The 2008 overall rate of death attributable to cardiovascular disease (CVD) (International Classification of Diseases, 10th Revision, codes I00–I99) was 244.8 per 100 000. The rates were 287.2 per 100 000 for white males, 390.4 per 100 000 for black males, 200.5 per 100 000 for white females, and 277.4 per 100 000 for black females.

From 1998 to 2008, the rate of death attributable to CVD declined 30.6%. Mortality data for 2008 show that CVD (I00–I99; Q20–Q28) accounted for 32.8% (811 940) of all 2 471 984 deaths in 2008, or 1 of every 3 deaths in the United States.

On the basis of 2008 mortality rate data, more than 2200 Americans die of CVD each day, an average of 1 death every 39 seconds. About 150 000 Americans killed by CVD (I00–I99) in 2008 were <65 years of age. In 2008, 33% of deaths due to CVD occurred before the age of 75 years, which is well before the average life expectancy of 77.9 years.

Coronary heart disease caused ≈1 of every 6 deaths in the United States in 2008. Coronary heart disease mortality in 2008 was 405 309. Each year, an estimated 785 000 Americans will have a new coronary attack, and ≈470 000 will have a recurrent attack. It is estimated that an additional 195 000 silent first myocardial infarctions occur each year. Approximately every 25 seconds, an American will have a coronary event, and approximately every minute, someone will die of one.

Each year, ≈795 000 people experience a new or recurrent stroke. Approximately 610 000 of these are first attacks, and 185 000 are recurrent attacks. Mortality data from 2008 indicate that stroke accounted for ≈1 of every 18 deaths in the United States. On average, every 40 seconds, someone in the United States has a stroke. From 1998 to 2008, the stroke death rate fell 34.8%, and the actual number of stroke deaths declined 19.4%.

In 2008, 1 in 9 death certificates (281 437 deaths) in the United States mentioned heart failure.

Data from the National Health and Nutrition Examination Survey (NHANES) 2005–2008 indicate that 33.5% of US adults ≥20 years of age have hypertension (Table 7-1). This amounts to an estimated 76 400 000 US adults with hypertension. The prevalence of hypertension is nearly equal between men and women. African American adults have among the highest rates of hypertension in the world, at 44%.

Among hypertensive adults, ≈80% are aware of their condition, 71% are using antihypertensive medication, and only 48% of those aware that they have hypertension have their condition controlled.

Despite 4 decades of progress, in 2010, among Americans ≥18 years of age, 21.2% of men and 17.5% of women continued to be cigarette smokers. In 2009, 19.5% of students in grades 9 through 12 reported current cigarette use.

The percentage of the nonsmoking population with detectable serum cotinine (indicating exposure to secondhand smoke) declined from 52.5% in 1999 to 2000 to 40.1% in 2007 to 2008, with declines occurring, and was higher for those 3 to 11 years of age (53.6%) and those 12 to 19 years of age (46.5%) than for those 20 years of age and older (36.7%).

An estimated 33 600 000 adults ≥20 years of age have total serum cholesterol levels ≥240 mg/dL, with a prevalence of 15.0% (Table 14-1).

In 2008, an estimated 18 300 000 Americans had diagnosed diabetes mellitus, representing 8.0% of the adult population. An additional 7 100 000 had undiagnosed diabetes mellitus, and 36.8% had prediabetes, with abnormal fasting glucose levels. African Americans, Mexican Americans, Hispanic/Latino individuals, and other ethnic minorities bear a strikingly disproportionate burden of diabetes mellitus in the United States (Table 17-1).

The estimated prevalence of overweight and obesity in US adults (≥20 years of age) is 149 300 000, which represents 67.3% of this group in 2008. Fully 33.7% of US adults are obese (body mass index ≥30 kg/m²). Men and women of all race/ethnic groups in the population are affected by the epidemic of overweight and obesity (Table 16-1).

Among children 2 to 19 years of age, 31.7% are overweight and obese (which represents 23.6 million children), and 16.9% are obese (12.6 million children). Mexican American boys and girls and African American girls are disproportionately affected. Over the past 3 decades, the prevalence of obesity in children 6 to 11 years of age has increased from ≈4% to >20%.

Obesity (body mass index ≥30 kg/m²) is associated with marked excess mortality in the US population. Even more notable is the excess morbidity associated with overweight and obesity in terms of risk factor development and incidence of diabetes mellitus, CVD end points (including coronary heart disease, stroke, and heart failure), and numerous other health conditions, including asthma, cancer, degenerative joint disease, and many others.

The prevalence of diabetes mellitus is increasing dramatically over time, in parallel with the increases in prevalence of overweight and obesity.

On the basis of NHANES 2003–2006 data, the age-adjusted prevalence of metabolic syndrome, a cluster of major cardiovascular risk factors related to overweight/obesity and insulin resistance, is ≈34% (35.1% among men and 32.6% among women).

The proportion of youth (≤18 years of age) who report engaging in no regular physical activity is high, and the proportion increases with age. In 2009, among adolescents in grades 9 through 12, 29.9% of girls and 17.0% of boys reported that they had not engaged in 60 minutes of moderate-to-vigorous physical activity, defined as any activity that increased heart rate or breathing rate, even once in the previous 7 days, despite recommendations that children engage in such activity ≥5 days per week.

Thirty-three percent of adults reported engaging in no aerobic leisure-time physical activity.

Data from NHANES indicate that between 1971 and 2004, average total energy consumption among US adults increased by 22% in women (from 1542 to 1886 kcal/d) and by 10% in men (from 2450 to 2693 kcal/d; see Chart 20-1).

The increases in calories consumed during this time period are attributable primarily to greater average carbohydrate intake, in particular, of starches, refined grains, and sugars. Other specific changes related to increased caloric intake in the United States include larger portion sizes, greater food quantity and calories per meal, and increased consumption of sugar-sweetened beverages, snacks, commercially prepared (especially fast food) meals, and higher energy-density foods.

Table 2-1 provides the specific definitions for ideal, intermediate, and poor cardiovascular health for each of the 7 health behaviors and health factors, for adults ≥20 years of age and children of selected ages (depending on data availability).

The prevalences of ideal, intermediate, and poor levels of each of the 7 cardiovascular health metrics are shown in Chart 2-1 (for children ages 12–19 years) and Chart 2-2 (for adults ≥20 years of age).

Age-standardized and age-specific prevalence estimates for ideal cardiovascular health and for ideal levels of each of its components are shown in Table 2-2.

Chart 2-3 displays the prevalence estimates for the population of US children meeting different numbers of criteria for ideal cardiovascular health (out of 7 possible).

Charts 2-4 and 2-5 display the age-standardized prevalence estimates for the population of US adults meeting different numbers of criteria for ideal cardiovascular health (out of 7 possible), overall and stratified by age groups, sex, and race.

Chart 2-6 displays the age-standardized percentages of US adults and percentages of children who have 5 or more of the metrics (out of 7 possible) at ideal levels.

Chart 2-7 displays the age-standardized percentages of US adults meeting different numbers of criteria for poor and ideal cardiovascular health. Meeting the AHA 2020 Strategic Impact Goals is predicated on reducing the relative percentage of those with poor levels while increasing the relative percentage of those with ideal levels for each of the 7 metrics.

The prevalence of risk factors and their awareness, treatment, and control are displayed in Table 2-3 separately for those with and without self-reported CVD. Among those without CVD, NHANES 2007–2008 data indicate the following:

In 2007, the age-standardized death rate attributable to all CVDs was 251.2 per 100 000 (Chart 2-8), down 4.3% from 262.5 in 2006 (baseline data for the 2020 Impact Goals on CVD and stroke mortality).

Data from NHANES 2007–2008 reveal that overall, 6.6% of Americans self-reported having some type of CVD (Table 2-3).

Among those with CVD, risk factor prevalence, awareness, treatment, and control in NHANES 2007 to 2008 were variable (Table 2-3).

Folsom et al² recently published the first examination of the community prevalence of ideal cardiovascular health and its association with incident CVD events in 12 744 white and African American participants of the ARIC study aged 45 to 64 years at baseline who were followed up for up to 20 years.

Taken together, these data continue to indicate the substantial progress that will need to occur for the AHA to achieve its 2020 Impact Goals over the next decade. If the goals can be met, there is evidence suggesting that CVD event rates could decrease significantly.

As shown in Table 2-4, relatively modest changes in population levels of health factors could result in important changes in the prevalence of overall and ideal cardiovascular health. For example, NHANES 2007–2008 data indicate that the current prevalence of ideal levels of BP among US adults is 43.8%. A 20% relative improvement by 2020 would mean the prevalence of ideal BP would need to increase to 52.6%. NHANES data indicate that a reduction in the population mean BP by just 2 mm Hg would result in 55.5% of US adults having ideal levels of BP. Further reductions in BP would mean even more people would achieve ideal levels. Such modest reductions could result from decreased salt intake at the population level of as little as 1 to 2 g per day, with significant projected decreases in CVD rates in US adults.³

Future issues of the Statistical Update will track progress toward the 2020 Strategic Impact Goals.

High BP (HBP)—76 400 000 (defined as systolic pressure ≥140 mm Hg and/or diastolic pressure ≥90 mm Hg, use of antihypertensive medication, or being told at least twice by a physician or other health professional that one has HBP).

Coronary heart disease (CHD)—16 300 000

The following age-adjusted prevalence estimates from the NHIS, NCHS are for diagnosed conditions for people ≥18 years of age in 2010¹:

Asian Indian adults (9%) are ≈2-fold more likely than Korean adults (4%) to have ever been told they have HD, based on data for 2004 to 2006.²

By 2030, 40.5% of the US population is projected to have some form of CVD.³

On the basis of the NHLBI’s FHS original and offspring cohort data from 1980 to 2003⁴:

Among American Indian men 45 to 74 years of age, the incidence of CVD ranges from 15 to 28 per 1000 population. Among women, it ranges from 9 to 15 per 1000.⁵

Data from the FHS indicate that the subsequent lifetime risk for all CVD in recipients starting free of known disease is 2 in 3 for men and >1 in 2 for women at 40 years of age (personal communication, Donald Lloyd-Jones, MD, Northwestern University, Chicago, IL; Table 3-4).

Analysis of FHS data among participants free of CVD at 50 years of age showed the lifetime risk for developing CVD was 51.7% for men and 39.2% for women. Median overall survival was 30 years for men and 36 years for women.⁶

Mortality data show that CVD (I00–I99, Q20–Q28) as the listed underlying cause of death (including congenital cardiovascular defects) accounted for 32.8% (811 940) of all 2 471 984 deaths in 2008, or 1 of every 3 deaths in the United States. CVD any-mentions (1 354 527 deaths in 2008) constituted 55.0% of all deaths that year (NHLBI; NCHS public-use data files).⁷

In every year since 1900 except 1918, CVD accounted for more deaths than any other major cause of death in the United States.^8,9

On average, >2200 Americans die of CVD each day, an average of 1 death every 39 seconds. CVD currently claims more lives each year than cancer, CLRD, and accidents combined.⁷

The 2008 death rate attributable to CVD (I00–I99) was 244.8 (excluding congenital cardiovascular defects) (NCHS).⁷ The rates were 287.2 for white males, 390.4 for black males, 200.5 for white females, and 277.4 for black females. From 1998 to 2008, death rates attributable to CVD (ICD-10 I00–I99) declined 30.6%. In the same 10-year period, the actual number of CVD deaths per year declined 14.1% (NHLBI tabulation).⁷ (Appropriate comparability ratios were applied.)

Among other causes of death in 2008, cancer caused 565 469 deaths; CLRD, 141 090; accidents, 121 902; and Alzheimer disease, 82 435.⁷

The 2008 CVD (I00–I99) death rates were 292.6 for males and 206.1 for females. There were 40 589 deaths due to breast cancer in females in 2008; lung cancer claimed 70 070 in females. Death rates for females were 22.5 for breast cancer and 39.0 for lung cancer. One in 31 deaths in females was attributable to breast cancer, whereas 1 in 6.6 was attributable to CHD. For comparison, 1 in 4.6 females died of cancer, whereas 1 in 3.0 died of CVD (I00–I99, Q20–Q28). On the basis of 2008 mortality data, CVD caused ≈1 death per minute among females, or 419 730 deaths in females in 2008. That represents more female lives than were claimed by cancer, CLRD, and Alzheimer disease combined (unpublished NHLBI tabulation).⁷

About 150 000 Americans died of CVD (I00–I99) in 2008 who were <65 years of age, and 33% of deaths attributed to CVD occurred before the age of 75 years, which is well below the average life expectancy of 77.9 years.⁷

According to the NCHS, if all forms of major CVD were eliminated, life expectancy could rise by almost 7 years. If all forms of cancer were eliminated, the estimated gain could be 3 years. According to the same study, the probability at birth of eventually dying of major CVD (I00–I78) is 47%, and the chance of dying of cancer is 22%. Additional probabilities are 3% for accidents, 2% for DM (unrelated to CVD), and 0.7% for HIV.¹⁰

In 2008, the leading causes of death in women ≥65 years of age were diseases of the heart (No. 1), cancer (No. 2), stroke (No. 3), and CLRD (No. 4). In older men, they were diseases of the heart (No. 1), cancer (No. 2), CLRD (No. 3), and stroke (No. 4).⁷

A study of the decrease in US deaths attributable to CHD from 1980 to 2000 suggests that ≈47% of the decrease was attributable to increased use of evidence-based medical therapies and 44% to changes in risk factors in the population attributable to lifestyle and environmental changes.¹¹

Analysis of data from NCHS was used to determine the number of disease-specific deaths attributable to all non-optimal levels of each risk factor exposure, by age and sex. In 2005, tobacco smoking and HBP were estimated to be responsible for 467 000 deaths, accounting for ≈1 in 5 or 6 deaths among US adults. Overweight/obesity and physical inactivity were each estimated to be responsible for nearly 1 in 10 deaths. High dietary salt, low dietary omega-3 fatty acids, and high dietary trans fatty acids were the dietary risks with the largest estimated excess mortality effects.¹²

Among an estimated 45 million people with functional disabilities in the United States, HD, stroke, and hypertension are among the 15 leading conditions that caused those disabilities. Disabilities were defined as difficulty with activities of daily living or instrumental activities of daily living, specific functional limitations (except vision, hearing, or speech), and limitation in ability to do housework or work at a job or business.¹³

Surveys conducted by the AHA in 1997, 2000, 2003, and 2006 to evaluate trends in women’s awareness, knowledge, and perceptions related to CVD found that in 2006, awareness of HD as the leading cause of death among women was 57%, significantly higher than in prior surveys. Awareness was lower among black and Hispanic women than among white women, and the racial/ethnic difference has not changed appreciably over time. In 2006, more than twice as many women felt uninformed about stroke compared with HD. Hispanic women were more likely than white women to report that there is nothing they can do to keep themselves from getting CVD. The majority of respondents reported confusion related to basic CVD prevention strategies.¹⁴

A nationally representative sample of women responded to a questionnaire about history of CVD risk factors, self-reported actions taken to reduce risk, and barriers to heart health. According to the study, published in 2006, the rate of awareness of CVD as the leading cause of death had nearly doubled since 1997, was significantly greater for whites than for blacks and Hispanics, and was independently correlated with increased PA and weight loss in the previous year. Fewer than half of the respondents were aware of healthy levels of risk factors. Awareness that their personal level was not healthy was positively associated with preventive action. Most women took steps to lower risk in family members and themselves.¹⁵

A total of 875 students in 4 Michigan high schools were given a survey to obtain data on the perception of risk factors and other knowledge-based assessment questions about CVD. Accidents were rated as the greatest perceived lifetime health risk (39%). Nearly 17% selected CVD as the greatest lifetime risk, which made it the third most popular choice after accidents and cancer. When asked to identify the greatest cause of death for each sex, 42% correctly recognized CVD for men, and 14% correctly recognized CVD for women; 40% incorrectly chose abuse/use behavior with a substance other than cigarettes as the most important CVD risk behavior.¹⁶

Seventy-nine percent of the lay public are confident that they know what actions to take in a medical emergency; 98% recognize an automated external defibrillator as something that administers an electric shock to restore a normal heart beat among victims of sudden cardiac arrest; and 60% are familiar with cardiopulmonary resuscitation (Harris Interactive survey conducted on behalf of the AHA among 1132 US residents ≥18 years of age, January 8, 2008, through January 21, 2008).

Data from the 2003 CDC BRFSS survey of adults ≥18 years of age showed the prevalence of respondents who reported having ≥2 risk factors for HD and stroke was successively higher at higher age groups. The prevalence of having ≥2 risk factors was highest among blacks (48.7%) and American Indian/Alaska Natives (46.7%) and lowest among Asians (25.9%); prevalence was similar in women (36.4%) and men (37.8%). The prevalence of multiple risk factors ranged from 25.9% among college graduates to 52.5% among those with less than a high school diploma (or its equivalent). People reporting household income of ≥$50 000 had the lowest prevalence (28.8%), and those reporting household income of <$10 000 had the highest prevalence (52.5%). Adults who reported being unable to work had the highest prevalence (69.3%) of ≥2 risk factors, followed by retired people (45.1%), unemployed adults (43.4%), homemakers (34.3%), and employed people (34.0%). Prevalence of ≥2 risk factors varied by state/territory and ranged from 27.0% (Hawaii) to 46.2% (Kentucky). Twelve states and 2 territories had a multiple risk factor prevalence of ≥40%: Alabama, Arkansas, Georgia, Indiana, Kentucky, Louisiana, Mississippi, North Carolina, Ohio, Oklahoma, Tennessee, West Virginia, Guam, and Puerto Rico.¹⁷

Data from the Chicago Heart Association Detection Project (1967–1973, with an average follow-up of 31 years) showed that in younger women (18–39 years of age) with favorable levels for all 5 major risk factors (BP, serum cholesterol, body mass index [BMI], DM, and smoking), future incidence of CHD and CVD is rare, and long-term and all-cause mortality are much lower than for those who have unfavorable or elevated risk factor levels at young ages. Similar findings applied to men in this study.^18,19

Analysis of several data sets by the CDC showed that in adults ≥18 years of age, disparities were common in all risk factors examined. In men, the highest prevalence of obesity (29.7%) was found in Mexican Americans who had completed a high school education. Black women with or without a high school education had a high prevalence of obesity (48.4%). Hypertension prevalence was high among blacks (41.2%) regardless of sex or educational status. Hypercholesterolemia was high among white and Mexican American men and white women regardless of educational status. CHD and stroke were inversely related to education, income, and poverty status. Hospitalization for total HD and acute MI (AMI) was greater among men, but hospitalization for congestive heart failure (CHF) and stroke was greater among women. Among Medicare enrollees, CHF hospitalization was higher among blacks, Hispanics, and American Indian/Alaska Natives than among whites, and stroke hospitalization was highest among blacks. Hospitalizations for CHF and stroke were highest in the southeastern United States. Life expectancy remains higher in women than in men and in whites than in blacks by ≈5 years. CVD mortality at all ages tended to be highest in blacks.²⁰

Analysis of 5 cross-sectional, nationally representative surveys from the National Health Examination Survey (NHES) 1960 to 1962 to the NHANES 1999 to 2000 showed that the prevalence of key risk factors (ie, high cholesterol, HBP, current smoking, and total DM) decreased over time across all BMI groups, with the greatest reductions observed among overweight and obese groups. Total DM prevalence was stable within BMI groups over time; however, the trend has leveled off or been reversed for some of the risk factors in more recent years.²¹

Data from BRFSS 2006 to 2008 demonstrated that during this 3-year period, 25.6% of non-Hispanic blacks, non-Hispanic whites, and Hispanics were obese, but prevalent obesity varied across groups: 35.7% for non-Hispanic blacks, 28.7% for Hispanics, and 23.7% for non-Hispanic whites.

Data from NHANES 2005 to 2006 showed that 90.4% of US adults exceeded their recommended target limit of daily dietary sodium intake.²²

Analysis of >14 000 middle-aged subjects in the ARIC study sponsored by the NHLBI showed that >90% of CVD events in black subjects, compared with ≈70% in white subjects, appeared to be explained by elevated or borderline risk factors. Furthermore, the prevalence of participants with elevated risk factors was higher in black subjects; after accounting for education and known CVD risk factors, the incidence of CVD was identical in black and white subjects. Thus, the observed higher CVD incidence rate in black subjects appears to be largely attributable to a greater prevalence of elevated risk factors. These results suggest that the primary prevention of elevated risk factors might substantially impact the future incidence of CVD, and these beneficial effects would likely be applicable not only for white but also for black subjects.²³

Data from the MEPS 2004 Full-Year Data File showed that nearly 26 million US adults ≥18 years of age were told by a doctor that they had HD, stroke, or any other heart-related disease²⁴:

Participants (18–64 years of age at baseline) in the Chicago Heart Association Detection Project in Industry without a history of MI were investigated to determine whether traditional CVD risk factors were similarly associated with CVD mortality in black and white men and women. In general, the magnitude and direction of associations were similar by race. Most traditional risk factors demonstrated similar associations with mortality in black and white adults of the same sex. Small differences were primarily in the strength and not the direction of the association.²⁵

A study of nearly 1500 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) study found that Hispanics with hypertension, hypercholesterolemia, and/or DM who speak Spanish at home and/or have spent less than half a year in the United States have higher systolic BP (SBP), low-density lipoprotein (LDL) cholesterol, and fasting blood glucose, respectively, than Hispanics who speak English and who have lived a longer period of time in the United States.²⁶

A family history of CVD increases risk of CVD, with the largest increase in risk if the family member’s CVD was premature.²⁷

There is consistent evidence from multiple large-scale prospective epidemiology studies for a strong and significant association of a reported family history of premature parental CHD with incident MI or CHD in offspring. In the FHS, the occurrence of a validated premature atherosclerotic CVD event in either a parent²⁸ or a sibling²⁹ was associated with an ≈2-fold elevated risk for CVD, independent of other traditional risk factors.

Addition of family history of premature CVD to a model that contained traditional risk factors provided modestly improved prognostic value in the FHS.²⁸ Family history of premature MI is also an independent risk factor in other multivariable risk models that contain traditional risk factors in large cohorts of women³⁰ and men.³¹

Parental history of premature CHD is associated with increased burden of subclinical atherosclerosis in the coronary arteries and the abdominal aorta.^32,33

In the FHS, a parental history of validated HF is associated with a 1.7-fold higher risk of HF in offspring, after multivariable adjustment.³⁴

A family history of early-onset sudden cardiac death in a first-degree relative is associated with a >2-fold higher risk for sudden cardiac death in offspring on the basis of available case-control studies.³⁵

The 2004 HealthStyles survey of 4345 people in the United States indicated that most respondents believe that knowing their family history is important for their own health, but few are aware of the specific health information from relatives necessary to develop a family history.³⁶

An accurate and complete family history may identify rare mendelian conditions such as hypertrophic cardiomyopathy (HCM), long-QT syndrome, or familial hypercholesterolemia. However, in the majority of people with a family history of a CVD event, a known rare mendelian condition is not identified.

Studies are under way to determine genetic variants that may help identify individuals at increased risk of CVD.

The lifetime risk for CVD and median survival were highly associated with risk factor presence and burden at 50 years of age among >7900 men and women from the FHS followed up for 111 000 person-years. In this study, optimal risk factor burden at 50 years of age was defined as BP <120/80 mm Hg, total cholesterol <180 mg/dL, absence of DM, and absence of smoking. Elevated risk factors were defined as stage 1 hypertension or borderline high cholesterol (200–239 mg/dL). Major risk factors were defined as stage 2 hypertension, elevated cholesterol (≥240 mg/dL), current smoking, and DM. Remaining lifetime risks for atherosclerotic CVD events were only 5.2% in men and 8.2% in women with optimal risk factors at 50 years of age compared with 68.9% in men and 50.2% in women with ≥2 major risk factors at age 50. In addition, men and women with optimal risk factors had a median life expectancy ≥10 years longer than those with ≥2 major risk factors at age 50 years.⁶

A recent study examined the association between low lifetime predicted risk for CVD (ie, having all optimal or near-optimal risk factor levels) and burden of subclinical atherosclerosis in younger adults in the Coronary Artery Risk Development in Young Adults (CARDIA) and MESA studies of the NHLBI. Among participants <50 years of age, nearly half had low and half had high predicted lifetime risks for CVD. Those with low predicted lifetime risk had lower prevalence and less severe amounts of coronary calcification and less carotid intima-media thickening, even at these younger ages, than those with high predicted lifetime risk. During follow-up, those with low predicted lifetime risk also had less progression of coronary calcium.³⁷

In another study, FHS investigators followed up 2531 men and women who were examined between the ages of 40 and 50 years and observed their overall rates of survival and survival free of CVD to 85 years of age and beyond. Low levels of the major risk factors in middle age were associated with overall survival and morbidity-free survival to ≥85 years of age.³⁸

A study of 366 000 men and women from the Multiple Risk Factor Intervention Trial (MRFIT) and Chicago Heart Association Detection Project in Industry defined low-risk status as follows: Serum cholesterol level <200 mg/dL, untreated BP 120/80 mm Hg, absence of current smoking, absence of DM, and absence of major electrocardiographic abnormalities. Compared with those who did not have low risk factor burden, those with low risk factor burden had between 73% and 85% lower relative risk (RR) for CVD mortality, 40% to 60% lower relative total mortality rates, and 6 to 10 years’ longer life expectancy.¹⁹

A study of 84 129 women enrolled in the Nurses’ Health Study identified 5 healthy lifestyle factors, including absence of current smoking, drinking half a glass or more of wine per day (or equivalent alcohol consumption), half an hour or more per day of moderate or vigorous PA, BMI <25 kg/m², and dietary score in the top 40% (which included diets with lower amounts of trans fats, lower glycemic load, higher cereal fiber, higher marine omega-3 fatty acids, higher folate, and higher polyunsaturated-to-saturated fat ratio). When 3 of the 5 healthy lifestyle factors were present, the RR for CHD over a 14-year period was 57% lower; when 4 were present, RR was 66% lower; and when all 5 factors were present, RR was 83% lower.³⁹ However, data from NHANES 1999 to 2002 showed that only about one third of adults complied with ≥6 of the recommended heart-healthy behaviors. Dietary recommendations, in general, and daily fruit intake recommendations, in particular, were least likely to be followed.⁴⁰

In the Chicago Heart Association Detection Project in Industry, remaining lifetime risks for CVD death were noted to increase substantially and in a graded fashion according to the number of risk factors present in middle age (40–59 years of age). However, remaining lifetime risks for non-CVD death also increased dramatically with increasing CVD risk factor burden. These data help to explain the markedly greater longevity experienced by those who reach middle age free of major CVD risk factors.⁴¹

Among individuals 70 to 90 years of age, adherence to a Mediterranean-style diet and greater PA are associated with 65% to 73% relatively lower rates of all-cause mortality, as well as lower mortality rates attributable to CHD, CVD, and cancer.⁴²

Seventeen-year mortality data from the NHANES II Mortality Follow-Up Study indicated that the RR for fatal CHD was 51% lower for men and 71% lower for women with none of 3 major risk factors (hypertension, current smoking, and elevated total cholesterol [≥ 240 mg/dL]) than for those with ≥1 risk factors. Had all 3 major risk factors not occurred, it is hypothesized that 64% of all CHD deaths among women and 45% of CHD deaths in men could theoretically have been avoided.⁴³

Investigators from the Chicago Heart Association Detection Project in Industry have also observed that risk factor burden in middle age is associated with better quality of life at follow-up in older age (≈25 years later) and lower average annual Medicare costs at older ages.

The presence of a greater number of risk factors in middle age is associated with lower scores at older ages on assessment of social functioning, mental health, walking, and health perception in women, with similar findings in men.⁴⁴

Similarly, the existence of a greater number of risk factors in middle age is associated with higher average annual CVD-related and total Medicare costs (once Medicare eligibility is attained).⁴⁵

From 1999 to 2009, the number of inpatient discharges from short-stay hospitals with CVD as the first-listed diagnosis decreased from 6 344 000 to 6 165 000 (NHDS, NCHS, and NHLBI). In 2009, CVD ranked highest among all disease categories in hospital discharges (NHDS, NCHS, and NHLBI).

In 2009, there were 94 871 000 physician office visits with a primary diagnosis of CVD (NCHS, NAMCS, NHLBI tabulation). In 2009, there were 4 761 000 ED visits and 7 261 000 hospital outpatient department visits with a primary diagnosis of CVD (NCHS, NHAMCS, NHLBI tabulation).

In 2005, ≈1 of every 6 hospital stays, or almost 6 million, resulted from CVD (Agency for Healthcare Research and Quality, NIS). The total inpatient hospital cost for CVD was $71.2 billion, approximately one fourth of the total cost of inpatient hospital care in the United States. The average cost per hospitalization was ≈41% higher than the average cost for all stays. Hospital admissions that originated in the ED accounted for 60.7% of all hospital stays for CVD. This was 41% higher than the rate of 43.1% for all types of hospital stays; 3.3% of patients admitted to the hospital for CVD died in the hospital, which was significantly higher than the average in-hospital death rate of 2.1% for all hospitalized patients.⁴⁶

In 2004, coronary artery disease (CAD) was estimated to be responsible for 1.2 million hospital stays and was the most expensive condition treated. This condition resulted in >$44 billion in expenses. More than half of the hospital stays for CAD were among patients who also received percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) during their stay. AMI resulted in $31 billion of inpatient hospital charges for 695 000 hospital stays. The 1.1 million hospitalizations for CHF amounted to nearly $29 billion in hospital charges.⁴⁷

In 2003, ≈48.3% of inpatient hospital stays for CVD were for women, who accounted for 42.8% of the national cost ($187 billion) associated with these conditions. Although only 40% of hospital stays for AMI and CAD were for women, more than half of all stays for nonspecific chest pain, CHF, and stroke were for women. There was no difference between men and women in hospitalizations for cardiac dysrhythmias.⁴⁸

Circulatory disorders were the most frequent reason for admission to the hospital through the ED, accounting for 26.3% of all admissions through the ED. After pneumonia, the most common heart-related conditions (in descending order) were CHF, chest pain, hardening of the arteries, and heart attack, which together accounted for >15% of all admissions through the ED. Stroke and irregular heart beat ranked seventh and eighth, respectively.⁴⁹

In 2004, 23.7% of nursing home residents had a primary diagnosis of CVD at admission, and 25% had CVD as the primary diagnosis at the time of interview. This was the leading primary diagnosis for these residents (NCHS, NNHS).⁴⁹

Among current home healthcare patients in 2007, 18.3% had a primary diagnosis of CVD at admission and 62.9% had any diagnosis of CVD at the time of interview (NCHS, NHHCS unpublished data).

Among patients discharged from hospice in 2007, 15.8% had a primary diagnosis of CVD at admission (NCHS, NHHCS unpublished data).

In 2009, an estimated 7 453 000 inpatient cardiovascular operations and procedures were performed in the United States; 4.2 million were performed on males, and 3.3 million were performed on females (NHLBI tabulation of NHDS, NCHS).

The estimated direct and indirect cost of CVD for 2008 is $297.7 billion (MEPS, Agency for Health-care Research and Quality, and NHLBI).

In 2006, $32.7 billion in program payments were made to Medicare beneficiaries discharged from short-stay hospitals with a principal diagnosis of CVD. That was an average of $10 201 per discharge.⁵⁰

Between 2010 and 2030, real (2008$) total direct medical costs of CVD are projected to triple, from $273 billion to $818 billion.³

In the NHLBI’s MESA study of white, black, Chinese, and Hispanic adults 45 to 84 years of age, carotid IMT and CAC were found to be commonly associated, but patterns of association differed somewhat by sex and race.²⁴

In a more recent analysis from the NHLBI’s MESA study, the investigators reported on follow-up of 6698 men and women in 4 ethnic groups over 5.3 years and compared the predictive utility of carotid IMT and CAC.²⁵

A conservative estimate for the number of discharges with ACS from hospitals in 2009 is 683 000. Of these, an estimated 399 000 are males and 284 000 are females. This estimate is derived by adding the first-listed inpatient hospital discharges for MI (634 000) to those for UA (49 000; NHDS, NHLBI).

When secondary discharge diagnoses in 2009 were included, the corresponding number of inpatient hospital discharges was 1 190 000 unique hospitalizations for ACS; 694 000 were males, and 496 000 were females. Of the total, 829 000 were for MI alone, 357 000 were for UA alone, and 4000 hospitalizations received both diagnoses (NHDS, NHLBI).

STEMI

NSTEMI

UA

Analysis of data from the GRACE multinational observational cohort study of patients with ACS found evidence of a change in practice for both pharmacological and interventional treatments in patients with either STEMI or non–ST-segment–elevation ACS. These changes have been accompanied by significant decreases in the rates of in-hospital death, cardiogenic shock, and new MI among patients with non–ST-segment–elevation ACS. The use of evidence-based therapies and PCI interventions increased in the STEMI population. This increase was matched with a statistically significant decrease in the rates of death, cardiogenic shock, and HF or pulmonary edema.⁵²

A study of patients with non–ST-segment–elevation ACS treated at 350 US hospitals found that up to 25% of opportunities to provide American College of Cardiology (ACC)/AHA guideline–recommended care were missed in current practice. The composite guideline adherence rate was significantly associated with in-hospital mortality.⁵²

A study of hospital process performance in 350 centers of nearly 65 000 patients enrolled in the CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines) National Quality Improvement Initiative found that ACC/AHA guideline–recommended treatments were adhered to in 74% of eligible instances.⁵³

After adjustment for clinical differences and the severity of CAD by angiogram, 30-day mortality after ACS is similar in men and women.⁵⁴

An estimated 7 000 000 Americans ≥ 20 years of age have had a stroke (extrapolated to 2008 using NCHS/NHANES 2005–2008 data). Overall stroke prevalence during this period is an estimated 3.0% (Table 6-1).

According to data from the 2010 BRFSS (CDC), 2.6% of men and 2.6% of women ≥18 years of age had a history of stroke; 2.4% of non-Hispanic whites, 4.0% of non-Hispanic blacks, 1.4% of Asian/Pacific Islanders, 2.5% of Hispanics (of any race), 5.8% of American Indian/Alaska Natives, and 4.1% of other races or multiracial people had a history of stroke (NHLBI tabulation of BRFSS).

The prevalence of silent cerebral infarction is estimated to range from 6% to 28%, with higher prevalence with increasing age.^1–3 The prevalence estimates also vary depending on the population studied (eg, ethnicity, sex, risk factor profile), definition of silent cerebral infarction, and imaging technique. It has been estimated that 13 million people had prevalent silent stroke in the 1998 US population.^4,5

The prevalence of stroke-related symptoms was found to be relatively high in a general population free of a prior diagnosis of stroke or transient ischemic attack (TIA). On the basis of data from 18 462 participants enrolled in a national cohort study, 17.8% of the population >45 years of age reported at least 1 symptom. Stroke symptoms were more likely among blacks than whites, among those with lower income and lower educational attainment, and among those with fair to poor perceived health status. Symptoms also were more likely in participants with higher Framingham stroke risk score (Reasons for Geographic and Racial Differences in Stroke study [REGARDS], NINDS).⁶

Projections show that by 2030, an additional 4 million people will have had a stroke, a 24.9% increase in prevalence from 2010.⁷

Each year, ≈795 000 people experience a new or recurrent stroke. Approximately 610 000 of these are first attacks, and 185 000 are recurrent attacks (GCNKSS, NINDS, and NHLBI; GCNKSS and NINDS data for 1999 provided July 9, 2008; estimates compiled by NHLBI). Of all strokes, 87% are ischemic and 10% are intracerebral hemorrhagic strokes, whereas 3% are subarachnoid hemorrhage strokes (GCNKSS, NINDS, 1999).

On average, every 40 seconds, someone in the United States has a stroke (AHA computation based on the latest available data).

Each year, ≈55 000 more women than men have a stroke (GCNKSS, NINDS).⁸

Women have a higher lifetime risk of stroke than men. In the FHS, lifetime risk of stroke among those 55 to75 years of age was 1 in 5 for women (20% to 21%) and approximately 1 in 6 for men (14% to 17%).⁹

Women have lower age-adjusted stroke incidence than men; however, sex differences in stroke risk may be modified by age.¹⁰ Data from FHS demonstrate that compared with white men, white women 45 to 84 years of age have lower stroke risk than men, but this association is reversed in older ages such that women >85 years of age have elevated risk compared with men.¹¹ Similarly, a population-based study in Sweden found stroke incidence to be lower for women than men at ages 55 to 64 years, but at 75 to 85 years of age, this association reversed, and women had a higher incidence than men.¹² Other studies report an excess risk of stroke in men compared with women that persists throughout the life course or diminishes but does not reverse with age.^13–15

On average, women are older at stroke onset than men (≈75 years compared with 71 years).¹¹

Blacks have a risk of first-ever stroke that is almost twice that of whites.¹⁶

In the national REGARDS cohort, in 27 744 participants followed up over 4.4 years (2003–2010), the overall age-and sex-adjusted black/white incidence rate ratio was 1.51, but for ages 45 to 54 years, it was 4.02, whereas for those ≥85 years of age, it was 0.86.¹⁷ Similar trends for decreasing incidence rate ratio were seen in the GCNKSS.¹⁸

Analysis of data from the FHS suggests that stroke incidence is declining over time in this largely white cohort. Data from 1950 to 1977, 1978 to 1989, and 1990 to 2004 showed that the age-adjusted incidence of first stroke per 1000 person-years in each of the 3 periods was 7.6, 6.2, and 5.3 in men and 6.2, 5.8, and 5.1 in women, respectively. Lifetime risk for incident stroke at 65 years of age decreased significantly in the latest data period compared with the first, from 19.5% to 14.5% in men and from 18.0% to 16.1% in women.¹⁹

In a similar fashion, data from the most recent GCNKSS show that compared with the 1990s, when incidence rates of stroke were stable, stroke incidence in 2005 was decreased for whites. Unfortunately, a similar decline was not seen in blacks. These changes for whites were driven by a decline in ischemic strokes for whites. There were no changes in incidence of ischemic stroke for blacks or for hemorrhagic strokes in blacks or whites.⁸

The BASIC (Brain Attack Surveillance in Corpus Christi) project (NINDS) demonstrated an increased incidence of stroke among Mexican Americans compared with non-Hispanic whites in a community in southeast Texas. The crude 3-year cumulative incidence (2000–2002) was 16.8 per 1000 in Mexican Americans and 13.6 per 1000 in non-Hispanic whites. Specifically, Mexican Americans had a higher cumulative incidence for ischemic stroke at younger ages (45–59 years of age: RR 2.04, 95% CI 1.55–2.69; 60–74 years of age: RR 1.58, 95% CI 1.31–1.91) but not at older ages (≥75 years of age: RR 1.12, 95% CI 0.94–1.32). Mexican Americans also had a higher incidence of intracerebral hemorrhage and subarachnoid hemorrhage than non-Hispanic whites, adjusted for age.²⁰

The age-adjusted incidence of first ischemic stroke per 1000 was 0.88 in whites, 1.91 in blacks, and 1.49 in Hispanics according to data from the Northern Manhattan Study (NOMAS; NINDS) for 1993 to 1997. Among blacks, compared with whites, the relative rate of intracranial atherosclerotic stroke was 5.85; of extracranial atherosclerotic stroke, 3.18; of lacunar stroke, 3.09; and of cardioembolic stroke, 1.58. Among Hispanics (primarily Cuban and Puerto Rican), compared with whites, the relative rate of intracranial atherosclerotic stroke was 5.00; of extracranial atherosclerotic stroke, 1.71; of lacunar stroke, 2.32; and of cardioembolic stroke, 1.42.²¹

Among 4507 American Indian participants without a prior stroke in the Strong Heart Study in 1989 to 1992, the age-and sex-adjusted incidence of stroke through 2004 was 6.79 per 100 person-years, with 86% of incident strokes being ischemic.²²

A review of published studies and data from clinical trials found that hospital admissions for intracerebral hemorrhage have increased by 18% in the past 10 years, probably because of increases in the number of elderly people, many of whom lack adequate BP control, as well as the increasing use of anticoagulants, thrombolytics, and antiplatelet agents. Mexican Americans, Latin Americans, blacks, Native Americans, Japanese people, and Chinese people have higher incidences than do white Americans.²³

In the GCNKSS, the annual incidence of anticoagulant-associated intracerebral hemorrhage per 100 000 people increased from 0.8 (95% CI 0.3–1.3) in 1988 to 1.9 (95% CI 1.1–2.7) in 1993/1994 and 4.4 (95% CI 3.2–5.5) in 1999 (P<0.001 for trend). Among people ≥80 years of age, the rate of anticoagulant-associated intracerebral hemorrhage increased from 2.5 (95% CI 0–7.4) in 1988 to 45.9 (95% CI 25.6–66.2) in 1999 (P<0.001 for trend). Over this period of time, incidence rates of cardioembolic ischemic stroke were similar, whereas warfarin distribution in the United States quadrupled on a per capita basis. The increase in incidence is therefore attributable to prescribing behavior and patterns of care.²⁴

In a nationwide survey of US adults, the estimated prevalence of self-reported physician-diagnosed TIA was 2.3%, which translates into ≈5 million people. The true prevalence of TIA is greater, because many patients who experience neurological symptoms consistent with a TIA fail to report it to their healthcare provider.²⁵

In the GCNKS, using data from 1993 and 1994, the age-, sex-, and race-adjusted incidence rates for TIA were 0.83 per 10 000. ²⁶ Age- and sex-adjusted incidence rates for TIA in Rochester, MN, were estimated at 0.68 per 1000 for the years 1985 through 1989.²⁷

The prevalence of physician-diagnosed TIA increases with age.²⁵ Incidence of TIA increases with age and varies by sex and race/ethnicity. Men, blacks, and Mexican Americans have higher rates of TIA than their female and non-Hispanic white counterparts.^20,26

Approximately 15% of all strokes are heralded by a TIA.²⁸

TIAs confer a substantial short-term risk of stroke, hospitalization for CVD events, and death. Of 1707 TIA patients evaluated in the ED of Kaiser Permanente Northern California, a large, integrated healthcare delivery system, 180 (10%) experienced a stroke within 90 days. Ninety-one patients (5%) had a stroke within 2 days. Predictors of stroke included age >60 years, DM, focal symptoms of weakness or speech impairment, and TIA that lasted >10 minutes.²⁹

Meta-analyses of cohorts of patients with TIA have shown the short-term risk of stroke after TIA is significant. Risk has been shown to be as high as 10% at 2 days and as high as 17% at 90 days.^30,31

Individuals who have a TIA and survive the initial high-risk period have a 10-year stroke risk of roughly 19% and a combined 10-year stroke, MI, or vascular death risk of 43% (4% per year).³²

Within 1 year of TIA, ≈12% of patients will die.²⁶

It is estimated that one third of episodes characterized as TIA according to the classic definition (ie, focal neurological deficits that resolve within 24 hours) would be considered infarctions on the basis of diffusion-weighted magnetic resonance imaging findings.³³

On average, every 4 minutes, someone dies of a stroke (NCHS, NHLBI).^33a

Stroke accounted for ≈1 of every 18 deaths in the United States in 2008.^33a

When considered separately from other CVDs, stroke ranks No. 4 among all causes of death, behind diseases of the heart, cancer, and CLRD (NCHS mortality data). Stroke mortality in 2008 was 134 148; any-mention mortality in 2008 was 223 841 and the death rate was 40.7.^33a See Chart 6-6 for sex and race comparisons.

From 1998 to 2008, the annual stroke death rate decreased 34.8%, and the actual number of stroke deaths declined 19.4% (NHLBI tabulation) (appropriate comparability ratios were applied).^33a,34

Conclusions about changes in stroke death rates from 1980 to 2005 are as follows:

Approximately 54% of stroke deaths in 2008 occurred out of the hospital (unpublished NHLBI tabulation of NCHS 2008 Mortality Data Set).

Among people 45 to 64 years of age, 8% to 12% of ischemic strokes and 37% to 38% of hemorrhagic strokes result in death within 30 days, according to 1987 to 2001 data from the ARIC study of the NHLBI.³⁵

In a study of people ≥65 years of age recruited from a random sample of Health Care Financing Administration Medicare Part B eligibility lists in 4 US communities (CHS), over the time period 1989 to 2000, the 1-month case fatality rate was 12.6% for all strokes, 8.1% for ischemic strokes, and 44.6% for hemorrhagic strokes.³⁶

More women than men die of stroke each year because of the larger number of elderly women. Women accounted for 60.1% of US stroke deaths in 2008.

From 1995 to 1998, age-standardized mortality rates for ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage were higher among blacks than whites. Death rates attributable to intracerebral hemorrhage also were higher among Asians/Pacific Islanders than among whites. All minority populations had higher death rates attributable to subarachnoid hemorrhage than did whites. Among adults 25 to 44 years of age, blacks and American Indian/Alaska Natives had higher risk ratios than did whites for all 3 stroke subtypes.³⁷

Age-adjusted stroke mortality rates began to level off in the 1980s and stabilized in the 1990s for both men and women, according to the Minnesota Heart Study. Women had lower rates of stroke mortality than did men throughout the period. Some of the improvement in stroke mortality may be the result of improved acute stroke care, but most is thought to be the result of improved detection and treatment of hypertension.³⁸

In 2002, death certificate data showed that the mean age at stroke death was 79.6 years; however, males had a younger mean age at stroke death than females. Blacks, American Indian/Alaska Natives, and Asian/Pacific Islanders had younger mean ages than whites, and the mean age at stroke death was also younger among Hispanics than non-Hispanics.³⁹

A report released by the CDC in collaboration with the Centers for Medicare & Medicaid Services, the Atlas of Stroke Hospitalizations Among Medicare Beneficiaries, found that in Medicare beneficiaries over the time period 1995 to 2002, 30-day mortality rate varied by age: 9% in patients 65 to 74 years of age, 13.1% in those 74 to 84 years of age, and 23% in those ≥85 years of age.⁴⁰

The black/white disparity in stroke mortality varies by age in a similar fashion to stroke incidence as described above.

There are substantial geographic disparities in stroke mortality, with higher rates in the southeastern United States, known as the “stroke belt” (Chart 6-7). This area is usually defined to include the 8 southern states of North Carolina, South Carolina, Georgia, Tennessee, Mississippi, Alabama, Louisiana, and Arkansas. These geographic differences have existed since at least 1940,⁴¹ and despite some minor shifts,⁴² they persist.^43–45 Within the stroke belt, a “buckle” region along the coastal plain of North Carolina, South Carolina, and Georgia has been identified with even a higher stroke mortality rate than the remainder of the stroke belt.⁴⁶ The overall average stroke mortality is ≈20% higher in the stroke belt than in the rest of the nation and ≈40% higher in the stroke buckle.

Racial and regional patterns in stroke incidence have been shown to be similar to patterns for stroke mortality, which suggests that disparities in incidence play a substantial role in mortality disparities. However, incidence only partly explains mortality disparities, and differences in case fatality or other factors likely contribute to racial and geographic disparities in stroke mortality.⁴⁷

High blood pressure: Chapter 7

Disorders of heart rhythm (including atrial fibrillation): Chapter 10

Smoking/Tobacco Use: Chapter 13

High blood cholesterol and other lipids: Chapter 14

Physical inactivity: Chapter 15

Diabetes mellitus: Chapter 17

End-stage renal disease and chronic kidney disease: Chapter 18

BP is a powerful determinant of risk for both ischemic stroke and intracranial hemorrhage. Subjects with BP <120/80 mm Hg have approximately half the lifetime risk of stroke of subjects with hypertension. The treatment and lowering of BP among hypertensive individuals was associated with a significant reduction in stroke risk.⁴⁸

In REGARDS (NINDS), black participants were more aware than whites of their hypertension and more likely to be undergoing treatment if aware of their diagnosis, but among those treated for hypertension, they were less likely than whites to have their BP controlled.⁴⁹

REGARDS (NINDS) also showed no evidence of a difference between the stroke belt and other regions in awareness of hypertension, but there was a trend for better treatment and BP control in the stroke belt region. The lack of substantial geographic differences in hypertension awareness and the trend toward better treatment and control in the stroke belt suggest that differences in hypertension management may not be a major contributor to the geographic disparity in stroke mortality.⁴⁹

Impaired glucose tolerance nearly doubled the stroke risk compared with patients with normal glucose levels and tripled the risks for patients with DM.⁵⁰

Age-specific incidence rates and rate ratios show that DM increases ischemic stroke incidence at all ages, but this risk is most prominent before 55 years of age in blacks and before 65 years of age in whites. Ischemic stroke patients with DM are younger, more likely to be black, and more likely to have hypertension, MI, and high cholesterol than nondiabetic patients.⁵¹

Atrial fibrillation (AF) is a powerful risk factor for stroke, independently increasing risk ≈5-fold throughout all ages. The percentage of strokes attributable to AF increases steeply from 1.5% at 50 to 59 years of age to 23.5% at 80 to 89 years of age.^52,53

Because AF is often asymptomatic^54,55 and likely frequently clinically undetected,⁵⁶ the stroke risk attributed to AF may be substantially underestimated.⁵⁷ Therefore, although AF is an important stroke risk factor, both patients and treating physicians may be unaware of its presence. A related point is that no strategy to pursue normal sinus rhythm, including cardioversion, antiarrhythmic drug therapy, and/or ablation, has definitively been shown to reduce the risk of stroke.

Data from the Honolulu Heart Program/NHLBI found that in Japanese men 71 to 93 years of age, low concentrations of HDL cholesterol were more likely to be associated with a future risk of thromboembolic stroke than were high concentrations.⁵⁸

In the FHS, a documented parental ischemic stroke by the age of 65 years was associated with a 300% increase in documented ischemic stroke risk in offspring, even after adjustment for other known stroke risk factors. The absolute magnitude of the increased risk was greatest in those in the highest quintile of the FRS. By age 65 years, people in the highest FRS quintile with an early parental ischemic stroke had a 25% risk of stroke compared with a 7.5% risk of ischemic stroke for those without such a history.⁵⁹

The CHS (NHLBI) showed people with creatinine ≥1.5 mg/dL were at increased risk for stroke, with an adjusted HR of 1.77 (95% CI 1.08–2.91).⁶⁰ Participants in REGARDS with a reduced estimated glomerular filtration rate (eGFR) were also shown to have increased risk of incident stroke symptoms.⁶¹

Analysis of data from the FHS found that women with natural menopause before 42 years of age had twice the ischemic stroke risk of women with natural menopause after age 42.⁶² Investigators from the Nurse’s Health Study, however, did not find an association between age at natural menopause and risk of ischemic or hemorrhagic stroke.⁶³

Overall, randomized clinical trial data indicate that the use of estrogen plus progestin, as well as estrogen alone, increases stroke risk in postmenopausal, generally healthy women and provides no protection for postmenopausal women with established HD.^64,65

Among postmenopausal women who were generally healthy, the Women’s Health Initiative (WHI), a randomized trial of 16 608 women (95% of whom had no preexisting CVD), found that estrogen plus progestin increased ischemic stroke risk by 44%, with no effect on hemorrhagic stroke.⁶⁴

In the WHI trial, among 10 739 women with hysterectomy, it was found that conjugate equine estrogen alone increased the risk of ischemic stroke by 55% and that there was no significant effect on hemorrhagic stroke.⁶⁶

In postmenopausal women with known CHD, the Heart and Estrogen/Progestin Replacement Study (HERS), a secondary CHD prevention trial, found that estrogen plus progestin hormone therapy did not reduce stroke risk.⁶⁷

The Women’s Estrogen for Stroke Trial (WEST) found that estrogen alone in postmenopausal women with a recent stroke or TIA had no significant overall effect on recurrent stroke or fatality.⁶⁸

Analysis of data from the FHS found that women with menopause at 42 to 54 years of age and at ≥55 years of age had lower stroke risk than those with menopause at <42 years of age, even after adjustment for potential confounders. Women with menopause before 42 years of age had twice the stroke risk of all other women in different age groups.⁶²

The risk of ischemic stroke or intracerebral hemorrhage during pregnancy and the first 6 weeks after giving birth was 2.4 times greater than for nonpregnant women of similar age and race, according to the Baltimore-Washington Cooperative Young Stroke Study. The risk of ischemic stroke during pregnancy was not increased during pregnancy per se but was increased 8.7-fold during the first 6 postpartum weeks. Intracerebral hemorrhage showed a small RR of 2.5 during pregnancy but increased dramatically to an RR of 28.3 in the first 6 postpartum weeks. The excess risk of stroke (all types except subarachnoid hemorrhage) attributable to the combined pregnancy/postpregnancy period was 8.1 per 100 000 pregnancies.⁶⁹

In the US Nationwide Inpatient Sample from 2000 to 2001, the rate of events per 100 000 pregnancies was 9.2 for ischemic stroke, 8.5 for intracerebral hemorrhage, 0.6 for cerebral venous thrombosis, and 15.9 for the ill-defined category of pregnancy-related cerebrovascular events, for a total rate of 34.2 per 100 000, not including subarachnoid hemorrhage. The risk was increased in blacks and among older women. Death occurred during hospitalization in 4.1% of women with these events and in 22% of survivors after discharge to a facility other than home.⁷⁰

Analyses of the US Nationwide Inpatient Sample from 1994 to 1995 and from 2006 to 2007 show a temporal increase in the proportion of pregnancy hospitalizations that were associated with a stroke, with a 47% increase for antenatal hospitalizations and 83% increase for postpartum hospitalizations, but no increase for delivery hospitalizations. Increases in the prevalence of heart disease and hypertensive disorders accounted for almost all the increase in postpartum stroke hospitalizations but not the antenatal stroke hospitalizations.⁷¹

Preeclampsia is a risk factor for ischemic stroke remote from pregnancy.⁷² The subsequent stroke risk of preeclampsia may be mediated by a 3.6- to 6.1-fold higher later risk of hypertension and a 3.1- to 3.7-fold higher later risk of DM, depending on whether the preeclampsia was mild or severe.⁷³

In NOMAS, a prospective cohort that included white, black, and Hispanic men and women in an urban setting followed up for a median of 9 years, baseline PA was associated with an overall 35% reduction in risk of ischemic stroke.⁷⁴

The NOMAS study found that only moderate- to vigorous-intensity exercise was associated with reduced stroke incidence, whereas light exercise (such as walking) showed no benefit.⁷⁵

Timing of PA in relation to stroke onset has also been examined in several studies. In a hospital-based case-control study from Heidelberg, Germany, recent activity (within the prior months) was associated with reduced odds of having a stroke or TIA, whereas sports activity during young adulthood that was not continued showed no benefit.⁷⁶ In a Danish case-control study, ischemic stroke patients were less physically active in the week preceding the stroke than age- and sex-matched control subjects, with the highest activity scores associated with the greatest reduction in odds of stroke.⁷⁷

Cigarette smoking is one of the well-established modifiable risk factors for stroke. This includes ischemic, intracerebral, and subarachnoid hemorrhage, but the data for intracerebral hemorrhage are less consistent.^78,79

Smoking is perhaps the most important modifiable risk factor in preventing subarachnoid hemorrhage, with the highest population attributable risk of any subarachnoid hemorrhage risk factor.⁸⁰

Current smokers have a 2 to 4 times increased risk of stroke compared with nonsmokers or those who have quit for more than 10 years.^78,79

Data also support a dose-response relationship across old and young age groups.^78,81

Discontinuation of smoking has been shown to reduce stroke risk across sex, race, and age groups.⁸¹

Sleep apnea is an independent risk factor for stroke, increasing the risk of stroke or death 2-fold.^82–85

Worsening sleep apnea severity is associated with greater stroke risk; patients with severe sleep apnea have 3- to 4-fold increased odds of stroke.^82,84,85

Continuous positive airway pressure improves a variety of outcomes after stroke.^86–88 For example, continuous positive airway pressure reduces the risk of recurrent vascular events among patients with stroke (relative risk reduction of 81.4%; number needed to treat of 3.4).⁸⁷

Sleep apnea is common after stroke, occurring in 60% to 96% of poststroke patients.^89–98

Correct knowledge of at least 1 stroke warning sign increased from 48% in 1995% to 68% in 2000, with no significant improvement to 2005 (68%) on the basis of a telephone survey conducted in a biracial population in the greater Cincinnati/Northern Kentucky region. Knowledge of 3 correct warning signs was low but increased over time: 5.4% in 1995, 12.0% in 2000, and 15.7% in 2005. Knowledge of at least 1 stroke risk factor increased from 59% in 1995% to 71% in 2000, but there was no improvement to 2005 (71%). Only 3.6% of those surveyed were able to independently identify tissue-type plasminogen activator as an available drug therapy, and only 9% of these were able to identify a window of <3 hours for treatment.⁹⁹

In the 2005 BRFSS, among respondents in 14 states, 38.1% were aware of 5 stroke warning symptoms and would first call 9-1-1 if they thought that someone was having a heart attack or stroke. Awareness of all 5 stroke warning symptoms and calling 9-1-1 was higher among whites than blacks and Hispanics (41.3%, 29.5%, and 26.8%, respectively), women than men (41.5% versus 34.5%), and people with higher versus lower educational attainment (47.6% for people with a college degree or more versus 22.5% for those who had not received a high school diploma).¹⁰⁰

A study was conducted of patients admitted to an ED with possible stroke to determine their knowledge of the signs, symptoms, and risk factors of stroke. Of the 163 patients able to respond, 39% did not know a single sign or symptom. Patients ≥65 years of age were less likely than those <65 years old to know a sign or symptom of stroke (28% versus 47%), and 43% did not know a single risk factor. Overall, almost 40% of patients did not know the signs, symptoms, and risk factors of stroke.¹⁰¹

In 2004, 800 adults ≥45 years of age were surveyed to assess their perceived risk for stroke and their history of stroke risk factors. Overall, 39% perceived themselves to be at risk. Younger age, current smoking, a history of DM, high BP, high cholesterol, HD, and stroke/TIA were independently associated with perceived risk for stroke. Respondents with AF were no more likely to report being at risk than were respondents without AF. Perceived risk for stroke increased as the number of risk factors increased; however, 46% of those with ≥3 risk factors did not perceive themselves to be at risk.¹⁰²

A study of patients who have had a stroke found that only 60.5% were able to accurately identify 1 stroke risk factor and that 55.3% were able to identify 1 stroke symptom. Patients’ median delay time from onset of symptoms to admission in the ED was 16 hours, and only 31.6% accessed the ED in <2 hours. Analysis showed that the appearance of nonmotor symptoms as the primary symptom and nonuse of the 9-1-1 system were significant predictors of delay >2 hours. Someone other than the patient made the decision to seek treatment in 66% of the cases.¹⁰³

Spanish-speaking Hispanics are less likely to know all stroke symptoms than English-speaking Hispanics, non-Hispanic blacks, and non-Hispanic whites. Lack of English proficiency is strongly associated with lack of stroke knowledge among Hispanics.¹⁰⁴

Stroke is a leading cause of serious long-term disability in the United States (Survey of Income and Program Participation, a survey of the US Bureau of the Census).¹⁰⁵

In the NHLBI’s FHS, among ischemic stroke survivors who were ≥65 years of age, these disabilities were observed at 6 months after stroke¹⁰⁶:

Data from the BRFSS (CDC) 2005 survey on stroke survivors in 21 states and the District of Columbia found that 30.7% of stroke survivors received outpatient rehabilitation. The findings indicated that the prevalence of stroke survivors receiving outpatient stroke rehabilitation was lower than would be expected if clinical practice guideline recommendations for all stroke patients had been followed.¹⁰⁷

Black stroke survivors had greater limitations in ambulation than did white stroke survivors, after adjustment for age, sex, and educational attainment but not stroke subtype, according to data from the NHIS (2000–2001, NCHS) as analyzed by the CDC.¹⁰⁸ A national study of inpatient rehabilitation after first stroke found that blacks were younger, had a higher proportion of hemorrhagic stroke, and were more disabled on admission. Compared with non-Hispanic whites, blacks and Hispanics also had a poorer functional status at discharge but were more likely to be discharged to home rather than to another institution even after adjustment for age and stroke subtype. After adjustment for the same covariates, compared with non-Hispanic whites, blacks also had less improvement in functional status per inpatient day.¹⁰⁹

After stroke, women have greater disability than men. A cross-sectional analysis of 5888 community-living elderly people (>65 years of age) in the CHS who were ambulatory at baseline found that women were half as likely to be independent in activities of daily living after stroke, even after controlling for age, race, education, and marital status.¹¹⁰ A prospective study from a Michigan-based stroke registry found that women had a 63% lower probability of achieving independence in activities of daily living 3 months after discharge, even after controlling for age, race, subtype, prestroke ambulatory status, and other patient characteristics.¹¹¹

From 1999 to 2009, the number of inpatient discharges from short-stay hospitals with stroke as the first-listed diagnosis remained about the same, with discharges of 961 000 and 971 000, respectively (NHLBI tabulation, NHDS, NCHS).

Data from 2009 from the Hospital Discharge Survey of the NCHS showed that the average length of stay for discharges with stroke as the first-listed diagnosis was 5.3 days.

In 2003, men and women accounted for roughly the same number of hospital stays for stroke in the 18- to 44-year-old age group. After 65 years of age, women were the majority. Among people 65 to 84 years of age, 54.5% of stroke patients were women, whereas among the oldest age group, women constituted 69.7% of all stroke patients.¹¹²

A first-ever county-level Atlas of Stroke Hospitalizations Among Medicare Beneficiaries was released in 2008 by the CDC in collaboration with the Centers for Medicare & Medicaid Services. It found that the stroke hospitalization rate for blacks was 27% higher than for the US population in general, 30% higher than for whites, and 36% higher than for Hispanics. In contrast to whites and Hispanics, the highest percentage of strokes in blacks (42.3%) occurred in the youngest Medicare age group (65–74 years of age).⁴⁰

In 2009, there were 768 000 ED visits and 127 000 outpatient department visits with stroke as the first-listed diagnosis. In 2009, physician office visits for a first-listed diagnosis of stroke totaled 3 327 000 (unpublished data, NCHS, NHAMCS, NHLBI tabulation).¹¹³

On the basis of pathogenic differences, pediatric strokes are typically classified as either perinatal, occurring at ≤28 days of life and including in utero strokes, or (later) childhood.

Recent estimates of the overall annual incidence of stroke in US children are 6.4 per 100 000 children (0–15 years) in 1999 in GCNKSS¹¹⁴ and 4.6 per 100 000 children (0–19 years) from 1997 to 2003 according to Kaiser Permanente of Northern California, a large, integrated healthcare delivery system.¹¹⁵ Approximately half of all incident childhood strokes are hemorrhagic.^114–116

The prevalence of perinatal strokes is 29 per 100 000 live births, or 1 per 3500 live births in the 1997 to 2003 Kaiser Permanente of Northern California population.¹¹⁵

A history of infertility, preeclampsia, prolonged rupture of membranes, and chorioamnionitis were found to be independent risk factors for perinatal arterial ischemic stroke in the Kaiser Permanente of Northern California population. The RR of perinatal stroke increased ≈25-fold, with an absolute risk of 1 per 200 deliveries, when ≥3 antenatally determined risk factors were present.¹¹⁷

Although children with sickle cell disease and congenital HD are at high risk for ischemic stroke, the most common cause in a previously healthy child is a cerebral arteriopathy, found in approximately two thirds of cases.¹¹⁸

Congenital HD accounted for 25% of pediatric arterial ischemic strokes in a population based study in Utah, Wyoming, Idaho, and Nevada; it increased the odds of stroke 16-fold compared with the general population.¹¹⁹

Thrombophilias (genetic and acquired) are risk factors for childhood stroke, with summary ORs ranging from 1.6 to 8.8 in a recent meta-analysis.¹²⁰

From 1979 to 1998 in the United States, childhood mortality resulting from stroke declined by 58% overall, with reductions in all major subtypes.¹²¹

The incidence of stroke in children has been stable over the past 10 years, whereas the 30-day case fatality rates declined from 18% in 1988–1989 to 9% in 1993–1994 and 9% in 1999 in the GCNKSS population.¹¹⁴

Compared with girls, boys have a 1.28-fold higher risk of stroke.¹²² Compared with white children, black children have a 2-fold risk of both incident stroke and death attributable to stroke.^121,122 The increased risk among blacks is not fully explained by the presence of sickle cell disease, nor is the excess risk among boys fully explained by trauma.¹²²

Strokes in children can be mistaken for a postictal Todd’s paresis: 22% of children with acute arterial ischemic stroke have a seizure on presentation; younger age predicts presentation with seizures.¹²³

At a median follow-up time of 6.3 years, half of 53 childhood ischemic stroke survivors and two thirds of 80 neonatal ischemic stroke survivors had at least 1 neurological deficit; only 10% to 20% had mild deficits, whereas the remainder had moderate or severe deficits.¹²⁴ Involvement of deep structures (basal ganglia, posterior limb of the internal capsule) as opposed to pure cortical lesions predicts motor deficits.¹²⁵

Despite current treatment, 1 of 10 children with ischemic or hemorrhagic stroke will have a recurrence within 5 years.^126,127 The 5-year recurrence risk is as high as 60% among children with cerebral arteriopathy. The recurrence risk after perinatal stroke, however, is negligible.¹²⁸

On the basis of NHIS data, the inability to afford medications among stroke survivors increased significantly from 8.1% to 12.7% between 1997 and 2004, totaling 76 000 US stroke survivors in 2004. Compared with stroke survivors able to afford medications, those unable to afford them more frequently reported lack of transportation, no health insurance, no usual place of care, income <$20 000, and out-of-pocket medical expenses ≥$2000.¹²⁹

In 2002, ≈21% of US counties did not have a hospital, 31% lacked a hospital with an ED, and 77% did not have a hospital with neurological services.¹³⁰

Of patients with ischemic stroke in the California Acute Stroke Pilot Registry, 23.5% arrived at the ED within 3 hours of symptom onset, and 4.3% received thrombolysis. If all patients had called 9-1-1 immediately, the expected overall rate of thrombolytic treatment within 3 hours would have increased to 28.6%. If all patients with known onset had arrived within 1 hour and had been treated optimally, 57% could have received thrombolytic treatment.¹³¹

Data from the Paul Coverdell National Acute Stroke Registry were analyzed from the 142 hospitals that participated in the 4 registry states. More patients were transported by ambulance than by other means (43.6%). Time of stroke symptom onset was recorded for 44.8% of the patients. Among these patients, 48% arrived at the ED within 2 hours of symptom onset. Significantly fewer blacks (42.4%) arrived within 2 hours of symptom onset than did whites (49.5%), and significantly fewer nonambulance patients (36.2%) arrived within 2 hours of symptom onset than did patients transported by ambulance (58.6%).¹³²

NHIS data from 1998 to 2002 found that younger stroke survivors (45–64 years) self-reported worse access to physician care and medication affordability than older stroke survivors. Compared with older patients, younger stroke survivors were more likely to be male (52% versus 47%), to be black (19% versus 10%), and to lack health insurance (11% versus 0.4%). Lack of health insurance was associated with reduced access to care.¹³³

Data from 142 hospitals participating in the Paul Coverdell National Acute Stroke Registry found that fewer than 48% of stroke patients arrived at the ED within 2 hours of symptom onset in 2005 to 2006. Blacks were less likely to arrive within the 2-hour window than whites (42.4% versus 49.5%). Among those arriving within 2 hours, 65.2% received imaging within 1 hour of ED arrival; significantly fewer women received imaging within 1 hour than men (62.9% versus 67.6%), but no differences were observed by racial group.¹³²

Results from the BASIC project found that women were less likely to arrive at the ED within 3 hours of stroke symptom onset than men (OR 0.7, 95% CI 0.5–0.9). Mexican Americans were 40% less likely to arrive by EMS than non-Hispanic whites, even after adjustment for age, National Institutes of Health Stroke Scale score, education, history of stroke, and insurance status. Language fluency was not associated with time to hospital arrival or use of EMS. The receipt of tissue-type plasminogen activator was low (1.5%) but did not differ by sex or race.¹³⁴

A national study of academic medical centers found no change in the proportion of patients with stroke arriving at hospitals within 2 hours of symptom onset between 2001 and 2004 (37% versus 38%); however, the rate of intravenous tissue-type plasminogen activator use increased over this time period (14% to 38%), which suggests system-level improvements in the organization of in-hospital care. In risk-adjusted analyses, black patients were 45% less likely to arrive within 2 hours than white patients.¹³⁵

In 2009, an estimated 93 000 inpatient endarterectomy procedures were performed in the United States. Carotid endarterectomy is the most frequently performed surgical procedure to prevent stroke (NHDS, NCHS, NHLBI tabulation).

Although rates of carotid endarterectomy in the Medicare population decreased slightly between 1998 and 2004, the use of carotid artery stenting increased dramatically¹³⁶ (Chart 6-12).

The randomized Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) compared carotid endarterectomy and stenting for symptomatic and asymptomatic carotid stenosis. There was no overall difference in the primary end point of stroke, MI, or death; however, carotid endarterectomy showed superiority with increasing age, with the crossover point at approximately age 70, and was associated with fewer strokes, which had a greater impact on quality of life than MI.¹³⁷

The estimated direct medical cost of stroke for 2008 is $18.8 billion. This includes hospital outpatient or office-based provider visits, hospital inpatient stays, ED visits, prescribed medicines, and home health care.¹³⁸

The mean expense per person for stroke care in the United States in 2007 was estimated at $7657.¹³⁸

The mean lifetime cost of ischemic stroke in the United States is estimated at $140 048. This includes inpatient care, rehabilitation, and follow-up care necessary for lasting deficits. (All numbers were converted to 1999 dollars by use of the medical component of the Consumer Price Index.)¹³⁹

The estimated cost of acute pediatric stroke in the United States was $42 million in 2003. The mean cost of short-term hospital care was $20 927 per discharge.¹⁴⁰

After adjustment for routine healthcare costs, the average 5-year cost of a neonatal stroke was $51 719 and that of a childhood stroke was $135 161. Costs among children with stroke continued to exceed those in age-matched control children even in the fifth year by an average of $2016.¹⁴¹

In a study of stroke costs within 30 days of an acute event between 1987 and 1989 in the Rochester Stroke Study, the average cost was $13 019 for mild ischemic strokes and $20 346 for severe ischemic strokes (4 or 5 on the Rankin Disability Scale).¹⁴²

Inpatient hospital costs for an acute stroke event account for 70% of first-year poststroke costs.¹¹⁵

The largest components of short-term care costs were room charges (50%), medical management (21%), and diagnostic costs (19%).¹⁴³

Death within 7 days, subarachnoid hemorrhage, and stroke while hospitalized for another condition are associated with higher costs in the first year. Lower costs are associated with mild cerebral infarctions or residence in a nursing home before the stroke.¹⁴²

Demographic variables (age, sex, and insurance status) are not associated with stroke cost. Severe strokes (National Institutes of Health Stroke Scale score >20) cost twice as much as mild strokes, despite similar diagnostic testing. Comorbidities such as ischemic HD and AF predict higher costs.^143,144

The total cost of stroke from 2005 to 2050, in 2005 dollars, is projected to be $1.52 trillion for non-Hispanic whites, $313 billion for Hispanics, and $379 billion for blacks. The per capita cost of stroke estimates is highest in blacks ($25 782), followed by Hispanics ($17 201) and non-Hispanic whites ($15 597). Loss of earnings is expected to be the highest cost contributor in each race/ethnic group.¹⁴⁵