In 1998, one of every 2.5 deaths in the United States was caused directly by CVD, and CVD was a contributing cause in an additional 20 percent of deaths.² More than 60 million Americans suffer from one or more types of heart or blood vessel diseases and conditions, which include, in order of prevalence, hypertension, or HTN; coronary heart disease, or CHD; stroke, congestive heart failure; rheumatic heart disease; and congenital cardiovascular defects. This cluster of maladies claims approximately 950,000 lives annually, equaling an average of one death every 33 seconds. The largest share of this high mortality is attributed to CHD, which was the primary contributing cause of death in an estimated 460,000 Americans in 1998.²

Nonfatal CHD events also are significantly associated with subsequent mortality and morbidity. An estimated 25 percent of men and 38 percent of women will die within one year after a myocardial infarction, or MI, while 18 percent of men and 35 percent of women will have another attack within six years. Furthermore, 22 percent of men and 46 percent of women will be disabled by heart failure after their initial MI.

Overall, there are an estimated 12,400,000 Americans (6,000,000 men and 6,400,000 women) alive who have experienced a heart attack, angina pectoris or both. These people have a 1.5 to 15 times increased risk of illness and death compared with the general population.²

Short-term projected risk—that over a period of 10 years or less—of development of major cardiovascular events, such as MI and angina pectoris, in people with CHD has been estimated to be 26 percent,³ while the short-term average risk of developing a fatal or non-fatal MI among patients with stable angina is 20 percent.⁴

Eradication of CVD may not be a realistic goal in the near future, but increased efforts in educating, screening and improving treatment can influence the morbidity and mortality associated with these diseases.⁵

Identifying people at high risk of developing CHD is paramount to preventing initial coronary events.⁶ Secondary prevention, defined as preventing recurrent coronary events, also shows promise of reducing morbidity and mortality in patients with CHD. Oral health care providers are in a position to aid with both screening for and monitoring of risk factors associated with CVD, as well as to facilitate and provide patient education. This article will discuss the role of oral health care providers in caring for patients with CVD, as well as review risk factors and markers for CHD. To compile this information, I conducted MEDLINE and Internet searches and reviewed publications from professional organizations for the most updated information on cardiovascular disease and associated risk factors. More than 450,000 articles and monographs on CVD were published in English between January 1990 and May 2001. Of these, approximately 45,000 discussed CVD and risk factors. I selected and reviewed more than 550 publications on the basis of their relevance to epidemiology, etiology, and primary and secondary prevention of CVD.

Oral health care providers can only perform a screening for, and not make, a diagnosis of cardiovascular disease.

	INVOLVEMENT OF ORAL HEALTH CARE PROVIDERS

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An appropriate medical history should to be obtained from all patients in dental settings. This type of history taking serves many different purposes, including that of detecting possible medical problems. For the purpose of screening patients for CVD, specific information needs to be elicited. This includes the presence and type of CVD and risk factors for CVD, including age; smoking habits; family history of CVD and diabetes mellitus, or DM; presence of HTN; DM and serum glucose levels; serum cholesterol levels; body weight and height; and level of physical activity. Although some of this information may not be obtained routinely from all patients, it will help the clinician develop a better overall view of a patient’s general health.

Examination of dental patients should include measure of blood pressure, which may suggest presence of HTN, as well as patients’ HTN control. It is beyond the scope of clinicians to diagnose HTN, but it is their responsibility to monitor blood pressure for all patients.⁷ Although oral health care providers may acquire readings of patients’ serum glucose and cholesterol levels, this has not been established as a routine practice in dental settings. However, there are no direct contraindications for performing such procedures if the dental clinicians use the acquired information to establish presence or risk of disease and to facilitate an appropriate referral to a qualified health care provider.

The combination of a medical history and a physical examination will assist clinicians in screening for the existence and severity of CVD. Any discussion of the findings of such information needs to be accompanied with the caveat that oral health care providers can only perform a screening for, and not make, a diagnosis of CVD. If patients are not aware of their risk factors for, or the presence of, CVD, or that the status of their CVD has changed, clinicians need to refer the patient to an appropriate medical provider for further evaluation.

	LIFETIME RISK OF DEVELOPING CORONARY HEART DISEASE

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The Framingham Heart Study, published in 1999, calculated the lifetime risk of developing CHD—a first event of angina pectoris, coronary insufficiency (unstable angina), MI or death from CHD.⁸ In a cohort of 7,733 study participants, the lifetime risk was estimated to be 48.6 percent in men at age 40 years and 31.7 percent among women of the same age.⁸

This study was the first of its kind and represents average values for a specific population, which may or may not be applicable to other patient groups. The presence or absence of risk factors for CHD will significantly modify the cumulative lifetime risk, both for a large cohort and for each person in the cohort. Importantly, risk factors for CHD begin at ages much younger than those at which a disease manifests its first symptoms. Therefore, interventions to reduce the risk factors for CHD—such as smoking cessation, lowering of blood pressure, reduction of hypercholesterolemia and decreasing plasma glucose levels—will change a person’s lifetime risk of experiencing an adverse coronary event. This was evident in another study, which estimated the 10-year risk of developing CHD in 55-year old men and women and in which multivariate risk factors for CHD were calculated.⁹ Elevated blood pressure (130/85 millimeters of mercury or higher) predicted CHD in 28 percent of men and in 29 percent of women, and elevated total cholesterol (200 milligrams/deciliter or higher) predicted CHD in 27 percent of men and in 34 percent of women. Table 1 (page 292) provides a guide to quantitative evaluation of multiple risk factors.

	RISK ASSESSMENT

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Both identification and summation of risk factors need to be characterized to reach a global assessment of people at risk of developing CHD and to facilitate targeted intervention. Risk factors that need to be chronicled include age; a smoking history, usually recorded as pack-years or number of cigarettes over time; blood pressure and flow rate, which includes the systolic blood pressure, diastolic blood pressure, the pulse and heart rate; estimating of serum cholesterol, which includes total, LDL and HDL levels; and fasting plasma glucose levels (Table 2). Predisposing risk factors also need to be assessed. These include family history; overweight and obesity, which are measured by body weight, body mass index and waist circumference; physical inactivity; family history of premature CHD; and insulin resistance. Combinations of more than one risk category will increase the absolute risk of developing CHD.

Older people have a higher risk of dying when they have an ischemic cardiac event. In one study, the fatality rate for men before the age of 50 years who had no pre-existing MI or stroke was 20 percent, while men aged 65 to 69 years had a mortality rate of more than 50 percent, which increased to up to 80 percent in those older than 70 years of age.¹²

Smoking. Smoking declined by 41.7 percent among adults from 1965 to 1997.¹³ However, this trend has not continued, as the prevalence of smokers has remained constant since 1990. In 1997, one-fourth of all adults and one-third of all high school students in the United States were cigarette smokers.¹³ Every day, more than 3,000 people younger than 18 years of age become daily smokers, which is an increase of 20 percent from the late 1970s to 1997. It is hard to establish the detrimental effect of smoking as it relates to CVD mortality, but an estimated 320,000 Americans were thought to have died annually of smoking-related illnesses between 1990 and 1994.¹⁴

Cigarette smoking has been established as a risk factor for CHD independent of other risk factors. In a large longitudinal study of a cohort with total serum cholesterol < 200 mg/dL, smoking was the main contributing factor in more than 40 percent of cases of ischemic heart disease.¹⁵ Cigarette smoking is assumed to promote the buildup of coronary plaques, destabilize coronary plaques, promote plaque rupture, increase platelet activation and cause endothelial dysfunction, all of which consequently cause coronary thrombosis. Furthermore, smoking increases catecholamine release and may cause coronary spasms. Not surprisingly, smoking is a significant risk factor for angina pectoris and MI. Smoking cessation is associated with reduced risk of experiencing MI, eradicating the risk associated with smoking as soon as about two to three years after cessation.^16–19

The incidence of cardiovascular disease increases stepwise with increased blood pressure.

HTN. An estimated 50 million Americans have elevated blood pressure, also called HTN. According to the 1997 report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure of the National Heart, Lung, and Blood Institute,²⁰ 31.6 percent of affected people are unaware of having HTN, 26.2 percent are treated without being controlled and 14.8 percent are diagnosed with HTN but are not treated. Uncontrolled HTN is a major health concern in the United States. It causes various illnesses associated with a high incidence of morbidity and mortality, including end-stage renal disease, stroke and CHD. Several clinical trials have suggested that lowering of blood pressure will reduce the risk of developing CHD.^21,22

Numerous features contribute to the detrimental association between HTN and CVD. They include promotion of atherosclerosis and thrombogenesis, reduced coronary vasodilatory reserve and left ventricular hypertrophy.^23–29

The incidence of CVD increases stepwise with increased blood pressure. Studies have indicated that the risk of a cardiac event increases by 1.6 in men and 2.5 in women when blood pressures increase from an optimal level (< 120/80 mm Hg) to high normal (130–139/85–89 mm Hg).³⁰

The most favorable blood pressure for reducing the risk of CHD development in nondiabetic patients and patients without renal disease is probably < 140/90 mm Hg.²⁰ Although HTN is an independent risk factor, it also is strongly related to other risk factors such as hyperlipidemia, age, sex and race.

High serum cholesterol levels. Hypercholesterolemia is a recognized reversible risk factor for CHD. This has been shown in several studies in which cholesterol and mortality rate have a close linear relationship.³¹ Accordingly, recommendations on cholesterol screening suggest that all adults aged 20 years and older should have a fasting lipoprotein profile (total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides) performed every five years.³²

The level of serum total cholesterol correlates directly with CHD.⁹ Each subsequent level of total cholesterol from 200 mg/dL to 239 mg/dL (6.20 millimolars per deciliter), 240 mg/dL to 279 mg/dL (7.21 mmol/L) and 280 mg/dL are associated with a higher risk of developing CHD. More than 31 percent of American adults have borderline high blood cholesterol levels of 200 to 239 mg/dL. An additional 21 percent have total cholesterol levels of 240 mg/dL or higher.

The National Cholesterol Education Program of the National Heart, Lung, and Blood Institute has established standards for serum LDL and HDL cholesterol³² (Table 3). Although the risk of developing CHD is very low when the serum LDL cholesterol level is below 100 mg/dL, atherogenesis occurs even at the near-optimal level of a LDL cholesterol of 100 to 129 mg/dL. Combination of several risk factors usually provides a more comprehensive picture of the overall risk. Thus, men aged 45 to 65 years are at an increased risk of developing CHD when their total serum cholesterol level is < 240 mg/dL and/or their LDL cholesterol levels are > 160 mg/dL. The risk of developing CHD is threefold in a middle-aged man who has LDL cholesterol levels > 160 mg/dL and two additional risk factors as compared with a man the same age who has a lower level of serum LDL cholesterol.⁹ Treatment aimed at reducing serum LDL and total cholesterol has been associated with lower risk of CHD and lower mortality.^33–38

View this table: [in this window] [in a new window]   TABLE 3 CLASSIFICATION OF LDL*, TOTAL AND HDL CHOLESTEROL AND TRIGLYCERIDES.

Serum glucose levels and DM. DM is a major contributing factor in the development of CHD.⁴² Interestingly, its impact may differ among ethnic groups. A prospective study conducted in 1997 concluded that the percentage of CHD cases attributable to DM was 27 percent and 8 percent in African-American women and men, respectively, and 15 percent and 12 percent for nonblack men and women, respectively.⁴³ Regardless, DM clearly increases the risk of developing CHD and experiencing cardiovascular mortality. In a similar study, the seven-year incidence of first MI among people with type 2 DM was 20.2 percent, which was significantly higher than in people who did not have DM (3.5 percent).⁴⁴ The mortality rate attributed to CHD among people who had DM but no history of MI (15.4 percent) was as high as among high-risk groups of people without DM who had had a prior MI (15.9 percent). Among people who had DM but no previous MI, the mortality rate due to CVD was 7.5 times greater than in people without DM and no previous MI.⁴⁴ DM negates the normal sex difference in the prevalence of CVD, in which women have a mortality risk due to CVD almost 1.5 times greater than that of men.⁴⁵

The association between fasting glucose and CHD mortality can be described as a linear relationship, in which increasing levels of serum glucose are associated with an increased risk of experiencing CHD mortality. This was highlighted in a multicenter study following more than 7,000 men for an average of 23 years.⁴⁶ A fasting glucose level of 140 mg/dL was associated with a 42 percent increased risk of death from CHD compared with a fasting glucose level of 108 mg/dL.

A cluster of disorders including insulin resistance, HTN, dyslipidemia, impaired glucose intolerance and CVD started to be referred to as the "insulin resistance syndrome" in the 1980s.⁴⁷ The direct role of insulin in causing CHD has been reviewed extensively, and it is evident that insulin has a symphathoexcitatory influence that is associated with CHD in both diabetic and non-diabetic people.^48,49

The presence of one or more risk factors such as systolic HTN, elevated cholesterol or cigarette smoking has a greater impact on CVD mortality in people with DM than in people without it.⁵⁰ Consequently, controlling for these risk factors has been shown to significantly affect the success of both primary and secondary prevention of CVD.⁵¹

Family history. Clustering of CHD in families has been recognized for several decades. It has been estimated that about 5 percent of families account for as much as 50 to 60 percent of CHD in people who have CHD before the age of 55 years.⁵² It is assumed that the risk of developing CHD within affected families is multifactorial, with genetic and environmental components, as well as associated behavioral factors. Nevertheless, family history has been shown to be an independent risk factor even in the presence of traditional risk factors such as age, smoking, HTN and hypercholesterolemia.⁵³

A recent study of people with premature CHD, defined as documented MI or greater than 50 percent occlusion in a major coronary artery in people younger than 60 years of age, indicated a significant correlation between early onset of CHD and family history of CHD (defined by angina, MI, coronary artery bypass surgery or positive cardiac catheterization before the age of 60 years).⁵⁴ The risk of developing premature CHD was increased more than threefold when any first-degree relative was affected; almost sixfold when a first-degree relative had exhibited CHD before the age of 45 years; and about sixfold when at least two first-degree relatives had a history of CHD.⁵⁴ Other research has yielded similar results, with increased relative risk of developing CHD ranging from 3.3 to 5.9 for people with two or more first-degree relatives who have CHD.⁵⁵

Obesity is the major factor associated with insulin resistance and the metabolic syndrome, and it is considered the number 1 factor predisposing Americans to develop coronary heart disease.

Although family history is a significant independent risk factor, most people who have a family history of CHD also have additional risk factors.⁵⁴ However, a substantial genetic component may explain why there are people who develop CHD despite low risk profiles but who have a positive family history of CHD.⁵⁶

The importance of predicting premature CHD in first-degree relatives to enhance prevention is clear, as many undiagnosed relatives have remediable risk factors. A recent study indicated that among siblings of patients with premature CHD, 87 percent of black men, 86 percent of black women, 79.5 percent of white men and 71.1 percent of white women had treatable risk factors.⁵⁷ Others have found similar findings when apparently healthy siblings of people with documented premature CHD had a high prevalence of coronary risk factors, particularly inadequately controlled HTN.⁵⁸ Timely interventions are essential, as many of the risk factors for CHD develop in childhood.⁵⁹

There seems to be a significant association between the presence of carotid plaques and a familial history of premature death caused by CHD.⁶⁰ This is of interest, as carotid plaques can be visualized on dental panoramic radiographs.^61,62 Studies have yet to show if there is a significant relationship between the findings of carotid plaques on dental panoramic radiographs and CHD.

Excess body weight. More than 43 million Americans older than 20 years of age are obese, based on a body mass index, or BMI, of 30.0 or higher. (The BMI is calculated by dividing weight in kilograms by height in meters.²) More than one-half of the entire U.S. population, including children, are considered overweight (having a BMI > 25). The cause of overweight and obesity in the United States is, for the most part, an excessive intake of food and sedentary life habits. BMI approximates total body fat, but fat distribution may be an adjunct predictor of CHD. Waist circumference gives a better indication of the degree of insulin resistance, and fat deposit around the waist appears more significant than fat accumulation at other sites in the development of CHD. Consequently, waist circumferences of more than 40 inches in men and more than 36 inches in women suggests significant insulin resistance and a high risk of developing CHD.⁶³

Obesity is the major factor associated with insulin resistance and the metabolic syndrome, and it is considered the number 1 factor predisposing Americans to develop CHD. In addition, a strong association has been found between overweight that begins in childhood and a progressive increased rate of developing other risk factors during adulthood.⁶⁴ Although overweight may have a direct effect on traditional risk factors, it also is an independent predictor of atherosclerosis.⁶⁵ Accordingly, the American Heart Association has proposed that obesity should be included as a major risk factor for CHD.⁶⁶ The impact of overweight on CHD is modified by different factors, including age, sex, ethnicity, fitness and body fat distribution.⁶⁷

It is not always possible to quantify the overweight people’s increased risk of developing CHD. However, one study estimated that middle-aged men increased their risk of developing fatal and nonfatal CHD by 72 percent when their BMI increased from less than 23 to a point in the range from 25 to 29.⁶⁸

Physical inactivity. Sedentary life habits predispose a person to obesity, increased insulin resistance, metabolic risk factors, early onset of type 2 DM, poor cardiovascular fitness and impaired body function, and they are a risk factor for developing coronary artery disease.⁶⁹ Physical fitness and regular exercise appear to protect against CHD.⁷⁰ Quantification of the association between physical fitness and CVD mortality has been attempted. Using a standardized treadmill exercise test, it was shown that increased fitness during a period of approximately five years reduced the risk of experiencing CVD mortality by 52 percent.⁷¹ Other research found a progressive decline in both fatal and nonfatal CHD with an increase of activity up to 2,000 kilocalories per week.⁷² A large cohort of more than 12,500 men followed over a period of six years showed that men with multiple coronary risk factors reduced their risk of developing CHD if they expended more than 1,000 kcal/week in physical activity such as climbing stairs, walking, sports and recreational activities.⁷³ Although total energy expenditure was related to decreased CHD risk, duration of physical activity was not.⁷⁴ A meta-analysis from 1990 indicated that physical activity was inversely related to the incidence of CHD, with a relative increased risk of 1.9 when inactive people were compared with active people.⁷⁵

The benefit of walking also has been used to quantify the risk of developing CHD. One study indicates that risk of developing CHD was reduced by 15 percent for every 0.5 mile of walking per day.⁷⁶

The favorable effect of exercising may be a changed plasma lipid profile (decreased LDL and triglyceride levels and an increased HDL level), loss of body fat, decreased insensitivity to insulin and lower blood pressure. The most beneficial effect of exercising on CVD mortality is thought to be through moderate-intensity activity (at a level of 40 percent to 60 percent of maximum oxygen uptake).⁶⁹

Other potential risk factors. Several other potential markers of increased CHD risk are being studied, including lipoprotein(a), small dense LDL, total plasma homocysteine, fibrinolytic capacity, fibrinogen, platelet reactivity, hypercoagulability, high-sensitivity C-reactive protein and infectious agents.^77,78 Discussion of these markers is beyond the scope of this review.

Of particular interest to oral health care workers is the possible causative relationship between periodontal infections and CVD. A model for this association still is emerging. Numerous articles on this topic have been published in the medical and dental literature, but no clear consensus regarding the true association between these conditions has been reached yet.⁷⁹

	SUMMARY

TOP ABSTRACT INVOLVEMENT OF ORAL HEALTH... LIFETIME RISK OF DEVELOPING... RISK ASSESSMENT SUMMARY REFERENCES

 
Most patients visit their dentists when they perceive themselves as healthy, but see their physicians only when they are sick. This type of conduct gives dental clinicians an opportunity to screen for underlying medical conditions for which the patient may be unaware. The concept of using dentists as screeners for underlying systemic conditions is an important aspect of early detection and prevention of numerous medical conditions that are associated with high morbidity and mortality.

Many severe chronic medical conditions are discovered only at a late stage of the disease when signs and symptoms compel the affected person to seek medical care. However, the symptomatic stage usually occurs many years after the inception of the disease process. In most cases, early recognition and intervention may have prevented, or significantly delayed, the onset of the disease, which may have resulted in decreased morbidity and mortality. Dentists can have an important impact on CVD by acting as screeners and educators, as well as monitors of risk factors.