Risk Factors

To predict incidence of cardiovascular disease, a number of risk factors have been proven to be indicative of cardiovascular disease risk. These traits can be broken up into two general categories; lipid and non-lipid risk factors (McGill, et al., 2001). Demographics for these risk factors are also available.

Lipid Risk Factors

Low Density Lipoprotein (LDL) Cholesterol

  • It has been known for many years that increased LDL cholesterol level result in increased cardiovascular disease incidence. This conclusion has been verified through decreased occurrence of coronary heart disease in patients treated with cholesterol-lowering therapy. In fact, when concentration levels were low enough, atherosclerosis no longer developed in patients (Gotto and Grundy 1999). Because of this direct correlation, LDL is the major risk factor in developing atherosclerotic disease and has been an area of significant prevention/treatment research
Low Density Lipoprotein Structure (Encyclopaedia Britannica 2007)
Low Density Lipoprotein Structure (Encyclopaedia Britannica 2007)

High Density Lipoprotein (HDL) Cholesterol

  • Studies have shown that there is generally an inverse association between HDL levels and coronary heart disease (Gordon, et al. 1989). This is in contrast to the LDL relationship. The exact mechanisms for this association are currently unknown, but there are several hypothesized that are being researched; most notable of these mechanisms is the “reverse transport” of cholesterol by HDL.

High Density Lipoprotein Structure (UC Davis 2008)
High Density Lipoprotein Structure (UC Davis 2008)

Non-Lipid Risk Factors


  • Smoking has been long associated with increased risk of cardiovascular disease. One study estimates that atherosclerotic disease increased by about 50% and incidence of coronary artery disease doubled in smokers (U.S. Department of Health and Human Services 1989). In addition to this, stopping smoking reduces the risk of cardiovascular disease significantly. Although the number of smokers has decreased in recent years, the disease is still prevalent among that population.


  • Hypertension is defined as having a systolic blood pressure greater than 140 mmHg or a diastolic blood pressure greater than 90 mmHg (Guibert and Franco 1996). There is an approximate linear relationship between elevated blood pressure and incidence of atherosclerotic disease (MacMahon 1990). Despite its ease of diagnosis and the availability of medical treatment, hypertension is still highly prevalent and is a major risk factor for cardiovascular disease.


  • The American Diabetes Association defines hyperglycemia as high glucose levels in the blood. Since glucose levels vary throughout the day, a subject with a consistent concentration above 7 mmol/L is said to be hyperglycemic. The risk of coronary atherosclerosis is 3 to 5 times greater when diabetic. The exact explanation for this requires further investigation; however, it is thought to be due to increased cholesterol esterification resulting in increased concentration of apolipoprotein E (Bierman 1992).

Plot of Coronary Heart Disease.jpg
Plot of Coronary Heart Disease Mortality Rates (Bierman 1992)


  • Age is the overriding risk factor out of every other factor listed here. It is an irreversible trait that increases the risk of developing cardiovascular disease. In a 10 year study consisting of 2489 men and 2956 women, aged 30 to 74 years at the time of their Framingham Heart Study, coronary heart disease (CHD) risk was found to increase with age. For example, males between 30-34 years old had a 3% 10 year CHD risk whereas males 70-74 years had a 30% 10 year CHD risk (Wilson, et al. 1998).

10 Year CHD Risk.jpg
Male (Left) and Female (Right) 10 Year Coronary Heart Disease Risks (Wilson, et al. 1998)


  • On average, females have less of a risk to develop coronary heart disease than males for a comparative age group (Wilson, et al. 1998). There are a few proposed reasons for this with suggested mechanisms, but none have been confirmed yet (Kannel, Hjortland and McNamara 1976). One possible explanation is that estrogen offers a protective effect to women. This is shown by increased coronary heart disease risk after menopause. Estrogen replacement therapy in post-menopausal woman has also been shown to reduce risk, thus verifying the hypothesis (Stampfer 1991). However, the exact mechanism of how estrogen offers protection is not known. Women also have higher HDL concentrations, which have been shown to decrease cardiovascular disease risk (Stocker and Keaney 2004).


  • Although the mechanisms are controversial on how obesity relates to atherosclerosis development, clustering of risk factors in patients usually occurs with obesity being included. Other risk factors included in the clustering are hypertension, low HDL cholesterol, and hyperglycemia. Obesity is defined as an excess in body fat; specifically, the World Health Organization classifies an adult with a BMI of 30.0 kg/m2 or higher as obese.


Bierman, E. L. (1992). George Lyman Duff memorial lecture. Atherogenesis in diabetes. Journal of the American Heart Association(12), 647-656.

Encyclopaedia Britannica. (2007). Low-Density Lipoprotein. Retrieved October 18, 2012, from Encyclopaedia Britannica: http://www.britannica.com/EBchecked/media/92254/Cutaway-view-of-a-low-density-lipoprotein-complex-The-LDL

Gordon, D. J., Probstfield, J. L., Garrison, R. J., Neaton, J. D., Castelli, W. P., Knoke, J. D., et al. (1989). High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. Circulation(79), 8 - 15.

Gotto, A. M., & Grundy, S. M. (1999). Lowering LDL cholesterol: questions from recent meta-analyses and subset analyses of clinical trial data issues from the interdisciplinary council on reducing the risk for coronary heart disease, ninth council meeting. Circulation(99), E1 - E7.

Guibert, R., & Franco, E. D. (1996). Choosing a definition of hypertension: impact on epidemiological estimates. (14, Ed.) Journal of Hypertension, 1275-1280.

Kannel, W. B., Hjortland, M. C., & McNamara, P. M. (1976). Menopause and risk of cardiovascular disease. Annals of Internal Medicine(85), 447-452.

MacMahon, S. (1990). Blood pressure, stroke, and coronary heart disease. Part 1, Prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet(335), 765.

McGill, H. C., McMahan, A. C., Zieske, A. W., Malcom, G. T., Tracy, R. E., & Strong, J. P. (2001). Effects of nonlipid risk factors on atherosclerosis in youth with a favorable lipoprotein profile. Circulation(103), 1546-1550.

Stampfer, M. J. (1991). Estrogen replacement therapy and coronary heart disease: a quantitative assessment of the epidemiologic evidence. Preventive Medicine(20), 47.

Stocker, R., & Keaney, J. F. (2004). Role of oxidative modifications in atherosclerosis. Physiol Rev(84), 1381-1478.

U.S. Department of Health and Human Services. (1989). Reducing the health consequences of smoking: 25 years of progress. A report of the surgeon general. U.S. Department of Health and Human Services.

UC Davis. (2008). HDL Composition Project. Retrieved October 18, 2012, from UCDavis Foods for Health Institute: http://ffhi.ucdavis.edu/prog/lnp/proj/comp

Wilson, P. W., D'Agostino, R. B., Levy, D., Belanger, A. M., Silbershatz, H., & Kannel, W. B. (1998). Prediction of coronary heart disease using risk factor categories. Circulation(97), 1837-1847.

Wilson, P. W., Kannel, W. B., Silbershatz, H., & D'Agostino, R. B. (1999). Clustering of metabolic factors and coronary heart disease. Arch Intern Medical(159), 1104-1109.