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Epidemiology of heart failure

Epidemiology of heart failure
Literature review current through: May 2024.
This topic last updated: Nov 23, 2022.

INTRODUCTION — Aging of the population and prolongation of the lives of cardiac patients by modern therapeutic innovations has led to an increasing prevalence of heart failure (HF). Despite improvements in therapy, the mortality rate in patients with HF has remained unacceptably high [1], making early detection of susceptible persons who would benefit from preventive measures imperative.

The epidemiology and causes of HF will be reviewed here. Diastolic dysfunction, asymptomatic left ventricular dysfunction, and causes of HF decompensation are discussed separately. (See "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis" and "Management and prognosis of asymptomatic left ventricular systolic dysfunction" and "Approach to diagnosis and evaluation of acute decompensated heart failure in adults".)

MAGNITUDE OF THE PROBLEM — The magnitude of the problem of HF cannot be assessed with precision since reliable, population-based estimates of its prevalence, incidence, and prognosis are lacking [2,3]. Part of the problem is that large differences exist among studies in their definition of the condition and the methods used to establish its presence. In addition, presymptomatic left ventricular (LV) dysfunction is now used increasingly as an indicator of impending, if not existing, HF [4].

Prevalence — There are an estimated 64 million people with HF worldwide [5]. The prevalence of HF varies geographically, with the highest prevalence rates of HF being reported from Central Europe, North Africa, and the Middle East, whereas lower rates are reported in Eastern Europe and Southeast Asia [6]. The American Heart Association (AHA) estimated that there were 6.2 million people with HF in the United States between 2013 and 2016 [7]. However, the uncertainty of establishing the HF diagnosis in large populations results in potentially inaccurate estimates; there at least six HF scoring methodologies for the diagnosis of HF that generally require history, physical examination, and chest radiographs [8,9].

Regardless of the definition used, the prevalence of HF and LV dysfunction increases with age [1,10-15]. As an example, the Framingham Heart Study found a prevalence of HF in males of 8 per 1000 at age 50 to 59 years, increasing to 66 per 1000 at ages 80 to 89 years; similar values (8 and 79 per 1000) were noted in females [1]. The prevalence in African-American populations is reported to be 25 percent higher than in White populations.

The Framingham Study estimates are primarily based upon symptomatic HF (table 1). These figures do not include asymptomatic patients with a reduced LV ejection fraction (LVEF). Investigations using echocardiography have found that only 50 percent of participants with LV dysfunction are symptomatic [12]. In a community survey from the Mayo Clinic, of 123 patients with an LVEF ≤50 percent, 30 (24 percent) had a diagnosis of HF; of 40 patients with an LVEF ≤40 percent, 21 (53 percent) had a diagnosis of HF [11]. (See "Tests to evaluate left ventricular systolic function".)

There has been an increase in the prevalence of HF in the population over time. In one study, the average increase from 1989 to 1999 was 1/1000 and 0.9/1000 for females and males, respectively [16]. This has been associated with a three- to fourfold rise in the rate of hospitalization for HF from 1971 to 1999 [16,17]. Several elements are contributing to this rise, particularly aging of the population. In addition, improved treatment of hypertension and valvular and coronary disease is allowing patients to survive an early death only to later develop HF. The prevalence of HF in the United States is projected to rise over the next four decades, with an estimated 772,000 new HF cases projected in the year 2040 [18] and a total of 8 million prevalent cases by 2030 [19].

However, these trends must be interpreted with caution because of the introduction of new diagnostic methodology, changes in hospital admission and reimbursement practices, increased awareness of the problem, and changes in the prevalence of comorbidity. Coexistent disease is often the chief reason for hospitalization of HF patients [20].

In 2004, there were over one million hospitalizations in the United States with a first listed discharge diagnosis of HF [17]. In addition, at least 20 percent of hospital admissions among persons older than 65 are due to HF [21].

Data from the United Kingdom indicate a rising prevalence of HF (23 percent increase in prevalent cases between 2002 and 2014) [22].

Preserved systolic function — It is now appreciated that HF often occurs with normal LV systolic function (ie, presumably on the basis of diastolic dysfunction) [23-25]. Various studies estimate that as many as 40 to 60 percent of patients with HF have diastolic dysfunction as defined by a normal LVEF [10,11,25-28]. However, there has been a marked variability in the reported prevalence of HF with preserved ejection fraction (HFpEF; ranging from 13 to 74 percent) due to the use of heterogeneous criteria and hospital-based data [10]. (See "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis".)

The prevalence of HFpEF increases with age [29-31]. In one review, the estimated prevalence of diastolic dysfunction among patients with HF was 15, 33, and 50 percent at ages less than 50, 50 to 70, and more than 70 years, respectively [29]. In addition, another 15 percent of elderly patients with HF have mildly abnormal systolic function (LVEF 45 to 54 percent), which should not produce symptoms on its own and is therefore probably associated with an important component of diastolic dysfunction [27].

In a study conducted in Olmsted County, Minnesota, 21 percent of the population had mild diastolic dysfunction, 7 percent had moderate diastolic dysfunction, 0.7 percent had severe diastolic dysfunction, and 5.6 percent had moderate or severe diastolic dysfunction with a normal LVEF [11]. Data from Olmsted County also indicate that the proportion of patients with HF with preserved systolic function may have increased in the community over time [32].

Incidence — The incidence of HF, like the prevalence, increases with age [15,33]. In the Framingham Study, the incidence approximately doubled over each successive decade of life, rising more steeply with age in females than in males (table 2). The annual incidence in males rose from 2 per 1000 at age 35 to 64 years to 12 per 1000 at age 65 to 94 years. Because the increase in risk with age is balanced by the decreased life expectancy with older age, the lifetime likelihood of developing HF is approximately 20 percent at all ages above 40 [33].

Data from the United Kingdom indicate a decrease in age-standardized HF incidence between 2002 and 2014 by 7 percent [22].

Relative incidence of HFrEF and HFpEF — HF may occur with either a preserved or a reduced LVEF (HFpEF or HFrEF). (See 'Preserved systolic function' above and "Pathophysiology of heart failure with preserved ejection fraction", section on 'HFpEF versus HFrEF'.)

The relative incidence of HFrEF (LVEF ≤40 percent) and HFpEF (LVEF ≥50 percent) was evaluated in the PREVEND community-based, cohort study of middle aged subjects [34]. A few patients with LVEF between 40 and 50 percent were excluded from the analysis. Among 8592 subjects, 4.4 percent were diagnosed with HF during a median of 11.5 years. Of these, 34 percent had HFpEF and 66 percent had HFrEF. These data are consistent with reports from the United States [35].

Older adults — Although the prevalence of HF is increasing due to aging of the population, the trend with regard to age-adjusted HF incidence is less clear. Four studies reached somewhat different conclusions.

An analysis from the Framingham study of 10,311 subjects (1075 with incident HF) found no change in age-adjusted incidence of HF in males between the time period of 1950 to 1969 and the time period of 1990 to 1999 [36]. Among females, there was a decline in age-adjusted incidence of HF in females between the time periods of 1950 to 1969 and 1970 to 1979 and no subsequent change in the period of 1990 to 1999. The mean age at the diagnosis of HF rose from 63 years in the 1950 to 1969 period to 80 years in the 1990 to 1999 period.

Similarly, a report from the Mayo Clinic based on 4537 individuals with incident HF (mean age 74 years) found no evidence of any significant change in age-adjusted HF incidence for either males or females between 1979 and 2000 [37].

In contrast, a retrospective Kaiser Permanente Center study of individuals ≥65 years old (1942 with incident HF) found a 14 percent increase in age-adjusted incidence of HF in the time period between 1970 to 1974 and 1990 to 1994 [38].

A larger study of HF incidence found a decline in rate over time in individuals ≥65 years old [39]. In a retrospective study of 622,789 Medicare beneficiaries ≥65 years old diagnosed with HF between 1994 and 2003, the incidence of HF declined from 32 per 1000 person-years in 1994 to 29 per 1000 person-years in 2003. Incidence declined most sharply among beneficiaries aged 80 to 84 years old (from 57.5 to 48.4 per 1000 person-years) and increased slightly among beneficiaries aged 65 to 69 years (from 17.5 to 19.3 per 1000 person-years).

Younger adults — Fewer data are available on the incidence of HF in younger adults. In the Framingham study, the five-year risk of HF among 40-year-old White subjects was 0.1 to 0.2 percent [33].

Younger patients with HF are more often from a Black than White population. A report from the CARDIA study of 5115 subjects aged 18 to 30 years who were prospectively followed for 20 years found that incident HF before 50 years of age was substantially more common among participants (1.1, 0.9, 0.08, and 0 percent in Black females, Black males, White females, and White males, respectively) [40]. It is conceivable that this race-related difference may be due to race-related disparities in health care access and socioeconomic factors. Among Black participants in the CARDIA study, independent predictors of HF before age 30 years (with HF occurring on average 15 years later) included higher diastolic blood pressure, higher body mass index, lower high-density lipoprotein-cholesterol, and kidney disease. LV systolic dysfunction on echocardiogram at age ≤35 years was also independently associated with later development of HF [40]. A report from the CHARM program found a larger percentage of Black patients among younger compared with older HF patient cohorts (age 20 to 39 years: 18 percent versus ≥70 years: 2 percent) [41].

Lifetime risk — In the Framingham Heart Study, at age 40, the lifetime risk of developing HF for both males and females was one in five [33]. At age 40, the lifetime risk of HF occurring without antecedent myocardial infarction (MI) was one in nine for males and one in six for females. Lower lifetime risk (one in seven at age 40) was observed in the Physicians' Health Study, which may be due to healthy lifestyle factors [42]. A report noted that the lifetime risk of HF varied by age, sex, and HF type.

Overall, the lifetime risk of all HF and of HFpEF is higher in White compared with Black populations, whereas lifetime risk of HFrEF is similar in White and Black populations. Likewise, lifetime risk of HFrEF is higher in females, but that of HFpEF is either similar in males and females [43] or slightly higher in females [44]. (See 'Risk factor reduction' below.)

An investigation from the Framingham Heart Study assessed temporal trends in the lifetime risk of HF in two 25-year epochs (1965 to 1989 and 1990 to 2014). In this report, the lifetime risk of HF at age 50 years increased across epochs from 18.86 to 22.55 percent in females, and from 19.19 to 25.25 percent in males. The increase in lifetime risk of HF was independent of body mass index, blood pressure, and history of MI. Of note, the mean age at onset of HF increased across the epochs by 6.6 years (females) to 7.2 years (males) [44].

Mortality — National statistics in the United States showed a rise in the death rate attributable to HF from 5.8 per 1000 in 1970 to 16.4 per 1000 in 1993 [45]. This upward trend contrasts with reported declines in overall and coronary mortality and at least in part reflects avoidance of premature mortality from these predisposing conditions, which are only palliated, not cured, by advances in therapy.

Among individuals with HF, analyses from Scotland, the Framingham Heart Study, the Mayo Clinic, and the cohort of older patients noted above, all found a progressive improvement in patient survival after 1980 [36-38,46]. However, average survival remained poor after hospitalization for a first episode of HF (eg, in Scotland in 2002 the median survival was 2.3 years in males and 1.7 years in females) [46]. (See "Prognosis of heart failure", section on 'Factors affecting mortality rates'.)

HFpEF appears to be associated with a better prognosis than HF due to systolic dysfunction (annual mortality 8 to 9 versus 19 percent) in some reports [47], although some investigators have reported similar mortality rates for HF due to systolic dysfunction and HFpEF [28]. A meta-analysis of nearly 42,000 patients with HF in 31 studies suggested that mortality of HFpEF is approximately 30 percent lower than that of HFrEF [48]. (See "Treatment and prognosis of heart failure with preserved ejection fraction", section on 'Prognosis'.)

RISK FACTORS FOR HEART FAILURE — Conditions or disease processes leading to the development of HF are discussed here. Precipitants (triggers or contributing factors) for decompensation in patients with heart disease and drugs to avoid or use with caution in patients with heart disease are discussed separately. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults" and "Drugs that should be avoided or used with caution in patients with heart failure".)

Frequency of various causes — In the 1970s, hypertension and coronary disease, particularly MI, were the primary causes of HF in the United States and Europe [1,49]. However, coronary disease and diabetes mellitus have become increasingly responsible for HF while hypertension and valve disease have become less common because of improvements in detection and therapy [50-52]. Over four decades of observation in the Framingham Study, the prevalence of coronary disease as a cause of HF increased 41 percent per calendar decade in males and 25 percent in females; the prevalence of diabetes as a contributing cause increased by more than 20 percent per decade [50].

Clinical trials suggest a higher prevalence (60 to 65 percent) of coronary disease. However, patients in these trials represent a selected group, since those with hypertension, diabetes, and diastolic dysfunction were often excluded [53].

Epidemiologically, the impact of the various predisposing conditions for HF is best determined by the population attributable risk (PAR) that takes into account both the hazard ratio and the prevalence of the predisposing condition in the population. As an example, the First National Health and Nutrition Examination Survey (NHANES I) of 13,643 males and females who were followed for 19 years found that the risk factors for HF and their PAR were as follows [51]:

Coronary heart disease – relative risk 8.1; overall PAR 62 percent, 68 percent in males and 56 percent in females.

Cigarette smoking – relative risk 1.6, PAR 17 percent.

Hypertension – relative risk 1.4, PAR 10 percent.

Obesity – relative risk 1.3, PAR 8 percent; the importance of obesity was also demonstrated in a long-term follow-up from the Framingham Heart Study that estimated that approximately 11 percent of cases of HF in males and 14 percent in females are attributable to obesity alone [54]. (See "Overweight and obesity in adults: Health consequences".)

Diabetes – relative risk 1.9, PAR 3 percent.

Valvular heart disease – relative risk 1.5, PAR 2 percent; however, valve disease is an increasingly common cause of HF at older ages, with calcific aortic stenosis being the most common disorder requiring surgery [55].

A large European study reported that overweight or obese and hypertension were the strongest risk factors for development of HF; together, they account for nearly 40 percent of incident HF [56].

A report from the United Kingdom indicated that increasing personal wealth was associated with a lower risk of HF, a later age of presentation, and lower mortality from HF [22].

A predominance of coronary disease and a lower incidence of hypertensive heart disease were also noted in an Italian registry of over 6200 unselected outpatients with HF [57]. The underlying cardiac diagnoses were:

Ischemic heart disease – 40 percent

Dilated cardiomyopathy – 32 percent

Primary valvular heart disease – 12 percent

Hypertensive heart disease – 11 percent

Other – 5 percent

A separate issue is the distribution of causes in patients in whom the diagnosis is not apparent. In an evaluation of 1230 patients with an initially unexplained cardiomyopathy, the following etiologies were noted [58]:

Idiopathic – 50 percent

Myocarditis – 9 percent

Ischemic heart disease – 7 percent

Infiltrative disease – 5 percent

Peripartum cardiomyopathy – 4 percent

Hypertension – 4 percent

HIV infection – 4 percent

Connective tissue disease – 3 percent

Substance abuse – 3 percent

Doxorubicin – 1 percent

Other – 10 percent

The reports discussed above did not attempt to evaluate cause according to age group. In a report from the CHARM program, the percent of patients with idiopathic dilated cardiomyopathy decreased as age increased (62 percent in patients aged 20 to 39, 35 percent in patients aged 40 to 49, 24 percent in patients aged 50 to 59, 17 percent in patients aged 60 to 69, and 9 percent in those aged ≥70 years) [41].

The definition and specific causes of dilated cardiomyopathy are discussed separately. (See "Causes of dilated cardiomyopathy".)

An association between obstructive sleep apnea and incident HF is discussed separately. (See "Obstructive sleep apnea and cardiovascular disease in adults", section on 'Cardiovascular events'.)

Geographic variation — Few data are available on the distribution of the causes of HF. HF in Africa has been conventionally thought to be caused predominantly by untreated rheumatic valvular disease, peripartum and idiopathic cardiomyopathy, and hypertension [59].

A different distribution of causes suggestive of an epidemiological transition was found in a later study of 844 de novo presentations of HF at an urban African hospital [60]. The mean age was 55 years and females (57 percent) and Black Africans (88 percent) predominated. The most common diagnoses were hypertensive HF (33 percent), idiopathic dilated cardiomyopathy (28 percent), right-sided HF (27 percent, nearly half with isolated right heart involvement), ischemic cardiomyopathy (9 percent), and valvular HF (8 percent). Black Africans had less ischemic cardiomyopathy but more idiopathic and other causes of cardiomyopathy than White Africans. It is unclear if these patterns are due to race per se or are related to the concomitant burden of comorbidities and associated health disparities.

Ischemic cardiomyopathy — As demonstrated by the above observations, ischemic cardiomyopathy is the most common cause of HF due to systolic dysfunction in Western countries. Ischemic cardiomyopathy is diagnosed in patients with HF who have had an MI or have evidence of hibernating myocardium or, on angiography, severe coronary disease. In contrast, patients with single vessel disease who have no evidence of MI or revascularization have a similar prognosis as those with nonischemic cardiomyopathy [61]. It was suggested that such patients should be classified as nonischemic cardiomyopathy, at least for prognostic purposes. (See "Treatment of ischemic cardiomyopathy".)

Hypertension — Hypertension increases the risk of HF at all ages. Data from the Framingham Heart Study found that, after age 40, the lifetime risk of developing HF was twice as high in subjects with a blood pressure ≥160/100 mmHg compared with <140/90 mmHg [33]. The risk of developing HF increases with the degree of blood pressure elevation. However, even moderate elevations contribute to risk in the long term [49]. The average blood pressure of hypertensive candidates for HF in the Framingham Study was 150/90 mmHg.

Another analysis from the Framingham study suggests that baseline systolic pressure and pulse pressure have a greater impact on the risk of subsequent HF than the diastolic pressure. In this analysis, 2040 participants ages 50 to 79 who were initially free of HF were followed for 17.4 years after baseline blood pressure measurements [62]. Clinical evidence of HF developed in 234 subjects (11.8 percent). Increments of one standard deviation in systolic pressure, pulse pressure, and diastolic pressure were associated with hazard ratios for HF of 1.56, 1.55, and 1.24, respectively, after adjustment for other risk factors. The investigators hypothesize that increased arterial stiffness may be important in the influence of hypertension on the development of HF. (See "Increased pulse pressure" and "Treatment of hypertension in older adults, particularly isolated systolic hypertension".)

Among hypertensive subjects, concurrent coronary disease, diabetes, LV hypertrophy, and valve disease increased the risk of HF [49]. As an example, 52 percent (in males) and 34 percent (in females) of hypertensive persons who developed HF in the Framingham Study had preceding MI, which increased the HF risk five to sixfold. Angina also increased the risk, but only half as much as an infarction. Diabetes, LV hypertrophy, and valve diseases escalate the hypertensive risk two- to threefold [49].

Post-MI — Antecedent hypertension has an impact on LV remodeling after an MI and increases the risk of HF in these patients. This was illustrated by a series of 1093 patients, 40 percent of whom had antecedent hypertension [63]. The following results were noted:

Hypertensive patients were more likely than normotensives to have early LV remodeling after the MI.

Hypertensive patients had a significantly greater incidence of HF during hospitalization (33 versus 24 percent for normotensives).

During a mean follow-up of two years, hypertensive patients had a significantly greater incidence of HF requiring hospitalization (12.4 versus 5.5 percent); this difference was especially evident in patients ≥65 years of age (20 versus 8 percent).

Limited data suggest that the incidence of post-MI HF in the community may be declining [64]. However, an analysis of Framingham data suggests that the increased survival of post-MI patients may be resulting in an increase in the incidence of HF post-MI [65].

Left ventricular hypertrophy — Whether due to hypertension, coronary disease, valve disease, or diabetes, LV hypertrophy is a prominent feature of evolving HF. Among patients with HF in the general population, antecedent evidence of LV hypertrophy is present in approximately 20 percent by electrocardiogram (ECG) and 60 to 70 by echocardiogram. The risk of HF of any cause increases progressively in relation to the LV mass with no discernible separation of compensatory from pathologic hypertrophy.

Each method of demonstrating LV hypertrophy (ECG, chest film, or echocardiogram) independently predicts HF. As a result, persons having any combination of them have a greater risk than those with any one alone. (See "Left ventricular hypertrophy: Clinical findings and ECG diagnosis".)

Obesity — Epidemiologic studies have identified obesity as a risk factor for both systolic and diastolic HF (see 'Frequency of various causes' above) and the prevalence is relatively greater in younger patients. In a report from the CHARM program, the youngest patients were more likely to be obese than the oldest (body mass index [BMI] ≥35 kg/m2: 23 versus 6 percent, comparing those aged 20 to 29 years with those ≥70 years) [41].

In a Mendelian randomization study (see "Mendelian randomization") that analyzed the relationships between the adiposity-associated variant rs9939609 and BMI, rs9939609 and 24 cardiometabolic traits, and BMI and these traits, evidence for a causal relationship between obesity and incident HF was found (hazard ratio, 1.19 per BMI-unit increase, 95% CI 1.03-1.39) [66].

Comparing predisposing conditions for HFpEF and HFrEF — Patients with HF can be broadly separated into those with preserved ejection fraction (HFpEF) or with reduced ejection fraction (HFrEF). (See 'Preserved systolic function' above and "Pathophysiology of heart failure with preserved ejection fraction", section on 'HFpEF versus HFrEF'.)

Conditions commonly associated with HFpEF and HFrEF include older age, hypertension, coronary disease, and diabetes mellitus [32]. Patients with HFpEF tend to be older, more frequently have hypertension, are overweight, and more often females, compared with patients with HFrEF. (See "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis".)

The predictors of these two types of HF were evaluated in the PREVEND community-based, cohort study of middle-aged subjects [34]. In multivariable analysis, incident HF was associated with the factors listed above as well as obesity, N-terminal pro brain natriuretic peptide (NT-proBNP), and highly sensitive troponin T (hs-TnT) in all subjects. In a comparison of etiological factors for HFpEF versus HFrEF, female sex, atrial fibrillation, increased urinary albumin excretion, and increased cystatin-C were preferentially associated with HFpEF, whereas male sex, smoking, hs-TnT, and prior MI were preferentially associated with HFrEF.

HFpEF is more often a condition of females than males [28]. In a study of 19,710 Medicare beneficiaries over age 65 hospitalized with a principal discharge diagnosis of HF, 34 percent had preserved LV function [31]. Females accounted for 71 percent of patients with HFpEF, compared with 49 percent of those with impaired LV function. In a multivariate analysis of predictors of HFpEF, female sex was significant (odds ratio 2.07, 95% CI 1.93-2.34).

Social determinants and heart failure — Social determinants of health are associated with HF incidence, severity, and prognosis [67,68]. The key risk factors include occupation, income, and conditions related to personal relationships and network [69]. In an investigation of more than 44,000 participants in the Women's Health Initiative, women who were socially isolated had a 23 percent greater risk of HF that was independent of traditional risk factors [70]. Social determinants of health correlate with physical frailty, and patients who are older and hospitalized often have "social frailty," which is a condition associated with all-cause mortality, recurrent HF hospitalization, and lack of advanced care planning [71-73].

PREVENTION OF HEART FAILURE — Prevention of HF requires early detection and treatment of predisposing conditions and of high-risk candidates by internists and general practitioners. Recommendations for the management of patients at high risk for HF and patients with asymptomatic left ventricular (LV) dysfunction were published in 2013 by an American College of Cardiology/American Heart Association (ACC/AHA) task force [74]. In this document, HF is divided into the following stages:

Stage A – At high risk for HF but without structural heart disease or symptoms of HF

Stage B – Structural heart disease but without signs or symptoms of HF

Stage C – Structural heart disease with prior or current symptoms of HF

Stage D – Refractory HF requiring specialized interventions

An updated classification from the ACC/AHA classifies Stage B HF as pre-HF [75]. It is estimated that the prevalence of pre-HF (ranging from 12.5 to 24.2 percent) is 5 to 10 times higher than that of symptomatic HF (estimated at 2.2 percent) [76].

Risk factor reduction — The high risk for HF associated with hypertension, diabetes, coronary disease, and obesity identifies these as priority areas for preventive efforts. As an example, major hypertension trials clearly indicate that treating hypertension reduces the risk of HF. One meta-analysis found that controlling hypertension in elderly adults can reduce HF incidence by 39 percent [77], a value close to the estimated population attributable risk for hypertension by the Framingham Study [49].

The impact of healthy lifestyle habits (normal body weight, not smoking, regular exercise [five or more times per week], moderate alcohol intake [5 to 14 drinks per week], consumption of breakfast cereals, and consumption of fruits and vegetables) on HF risk was examined in a study of 20,900 males from the Physicians' Health Study [42]. The analysis revealed that healthy lifestyle habits were associated with lower lifetime risk, with highest risk (21 percent) in males adhering to none of the six lifestyle factors and the lowest risk (10 percent) in males adhering to four or more of these factors.

The Physicians' Health Study and other observational studies suggest that increased physical activity, higher cardiorespiratory fitness, and lower sedentary time are associated with reduced HF incidence [78]. These associations are consistent for occurrence of HF with both preserved and reduced ejection fraction.

Clinical trials in high-risk patients with diabetes mellitus have found that sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of heart failure hospitalization and other adverse cardiovascular events, as discussed separately (see "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Cardiovascular effects'). The cardioprotective effects are believed to be multifactorial, including favorable effects on weight, blood pressure, blood glucose, and diuresis. The use of SGLT2 inhibitors in selected patients with diabetes is discussed separately. (See "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Suggested approach to the use of SGLT2 inhibitors' and "Initial management of hyperglycemia in adults with type 2 diabetes mellitus", section on 'Initial pharmacologic therapy' and "Management of persistent hyperglycemia in type 2 diabetes mellitus", section on 'Our approach'.)

SGLT2 inhibitors for the treatment of diabetic nephropathy and heart failure with reduced ejection fraction are reviewed separately. (See "Treatment of diabetic kidney disease" and "Secondary pharmacologic therapy for heart failure with reduced ejection fraction".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Beyond the Basics topic (see "Patient education: Heart failure (Beyond the Basics)")

SUMMARY

Prevalence – The worldwide magnitude of the heart failure (HF) problem cannot be assessed with precision since reliable, population-based estimates of its prevalence, incidence, and prognosis are lacking for many regions of the globe, and a variety of methods that include history, physical examination, and heart function have been used to diagnose the condition. There were an estimated 6.2 million people with HF in the United States in 2013 to 2016. There are an estimated 64 million people with HF worldwide. (See 'Prevalence' above.)

The prevalence and incidence of HF increases with age, and trend data suggest that the prevalence in the United States has increased in persons aged >65 years. (See 'Prevalence' above and 'Incidence' above.)

Risk factors – Risk factors for HF include coronary heart disease, cigarette smoking, hypertension, overweight, diabetes, and valvular heart disease. (See 'Risk factors for heart failure' above.)

Social determinants of health also contribute to the overall burden of HF.

Risk factor reduction – Prevention of HF requires early detection and treatment of predisposing conditions and of high-risk candidates by internists and general practitioners. The high risk for HF associated with hypertension, diabetes, coronary disease, and obesity identifies these as priority areas for preventive efforts. (See 'Risk factor reduction' above.)

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Topic 3479 Version 24.0

References

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