July 2017

Suggested Citation: Garko, M.G. (2017, July). Coronary heart disease – Part VI:  Smoking cessation as part of a personal prevention program to combat coronary heart disease. Health and Wellness Monthly. Retrieved (insert month, day, year), from www.letstalknutrition.com.


Coronary heart disease – Part VI:  Smoking Cessation as Part of a Personal  

Prevention Program to Combat Coronary Heart Disease




Sudden Cardiac Death (SCD) takes the lives of nearly 1,000 people a day in the United States. This rate of mortality is equivalent to one death every two minutes or two jumbo 747 jets crashing per day (Heart Rhythm Foundation, 2006; National Heart Attack Alert Program, 2001). SCD is the most pervasive lethal manifestation of cardiovascular disease (CVD).


Although all known diseases of the heart can cause an abrupt loss of heart function (i.e., cardiac arrest) resulting in SCD, the most common underlying cause of SCD is coronary heart disease (CHD). Approximately 90% of adult SCD victims suffer from two or more diseased coronary arteries clogged by atherosclerosis (American Heart Association, 2006a & 2006b).


Unfortunately, SCD is the first and only symptom of a cardiac victim’s unexpected death. There is such little warning that approximately 335,000 people die annually of CHD without having the opportunity to be admitted to a hospital or taken to an emergency room. This amounts to about half of all deaths attributable to CHD. The majority of these are sudden cardiac deaths caused by cardiac arrest (American Heart Association (2006b).


Dying unexpectedly from cardiac arrest dramatizes the importance of maintaining cardiovascular health and preventing CHD. One of the prevailing themes running throughout the Health and Wellness Monthly series on coronary heart disease is that people must take personal responsibility for their health. For example, in the February, 2013, issue of Health and Wellness Monthlyit was proposed that people can take three action steps in taking personal responsibility for their cardiovascular health. First, they can become informed about the risk factors associated with CHD. Second, they can determine their individual level of risk for CHD. Third, they can adopt a lifestyle that excludes smoking and includes a heart-healthy diet and regular physical activity (see Garko, 2013, February).


The first five installments of the Health and Wellness Monthly series on coronary heart disease focused primarily on the first two action steps. The remaining installments in the series will spotlight dietary and lifestyle recommendations. It will be proposed that people can take personal responsibility for their health by creating, along with the assistance of a healthcare professional, a Personal Prevention Program based on the state of their cardiovascular health and level of risk for CHD.[1] The recommendations in the remaining issues in the series will focus on the three most important diet and lifestyle factors to promote cardiovascular health and prevent CHD (e.g., smoking cessation, heart-healthy nutrition, regular physical activity, etc.).


In this July, 2017, issue of Health and Wellness Monthly is an update of an earlier article focusing on smoking cessation to improve overall and cardiovascular health and minimize the odds of developing, dying from or being debilitated by CHD. Along the way, reference will be made to biochemical and physiological factors such as blood pressure, LDL and HDL cholesterol, homocysteine and C-reactive protein and how they become implicated with tobacco smoke, atherosclerosis and CHD.


Diet, Lifestyle and Cardiac Health


For almost a century researchers have accumulated a body of scientific evidence from cross-sectional studies, case-control studies, cohort studies and intervention studies identifying the causes of CHD, showing the effectiveness of diet and lifestyle on heart health and demonstrating that cardiovascular diseases (CHD in particular) are preventable (see Kromhout, 2002; Connor, 1999). A healthy diet and lifestyle factors such as regular physical exercise, moderate alcohol consumption of alcohol and not smoking, along with low serum cholesterol levels and low blood pressure, are correlated with a low risk of CHD (see Kromhout et al., 2002; Stamler, et al., 1999; Stampfer et al., 2000; Thomas et al., 2002).


Stated another way, notwithstanding the influence of aging, genes and environment and other factors bearing upon cardiac health, it is axiomatic that the biochemical and physiological risk factors associated with CHD such as diabetes, overweight-obesity, high blood pressure, high LDL levels, low HDL levels and increased fibrinogen, homocysteine and C-reactive protein levels track back to an unhealthy, risk-prone diet and lifestyle. Hence, the road to cardiovascular health is traveled most often by route of a healthy diet and lifestyle.

Distinguishing Between Diet and Lifestyle


It is quite common for cardiovascular recommendations to be divided into the categories of diet and lifestyle. Generally speaking, lifestyle refers to the way an individual lives on a day-to-day basis. It includes behavioral, cognitive (i.e., attitudes, values & beliefs) and emotional factors associated with everything from dress to diet. It is not uncommon to separate conceptually diet and lifestyle in discussions focusing on either modifiable risk factors associated with CHD or factors promoting cardiovascular health. Yet, dietary behaviors help make-up a person’s lifestyle because what people eat, why they eat, when they eat and with whom they eat are an important part of their day-to-day living and dietary rituals. That being said, diet is distinguished from lifestyle in this discussion in order to put a special focus on the impact of nutrition on maintaining cardiovascular health and preventing CHD. Otherwise, it is assumed that dietary behaviors are inherent to the concept of lifestyle.


Moreover, since biochemical and physiological processes related to cardiovascular functioning and heart health are so influenced by diet and lifestyle, keeping blood pressure, LDL and HDL cholesterol, insulin, homocysteine and C-reactive protein levels within heart-healthy ranges is considered to be a crucial part of individuals’ personal responsibility and, therefore, lifestyle.

Distinguishing Between Primary and Secondary Prevention


When it comes to CHD, the concept of prevention is divided typically into the two main categories of primary and secondary prevention. Generally speaking, primary prevention refers to “the effort to modify risk factors or prevent their development with the aim of delaying or preventing new-onset CHD,” while secondary prevention means “therapy to reduce recurrent CHD events and decrease coronary mortality in patients with established CHD” (Grundy, et al., 1998, p. 1879).[2]


Recommendation – Stop Smoking and Don’t Start


Most researchers and healthcare providers, including the Surgeon General of the United States, consider smoking to be the most important, lethal and preventable modifiable independent risk factor for CVD, generally, and CHD, specifically (see U.S. Department of Health and Human Services, 2004).




Effects of Tobacco Smoke on Overall and Cardiovascular Health


The Surgeon General’s 2004 report on The Health Consequences of Smoking is a sobering account of the devastating effects of tobacco smoke on virtually every cell, organ and major system of the human body, including the heart and cardiovascular system.


Studies reveal that compared to nonsmokers regular smokers and individuals exposed repeatedly to passive tobacco smoke have more of an increased  chance for (1) biomolecular oxidative damage to DNA, proteins and lipids than nonsmokers, (2) endothelial injury and dysfunction, a primary determinant in the development in atherosclerosis, (3) blood clots/thrombi along the arterial walls (4) plasma fibrinogen, a protein increasing the formation of blood clots, (5) localized arterial inflammation and systemic inflammation, reflected by increased levels of such biomarkers as leukocytes and C-reactive protein, (6) adverse lipid profiles, measured by higher concentrations of low density lipoprotein (LDL) and lower concentrations of higher density lipoprotein (HDL), (7) a higher oxygen demand induced by the release of catecholamines, which are associated with an increase in baseline heart rate, contractability and vascular tone, (9) deficient blood flow to the heart caused by a constriction of proximal an distal arteries and increase in coronary vessel tone, all of which results in a decreased oxygen supply to heart tissues and (10) lower levels of antioxidant micronutrients such as Vitamin C and carotenoids to neutralize free oxygen radicals that damage the endothelium of the coronary arteries  (see U.S. Department of Health and Human Services, 2004).


Even 42 years after the Surgeon General’s first report of the effects of smoking on human health, the catalogue of diseases and harmful effects associated with tobacco smoke continues to grow. In addition to CHD and all other forms of  cardiovascular disease, there is now substantial evidence to infer a causal relationship between active smoking and abdominal aortic aneurysm, acute myeloid leukemia, cataract, cervical cancer, kidney cancer, pancreatic cancer, pneumonia, periodontitis, stomach, bladder, esophageal, laryngeal, lung, oral, and throat cancers, chronic lung diseases, reproductive effects and sudden infant death syndrome (U.S. Department of Health and Human Services, 2004).


Tobacco Smoke, Atherosclerosis and CHD


It is widely recognized and accepted that atherosclerosis is the underlying pathogenic process responsible for the development of cardiovascular diseases, including CHD. Although considerable theoretical progress has been made in explaining the development of atherosclerosis, researchers are still debating and hypothesizing about the exact pathological sequence of events leading to CHD and other forms of cardiovascular disease. Nevertheless, a significant amount of empirical evidence now exists to conclude that atherosclerosis is an inflammatory disease and is the disease mechanism for CHD.


Response to injury hypothesis. The dominant explanation implicating inflammation in the development of atherosclerosis is Ross and Glomset’s (1973) response-to-injury hypothesis. Ross and Glomset (1973) hypothesized that atherosclerosis is caused by a localized injury to the endothelium of arteries. The injury can stem from a number of factors including physical stress on the arterial lining (i.e., high blood pressure), oxidative stress involving an increase in free radicals and/or decrease in antioxidants, elevated cholesterol levels and infection.


Endothelial damage can also be caused by the constellation of adverse chemicals found in tobacco smoke. When tobacco smoke reaches the airways and alveoli of the lungs, the gaseous and particulate components of the tobacco smoke (e.g., carbon monoxide, nicotine, benzo[a]pyrene) are circulated by the bloodstream throughout the body into the cells, tissues and organs. The chronic exposure of the coronary arteries to the adverse chemicals of tobacco smoke initiates oxidative stress and oxygen free radicals causing structural and functional damage to the endothelium.


Damage to the endothelial cells is a key event in the development of atherosclerosis in that the endothelium serves as a barrier between the blood flowing through the cavity of the artery (i.e., the lumen) and the inner most layer of the arterial wall (i.e., intima). One of the primary functions of the endothelium is to prevent substances flowing in the blood from entering the arterial wall.


Oxidative damage to the endothelium triggers a chronic inflammation response by the immune system to repair the endothelium and respond to the foreign substances (e.g., LDL cholesterol) now allowed to enter into the inner most layer of the arterial wall (i.e., intima). Over a person’s lifetime the continual switching on of the immune system in response to damaged endothelial cells and oxidized LDL cholesterol results in the formation of atherosclerotic plaque in the innermost layer of the arterial wall.[3] Paradoxically, the body’s immune system in its attempt to repair the damage to the coronary arteries ends-up becoming instrumental in the development of atherosclerosis.


Health Benefits of Smoking Cessation

There are a host of confirmed benefits associated with quitting smoking. The following are the major conclusions regarding the health benefits associated with smoking cessation found in the Surgeon


General’s 1990 Report on the Health Benefits of Smoking Cessation:

  • Smoking cessation has major and immediate health benefits for men and women of all ages. Benefits apply to persons with and without smoking-related disease.
  • Former smokers live longer than continuing smokers. For example, persons who quit smoking before age 50 have one-half the risk of dying in the next 15 years compared with continuing smokers.
  • Smoking cessation decreases the risk of lung cancer, other cancers, heart attack, stroke, and chronic lung disease.
  • Women who stop smoking before pregnancy or during the first 3 to 4 months of pregnancy reduce their risk of having a low birth weight baby to that of women who never smoked.
  • The health benefits of smoking cessation far exceed any risks from the average 5-pound (2.3-kg) weight gain or any adverse psychological effects that may follow quitting(U.S. Department of Health and Human Services, 1990, p.6).


The Surgeon General’s 1990 Report on the Health Benefits of Smoking Cessation provides the following on the impact smoking cessation has on overall mortality and morbidity:

  • Former smokers live longer than continuing smokers, and the benefits of quitting extend to those who quit at older ages. For example, persons who quit smoking before age 50 have one-half the risk of dying in the next 15 years compared with continuing smokers.
  • Smoking cessation at all ages reduces the risk of premature death.
  • Among former smokers, the decline in risk of death compared with continuing smokers begins shortly after quitting and continues for at least 10 to 15 years. After 10 to 15 years of abstinence, risk of all-cause mortality returns nearly to that of persons who never smoked.
  • Former smokers have better health status than current smokers as measured in a variety of ways, including days of illness, number of health complaints, and self-reported health status (U.S. Department of Health and Human Services, 1990, p.8).



With respect to smoking cessation and cardiovascular benefits, the Surgeon General’s 1990 Report on the Health Benefits of Smoking Cessation provides the following conclusions:

  • Compared with continued smoking, smoking cessation substantially reduces risk of coronary heart disease (CHD) among men and women of all ages.
  • The excess risk of CHD caused by smoking is reduced by about half after 1 year of smoking abstinence and then declines gradually. After 15 years of abstinence, the risk of CHD is similar to that of persons who have never smoked.
  • Among persons with diagnosed CHD, smoking cessation markedly reduces the risk of recurrent infarction and cardiovascular death. In many studies, this reduction in risk of recurrence or premature death has been 50 percent or more.
  • Smoking cessation substantially reduces the risk of peripheral artery occlusive disease compared with continued smoking.
  • Among patients with peripheral artery disease, smoking cessation improves exercise tolerance, reduces the risk of amputation after peripheral artery surgery, and increases overall survival.
  • Smoking cessation reduces the risk of both ischemic stroke and subarachnoid hemorrhage compared with continued smoking. After smoking cessation, the risk of stroke returns to the level of never smokers; in some studies this has occurred within 5 years, but in others as long as 15 years of abstinence were required (U.S. Department of Health and Human Services, 1990, p.10).


As reported by the Surgeon General, the following are specific health benefits that can be experienced at specific time intervals upon the cessation of smoking:

  • Within 20 minutes after quitting the heart rate drops.
  • Twelve hours after quitting, carbon monoxide levels in the blood drop to normal.
  • Two to three weeks after quitting, circulation improves and lung function increases.
  • One to nine months after quitting, coughing and shortness of breath decrease; cilia (i.e., tiny hair like structures responsible for moving mucus out of the lungs) regain their normal function, thereby, improving the ability to handle mucus, clean the lungs, and reduce the risk of infection.
  • One year after quitting, the increased risk of CHD is reduced to half that of smokers’ risk
  • Five years after quitting, the risk for stroke is reduced to that of a nonsmoker 5-15 years after quitting.
  • Ten years after quitting, the death rate for lung cancer death is approximately half that of a continuing smokers’ rate. Also, there is a decreased risk for cancer of the mouth, throat, esophagus, bladder, cervix and pancreas.
  • Fifteen years after quitting, the risk for CHD is that of nonsmokers (see Department of Health and Human Services, 1988; Department of Health and Human Services, 1990).




Smoking is tantamount to playing Russian roulette with one’s health and life. Given its lethalness and causal connection to atherosclerosis and CHD, tobacco smoke is certainly among the primary underlying causes responsible for the 1,000 sudden cardiac deaths occurring daily.

Decades worth of data on the effects of tobacco smoke on human health reveal that tobacco smoke harms virtually every organ of the body and is the cause of numerous diseases. Specifically, tobacco smoke causes cancer of many different types, cardiovascular diseases, respiratory diseases, reproductive defects, along with an increased risk for cataract, diminished overall health status, hip fractures, low bone density and peptic ulcer disease.


The good news is that while exposure to tobacco smoke is the most lethal cause of chronic disease-related death, it is the most preventable cause. There is a mountain of scientific evidence demonstrating that smoking cessation has immediate and long-term health benefits. In particular, the degree of death and disability stemming from CHD can be almost instantly reduced if there were a reduction in the number of people who smoked. It is not a medical mystery that tobacco smoke is a major contributor to the development of atherosclerosis and one of its most deadly outcomes, CHD.


For smokers, quitting smoking would a priority goal in their Personal Prevention Program to prevent CHD, in addition to all the other mentioned diseases. Admittedly, quitting smoking is a difficult challenge. It is beyond the scope of this newsletter to address how to start and succeed at a smoking cessation program. How to quit smoking is a topic that merits an in-depth discussion. Although there are numerous other helpful and credible sources, it is recommended that smokers refer to the American Cancer Society’s Guide to Quitting Smoking (2006) for insights and suggestions on how to initiate a successful smoking cessation program. It is a good way to become informed about what is involved in an effort to quit smoking. Smoking cessation is a process that involves biochemical, psychological and behavioral factors, among others.


Hence, a good first step in an effort to quit smoking is to become armed with the necessary information to understand the process involved in a smoking cessation program, which will increase the odds of succeeding. Many people embark upon a smoking cessation program by just trying to stop smoke. Some succeed most fail with this approach. A better approach is to learn in advance what the journey will entail and what to expect. It is recommended that a qualified health professional specializing in smoking cessation be enlisted to provide guidance and support.


In the meantime, it is recommended that a simultaneous effort be made to learn about and implement specific dietary and other lifestyle strategies (e.g., regular physical activity) to improve cardiovascular health and combat CHD. Some of these proposed strategies will be addressed in upcoming issues of Health and Wellness Monthly and can be included in a Personal Prevention Program to help prevent, delay and reverse CHD, depending on the particular cardiovascular status of those willing to take personal responsibility for their health.



American Cancer Society (n.d.). Guide to quitting smoking. Retrieved October 29, 2006, from http://cancer.org/docroot/PED/content/PED_10_13X_Guide_for_Quitting_Smoking.asp?sitearea cardiacthful Hints and can be included in a Personal Prevention Pr


American Heart Association (n.d.). About sudden death and cardiac arrest.  Retrieved October 15, 2006a, from


American Heart Association (n.d.). Sudden cardiac death.  Retrieved October 15, 2006b, from


Centers for Disease Control and Prevention (1990). The surgeon General’s 1990 report on the health benefits of smoking cessation: Executive Summary – introduction, overview, and conclusions. (Mortality and Morbidity Weekly Report, 39(RR-12), pp. 2-10). Atlanta, GA: Centers for Disease Control and Prevention.


Garko, Michael (2006, September). Cardiovascular health – Part VI: Modifiable risk factors for coronary heart disease. Healthful Hints. http://letstalknutrition.com  


Garko, M.G. (2013, February). Coronary heart disease – Part IV: Modifiable Risk Factors. Health and Wellness Monthly. Retrieved (insert month, day, year), from www.letstalknutrition.com.


Grundy, S.M., Balady, G.J, Criqui, M.H., Fletcher, G. et al. (1998). Primary prevention of coronary heart disease: Guidance from Framingham: A statement for healthcare professionals from the AHA task force on risk reduction. Circulation, 97,  1876-1887.


Heart Rhythm Foundation (n.d.), Sudden cardiac arrest key facts. Retrieved October, 15, 2006, from http://heartrhythmfoundation.org/facts/scd.asp


Kromhout, D, Menotti, A., Kesteloot, H & Sans, S. (2002). Prevention of coronary heart disease by diet and lifestyle: Evidence from prospective cross-cultural, cohort, and intervention studies. Circulation, 105, 893-898.


Pearson, T.A., Blair, S.N., Daniels, S.R., Eckel, R.H., et al. (2002). Circulation, 106, 388-391.


Ross, R. & Glomset, J.A. (1976). The pathogenesis of atherosclerosis (first of two parts). New England Journal of Medicine, 295: 369-377.


Ross, R. & Glomset, J.A. (1976). The pathogenesis of atherosclerosis (second of two parts). New England Journal of Medicine, 295: 420-525.


Stampfer, M.J., Hu, F.B., Manson, J.E., et al. (2000). Primary prevention of coronary heart disease in women through diet and lifestyle. New England Journal of Medicine, 343, 16-22.


Stamler, J. Stamler, R., Neaton, J.D. et al. (1999). Low risk-factor profile and long-term cardiovascular and noncardiovascular mortality and life expectancy. JAMA, 282, 2012-2018.


U.S. Department of Health and Human Services (2001). National heart attack alert program: National heart, lung, and blood institute coordinating committee meeting 10 year anniversary meeting. Retrieved October 25, 2006 from http://nhlbi.nih.gov/about/nhaap_hi601.htm


U.S. Department of Health and Human Services (2004). The health consequences of smoking: A report of the surgeon general. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. Atlanta, GA.


U.S. Department of Health and Human Services (1988). The health consequences of smoking: Nicotine addiction.U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Center for Health Promotion and Education, Office on Smoking and Health. DHHS Publication NO. (CDC) 88-8406.


Suggested Citation: Garko, M.G. (2017, July). Coronary heart disease – Part VI:  Smoking cessation as part of a personal prevention program to combat coronary heart disease. Health and Wellness Monthly. Retrieved (insert month, day, year), from www.letstalknutrition.com.


[1] It cannot be emphasized enough that the dietary and lifestyle recommendations offered in this month’s newsletter should not be construed to mean that readers should replace or abandon any current or future cardiovascular care or treatment provided by a healthcare professional. On the contrary, readers are encouraged to consult with a qualified healthcare professional before putting into practice any of the offered recommendations, especially if they have been or are being treated for cardiovascular disease in any of its various forms.


[2] The diet and lifestyle recommendations that will be offered are applicable to both types of prevention. However, secondary prevention may involve more aggressive medical treatment and intervention, underscoring the importance of those, who are cardiac patients, consulting a healthcare professional before adopting any of the recommendations.


[3] For an in depth treatment of atherosclerosis as an inflammation disease and the response-to-injury hypothesis see (1976a) and Ross & Glomset (1976b).