD is crucial to grasping what it is, how it comes about and its health consequences (i.e., death or disability). Moreover, knowing about the cause, disease development and effects (i.e., pathogenesis) of CHD provides insight into how best to prevent or reverse it or otherwise maintain long term cardiovascular health.

CHD is a direct consequence of atherosclerosis, an inflammatory disease process involving the gradual accumulation of plaque taking the form of lipid laden lesions (atheromas) on the inner walls of the coronary arteries. Atherosclerosis begins in early childhood (before age 10) with the appearance of soft, fatty streaks along the inner walls of the coronary arteries (McGill et. al, 2000). They do not block the flow of blood in the early stages of their development. However, over an extended period of time these fatty streaks evolve into thickened and hardened fibrous plaques/lesions. The atheromatous plaque builds up narrowing (i.e., stenosis) the open space (i.e., the lumen) within the arteries and preventing blood to flow freely.

One of the consequences of plaque narrowing the lumen is that the heart cannot receive a sufficient supply of fresh oxygenated blood, weakening the structure and function of the heart muscle. Another consequence is that the hard, fibrous outer shell of the plaque can rupture. When this happens platelets form a blood clot around the lesion. The clot can then block the flow of oxygenated blood through the already obstructed artery. If the artery becomes blocked completely, then within a short period of time the heart becomes starved for oxygen (ischemia) and the heart muscle cells begin to die resulting in permanent damage. This is medically termed a myocardial infarction. In common parlance, it is called a heart attack.

Typically, red blood cells, low-density lipoproteins (LDL), high-density lipoproteins (HDL), monocytes, and platelets course easily through healthy coronary arteries. However, when damage is done to the endothelial cells lining the arteries the immune system’s inflammation response is triggered to repair the damage.

What sets the inflammation response into motion is debated vigorously in the literature. Among other factors, viruses, bacteria, excessive, oxidized LDL cholesterol, hypertension/high blood pressure, homocysteine, tobacco smoke toxins, industrial chemical toxins, alcohol, refined sugar, excess saturated and trans-fats, insulin, excess refined, processed carbohydrates have all been mentioned as causes of inflammation or at least risk factors for it.  The debate about what causes atherosclerotic inflammation will not be settled in this article

Nevertheless, one plausible explanation derived from various scientific studies involves the oxidation of lipids (in particular LDL cholesterol) or what is termed as the lipid peroxidation hypothesis. It is hypothesized that when one or another inflammatory agent(s) damage(s) the endothelium lining of the coronary arteries the immune system kicks in and sends white blood cells to repair the injured site. Because it is a large-sized transporter of cholesterol, the LDL becomes trapped in the inner most layer of the arterial wall called the intima, which consists of a continuous layer of endothelial cells. Some of the trapped LDL then becomes oxidized by free radicals producing an inflammation response.

As the LDL is oxidized within the intima, monocytes flood to the inflamed site to then become macrophages. The macrophages literally consume the now oxidized LDL and grow into foam cells, which in turn become oxidized, thereby, promoting even more inflammation and immune scavenging macrophages to try and undo the cellular damage done to the endothelium. In the attempt to repair the oxidative damage, there is a proliferation of smooth muscle cells lining the arterial wall. The smooth muscle cells and macrophages produce connective tissue, all of which becomes mixed with the foam cells resulting in the scar-like tissue of fibro-lipid plaque to form along the arterial wall. Mineralization takes place further hardening the plaques and advancing the disease. This process repeats itself resulting in multiple layers and larger areas of plaque developing in the coronary arteries (e.g., see Berliner et al., 1995; Heinecke, 1998; Navab, et al., 1996; Raines et al., 1996; Ross, 1992, 1999; Witztum & Steinberg, 1991).

 

Summary

 

Notwithstanding the debate about what triggers inflammation in the coronary arteries, there is considerable theoretical and empirical support for viewing atherosclerosis as an inflammation disease. Research has revealed that immune implicated substances such as cytokines, T-lymphocytes, leukocytes, fibrinogen, Interlukin-1b, Interlukin-6, C-Reactive Protein (CRP), Macrophage-Monocyte Colony Stimulating Factor (MCSF) are associated with atherosclerosis (e.g., see Andreotti et al., 1999; Bauer et al., 1988; Cermak et al., 1993; Danesh et al., 1998; Dinarello, 1993; Libby & Ross, 1996; Luster, 1998; Rajavashisth et al., 1990; Ross, 1992, 1999; Shyy et al., 1993; Sironi et al., 1989); this research provides further evidence that atherosclerosis is an inflammation disease. Hence, if atherosclerosis is the underlying disease process of CHD and is inflammation based, then this suggests that the origination and development of CHD is connected to an immune or autoimmune response to injured endothelium by inflammation triggering agents.

Conclusion 

The human heart is a phenomenally powerful pump supplying fresh oxygenated, nutrient rich blood to every cell, tissue and organ in the body. It is paradoxically durable and capable of a sustained workload but vulnerable and susceptible to disease and failure. It beats relentlessly without ever pausing to rest. It is made of fatigue-proof muscle. The only time cardiac muscle loses its endurance and the heart is unable to continue its rhythmical beating is when it becomes diseased. Unfortunately, the diseasing of the heart takes place quietly and over a long period of time. It is as if it does not want to disappoint. But then one day it sends out a signal of serve pain in the chest. Depending on the extent of its diseased condition you either experience angina or suffer a fatal or near fatal heart attack. Too bad it does not signal in an overt way when atherosclerosis is in its early stages. Of course, it is our responsibility to practice preventative care by getting periodic check-ups. If you suspect you suffer from atherosclerosis, there are a variety of cardiac screening and diagnostic tests that can be performed for patients who are asymptomatic for cardiovascular disease.

 

Although there is an ongoing scientific debate about what triggers it, there is little debate among medical investigators that atherosclerotic inflammation is the underlying cause of CHD. Just as it is the responsibility of health consumers to monitor the condition their hearts, it is their responsibility to understand the role of inflammation in the pathogenesis of CHD and to learn about the various inflammation promoting risk factors associated with CHD, a topic which will be explored in an upcoming issue of Health and Wellness Monthly.

 

In the upcoming issue, it will be learned that researchers have identified a whole host of nutritional, genetic and lifestyle factors associated with CHD. Nevertheless, it is unlikely that CHD is caused by one factor (e.g., cholesterol). It is more likely that its origination and development is multi-factorial implicating biological, psychological and sociological factors that serve to switch on the immune system and trigger the inflammation process. The immune system starts out to repair coronary arterial damage. However, it ends up setting into motion a process that destroys the very thing it wanted to restore, yet another paradoxical feature of the heart. The immune system is the sentinel of the body. Regrettably, it is not an infallible one.

References 

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Bauer, J. et al. (1989). Regulation of interleukin 6 expression in cultured human blood monocytes and monocytes derived macrophages. Blood 72, 1134-1140.

Berliner, J.A. et al. (1995). Atherosclerosis: Basic mechanisms. Oxidation, inflammation, and genetics. Circulation, 91(9), 2488-2496.

Cermak, J., et al. (1993). C-reactive protein induces human peripheral blood monocytes to synthesize tissue factor. Blood  82, 513-520.

Danesh, J., et al. (1998). Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary artery disease. Meta-analyses of prospective studies. JAMA  279, 1477-1482.

Dinarello, C.A., et al. (1993). The role of interleukin-1 in disease. New England Journal of Medicine  328, 106-112.

Heinecke, J.W. (1988). Oxidants and antioxidants in the pathogenesis of

atherosclerosis: Implications for the oxidized low density lipoprotein hypothesis. Atherosclerosis. 141, 1-15.

Libby, P., et al. (1996). Cytokines and growth regulatory molecules in atherosclerosis. In V. Fuster, R. Ross & E.J. Topol (Eds.), Atherosclerosis and coronary artery disease (pp. 585-592). Philadelphia: Lippincott Raven Publishers.

Luster, A.D. (1998). Chemokines – Chemotactic cytokines that mediate inflammation. New England Journal of Medicine 338, 436-445.

Navab, M., et al. (1996). The Yin and Yang of oxidation in the development of the fatty streak: A review based on the 1994 George Lyman Duff Memorial Lecture. Arteriosclerosis, Thrombosis, Vascular Biology 16, 831-842.

McGill, H.C., et al. (2000). Origin of atherosclerosis in childhood and adolescence.

American Journal of Clinical Nutrition 72, 13075-13255.

Raines, E.W. et al. (1996). The role of macrophages. In V. Fuster, R. Ross & E.J. Topol (Eds.), Atherosclerosis and coronary artery disease: Chapter 30. Philadelphia: Lippincott Raven Publishers.

Rajavashisth, T.B., et al. (1990). Induction of endothelial cell expression of granulocyte and macrophage colony stimulating factors by modified low density lipoproteins. Nature 334, 254-257.

Ross, R. (1992). The pathogenesis of atherosclerosis. In E. Braunwald (Ed.), Heart disease (pp. 1106-1124). Philadelphia: W. B. Saunders.

Ross, R. (1999). Atherosclerosis-an inflammatory disease. New England Journal of Medicine 340, 115-126.

Roger, V., Go, A.S., Lloyd-Jones, D.M., Benjamin, E.J., Berry, J.D., Borden, W.B., Bravata, D.M., Dai, S., Ford, E.S., Fox, C.S., Fullerton, H.J., Gillespie, C., Hailpern, S.M., Heit, J.A., Howard, V.J., Kissela, jB.M., Kittner, S.J., Lackland, D.T.., Lichtman, J.H., Lisabeth, L.D., Makuc, D.M., Marcus, G.M., Marelli, A., Matchar, D.G., Mou, C.S., Mozaffarian, D., Mussolino, M.E., Nichol, G., Paynter, N.P., Soliman, E.Z., Sorlie, P.D., Sotoodehnia, N., Turan, T.N., Virani, S.S., Wong, N.D. Woo, D. & Turner, M.B. (2011). Heart disease and stroke statistics – 2012 Update: A report from the American Heart Association. Circulation. Retrieved January, 2012, from http://circ.ahajournals.org/content/early/2011/12/15/12/CIR.0b013e31823ac046.DC1.html

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Suggested Citation: Garko, M.G. (2012, September). Coronary heart disease – Part I: The prevalence, incidence, mortality and pathogenesis of the leading cause of death in the United States. Health and Wellness Monthly. Retrieved (insert month, day, year), from www.letstalknutrition.com.

[1] CHD is variously referred to in the literature as coronary artery disease (CAD), atherosclerotic heart disease and ischemic heart disease. At the same time, some writers even make a distinction between CHD and CAD. The terminological and definitional inconsistencies in the literature on CHD have contributed to the conceptual confusion confronting health consumers on cardiovascular disease (CVD), generally, and CHD, specifically.

[2] The arteries that supply oxygenated blood to the heart are termed “coronary” because they surround the heart in the form of a crown.

[3] Atheromatous plaque is made-up of such substances as cholesterol, proteins, calcium, fibrin, foam cells, smooth muscle cells and other elements. Structurally, atheromatous plaque can be divided into three distinguishable parts. There is the 1.atheroma (a mound or nodule of accumulated soft, flaky, yellowish material) occupying the center of larger plaques, 2. an underlying area of cholesterol crystals, and 3. calcification located at the outer area of more advanced lesions (Wikipedia, 2006).

 

 

 

 

[4] Prevalence means the total number of cases in a population at a given point in time. Incidence means the total number of new cases in a population in a one year period. Mortality means the total number of deaths in a population in a given year.

 

[5] Cardiovascular disease (CVD) includes all diseases related to the circulatory system, including congenital CVD (see Roger et al. 2012). Further, the prevalence of CVD includes those suffering from hypertension, heart disease (HD), stroke, peripheral artery disease (PAD) and diseases of the veins (see Roger et al., 2011).