Heart Failure: Practice Essentials, Background, Pathophysiology (original) (raw)

Practice Essentials

Heart failure develops when the heart, via an abnormality of cardiac function (detectable or not), fails to pump blood at a rate commensurate with the requirements of the metabolizing tissues or is able to do so only with an elevated diastolic filling pressure. See the image below.

Heart Failure. This chest radiograph shows an enla

Heart Failure. This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases, signs of acute heart failure.

Signs and symptoms

Signs and symptoms of heart failure include the following:

See Presentation for more detail.

Diagnosis

Heart failure criteria, classification, and staging

The Framingham criteria for the diagnosis of heart failure consists of the concurrent presence of either two major criteria or one major and two minor criteria. [1]

Major criteria comprise the following:

Minor criteria (accepted only if they cannot be attributed to another medical condition) are as follows:

The New York Heart Association (NYHA) classification system categorizes heart failure on a scale of I to IV, [2] as follows:

The American College of Cardiology/American Heart Association (ACC/AHA) staging system is defined by the following four stages [3] :

Additional ACC/AHA/ and Heart Failure Society of America (HFSA) disease-staging terminology characterizes the syndrome as a continuum [4, 5, 6, 7] :

Testing

The following tests may be useful in the initial evaluation for suspected heart failure [3, 8, 9] :

See Workup for more detail.

Management

Treatment includes the following:

Surgical options

Surgical treatment options include the following:

See Treatment and Medication for more detail.

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Background

Heart failure is the pathophysiologic state in which the heart, via an abnormality of cardiac function (detectable or not), fails to pump blood at a rate commensurate with the requirements of the metabolizing tissues or is able to do so only with an elevated diastolic filling pressure.

Heart failure (see the images below) may be caused by myocardial failure but may also occur in the presence of near-normal cardiac function under conditions of high demand. Heart failure always causes circulatory failure, but the converse is not necessarily the case, because various noncardiac conditions (eg, hypovolemic shock, septic shock) can produce circulatory failure in the presence of normal, modestly impaired, or even supranormal cardiac function. To maintain the pumping function of the heart, compensatory mechanisms increase blood volume, cardiac filling pressure, heart rate, and cardiac muscle mass. However, despite these mechanisms, there is a progressive decline in the ability of the heart to contract and relax, resulting in worsening heart failure.

Heart Failure. This chest radiograph shows an enla

Heart Failure. This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases, signs of acute heart failure.

Heart Failure. A 28-year-old woman presented with

Heart Failure. A 28-year-old woman presented with acute heart failure secondary to chronic hypertension. The enlarged cardiac silhouette on this anteroposterior (AP) radiograph is caused by acute heart failure due to the effects of chronic high blood pressure on the left ventricle. The heart then becomes enlarged, and fluid accumulates in the lungs (ie, pulmonary congestion).

Signs and symptoms of heart failure include tachycardia and manifestations of venous congestion (eg, edema) and low cardiac output (eg, fatigue). Breathlessness is a cardinal symptom of left ventricular (LV) failure that may manifest with progressively increasing severity.

Heart failure can be classified according to a variety of factors (see Heart Failure Criteria, Classification, and Staging). The New York Heart Association (NYHA) classification for heart failure comprises four classes, based on the relationship between symptoms and the amount of effort required to provoke them, as follows [2] :

The American College of Cardiology/American Heart Association (ACC/AHA) heart failure guidelines complements the NYHA classification to reflect the progression of disease, divided into four stages, as follows [3] :

More recently, the ACC/AHA and Heart Failure Society of America (HFSA) introduced additional disease-staging terminology to characterize the syndrome of heart failure as a continuum, as follows [4, 5, 6, 7] :

Laboratory studies for heart failure should include a complete blood count (CBC), electrolyte levels, and hepatorenal function studies. Imaging studies such as chest radiography and two-dimensional echocardiography are recommended in the initial evaluation of patients with known or suspected heart failure. B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels can be useful in differentiating cardiac and noncardiac causes of dyspnea. (See Workup for more information.)

In acute heart failure, patient care consists of stabilizing the patient's clinical condition; establishing the diagnosis, etiology, and precipitating factors; and initiating therapies to provide rapid symptom relief and survival benefit. Surgical options for heart failure include revascularization procedures, electrophysiologic intervention, cardiac resynchronization therapy (CRT), implantable cardioverter-defibrillators (ICDs), valve replacement or repair, ventricular restoration, heart transplantation, and ventricular assist devices (VADs). (See Treatment for more information.)

The goals of pharmacotherapy are to increase survival and to prevent complications. Along with oxygen, medications assisting with symptom relief include diuretics, digoxin, inotropes, and morphine. Drugs that can exacerbate heart failure should be avoided (nonsteroidal anti-inflammatory drugs [NSAIDs], calcium channel blockers [CCBs], and most antiarrhythmic drugs). (See Medication for more information.)

For further information, see the Medscape Drugs & Diseases articles Pediatric Congestive Heart Failure, Congestive Heart Failure Imaging, Heart Transplantation, Pediatric Heart Transplantation, Coronary Artery Bypass Grafting, and Implantable Cardioverter-Defibrillators.

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Pathophysiology

The common pathophysiologic state that perpetuates the progression of heart failure is extremely complex, regardless of the precipitating event. Compensatory mechanisms exist on every level of organization, from the subcellular all the way through to organ-to-organ interactions. Only when this network of adaptations becomes overwhelmed does heart failure ensue. [11, 12, 13, 14, 15]

Adaptations

Most important among the adaptations are the following [16] :

The release of norepinephrine by adrenergic cardiac nerves augments myocardial contractility and includes activation of the renin-angiotensin-aldosterone system [RAAS], the sympathetic nervous system [SNS], and other neurohumoral adjustments that act to maintain arterial pressure and perfusion of vital organs.

In acute heart failure, the finite adaptive mechanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac performance. [17]

The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and regeneration. [18] This process eventually leads to remodeling, usually the eccentric type. Eccentric remodeling further worsens the loading conditions on the remaining myocytes and perpetuates the deleterious cycle. The idea of lowering wall stress to slow the process of remodeling has long been exploited in treating heart failure patients. [19]

The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of neuroendocrine systems, most notably the above-mentioned adrenergic systems and RAAS. [20]

The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which increases calcium afterload and, via an increase in cyclic adenosine monophosphate (cAMP), causes an increase in cytosolic calcium entry. The increased calcium entry into the myocytes augments myocardial contractility and impairs myocardial relaxation (lusitropy).

The calcium overload may induce arrhythmias and lead to sudden death. The increase in afterload and myocardial contractility (known as inotropy) and the impairment in myocardial lusitropy lead to an increase in myocardial energy expenditure and a further decrease in cardiac output. The increase in myocardial energy expenditure leads to myocardial cell death/apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a cycle of further increased neurohumoral stimulation and further adverse hemodynamic and myocardial responses.

In addition, the activation of the RAAS leads to salt and water retention, resulting in increased preload and further increases in myocardial energy expenditure. Increases in renin, mediated by a decreased stretch of the glomerular afferent arteriole, reduce delivery of chloride to the macula densa and increase beta1-adrenergic activity as a response to decreased cardiac output. This results in an increase in angiotensin II (Ang II) levels and, in turn, aldosterone levels, causing stimulation of the release of aldosterone. Ang II, along with ET-1, is crucial in maintaining effective intravascular homeostasis as mediated by vasoconstriction and aldosterone-induced salt and water retention.

The concept of the heart as a self-renewing organ is a relatively recent development. [21] This paradigm for myocyte biology created an entire field of research aimed directly at augmenting myocardial regeneration. The rate of myocyte turnover has been shown to increase during times of pathologic stress. [18] In heart failure, this mechanism for replacement becomes overwhelmed by an even faster increase in the rate of myocyte loss. This imbalance of hypertrophy and death over regeneration is the final common pathway at the cellular level for the progression of remodeling and heart failure.

Angiotensin II

Research indicates that local cardiac Ang II production (which decreases lusitropy, increases inotropy, and increases afterload) leads to increased myocardial energy expenditure. Ang II has also been shown in vitro and in vivo to increase the rate of myocyte apoptosis. [22] In this fashion, Ang II has similar actions to norepinephrine in heart failure.

Ang II also mediates myocardial cellular hypertrophy and may promote progressive loss of myocardial function. The neurohumoral factors above lead to myocyte hypertrophy and interstitial fibrosis, resulting in increased myocardial volume and increased myocardial mass, as well as myocyte loss. As a result, the cardiac architecture changes which, in turn, leads to further increase in myocardial volume and mass.

Myocytes and myocardial remodeling

In the failing heart, increased myocardial volume is characterized by larger myocytes approaching the end of their life cycle. [23] As more myocytes drop out, an increased load is placed on the remaining myocardium, and this unfavorable environment is transmitted to the progenitor cells responsible for replacing lost myocytes.

Progenitor cells become progressively less effective as the underlying pathologic process worsens and myocardial failure accelerates. These features—namely, the increased myocardial volume and mass, along with a net loss of myocytes—are the hallmark of myocardial remodeling. This remodeling process leads to early adaptive mechanisms, such as augmentation of stroke volume (Frank-Starling mechanism) and decreased wall stress (Laplace law) and, later, to maladaptive mechanisms such as increased myocardial oxygen demand, myocardial ischemia, impaired contractility, and arrhythmogenesis.

As heart failure advances, there is a relative decline in the counterregulatory effects of endogenous vasodilators, including nitric oxide (NO), prostaglandins (PGs), bradykinin (BK), atrial natriuretic peptide (ANP), and B-type natriuretic peptide (BNP). This decline occurs simultaneously with the increase in vasoconstrictor substances from the RAAS and the adrenergic system, which fosters further increases in vasoconstriction and thus preload and afterload. This results in cellular proliferation, adverse myocardial remodeling, and antinatriuresis, with total body fluid excess and worsening of heart failure symptoms.

Systolic and diastolic failure

Systolic and diastolic heart failure each result in a decrease in stroke volume. [24, 25] This leads to activation of peripheral and central baroreflexes and chemoreflexes that are capable of eliciting marked increases in sympathetic nerve traffic.

Although there are commonalities in the neurohormonal responses to decreased stroke volume, the neurohormone-mediated events that follow have been most clearly elucidated for individuals with systolic heart failure. The ensuing elevation in plasma norepinephrine directly correlates with the degree of cardiac dysfunction and has significant prognostic implications. Norepinephrine, while directly toxic to cardiac myocytes, is also responsible for a variety of signal-transduction abnormalities, such as downregulation of beta1-adrenergic receptors, uncoupling of beta2-adrenergic receptors, and increased activity of inhibitory G-protein. Changes in beta1-adrenergic receptors result in overexpression and promote myocardial hypertrophy.

Atrial natriuretic peptide and B-type natriuretic peptide

ANP and BNP are endogenously generated peptides activated in response to atrial and ventricular volume/pressure expansion. ANP and BNP are released from the atria and ventricles, respectively, and both promote vasodilation and natriuresis. Their hemodynamic effects are mediated by decreases in ventricular filling pressures, owing to reductions in cardiac preload and afterload. BNP, in particular, produces selective afferent arteriolar vasodilation and inhibits sodium reabsorption in the proximal convoluted tubule. It also inhibits renin and aldosterone release and, therefore, adrenergic activation. ANP and BNP are elevated in chronic heart failure. BNP especially has potentially important diagnostic, therapeutic, and prognostic implications.

For more information, see the Medscape Drugs & Diseases article Natriuretic Peptides in Congestive Heart Failure.

Other vasoactive systems

Other vasoactive systems that play a role in the pathogenesis of heart failure include the ET receptor system, the adenosine receptor system, vasopressin, and tumor necrosis factor-alpha (TNF-alpha). [26] ET, a substance produced by the vascular endothelium, may contribute to the regulation of myocardial function, vascular tone, and peripheral resistance in heart failure. Elevated levels of ET-1 closely correlate with the severity of heart failure. ET-1 is a potent vasoconstrictor and has exaggerated vasoconstrictor effects in the renal vasculature, reducing renal plasma blood flow, glomerular filtration rate (GFR), and sodium excretion.

TNF-alpha has been implicated in response to various infectious and inflammatory conditions. Elevations in TNF-alpha levels have been consistently observed in heart failure and seem to correlate with the degree of myocardial dysfunction. Some studies suggest that local production of TNF-alpha may have toxic effects on the myocardium, thus worsening myocardial systolic and diastolic function.

In individuals with systolic dysfunction, therefore, the neurohormonal responses to decreased stroke volume result in temporary improvement in systolic blood pressure and tissue perfusion. However, in all circumstances, the existing data support the notion that these neurohormonal responses contribute to the progression of myocardial dysfunction in the long term.

Heart failure with preserved ejection fraction

In diastolic heart failure (heart failure with preserved ejection fraction [HFpEF]), the same pathophysiologic processes occur that lead to decreased cardiac output in systolic heart failure, but they do so in response to a different set of hemodynamic and circulatory environmental factors that depress cardiac output. [27]

In HFpEF, altered relaxation and increased stiffness of the ventricle (due to delayed calcium uptake by the myocyte sarcoplasmic reticulum and delayed calcium efflux from the myocyte) occur in response to an increase in ventricular afterload (pressure overload). The impaired relaxation of the ventricle then leads to impaired diastolic filling of the left ventricle (LV).

Morris et al found that right venticular (RV) subendocardial systolic dysfunction and diastolic dysfunction, as detected by echocardiographic strain rate imaging, are common in patients with HFpEF. This dysfunction is potentially associated with the same fibrotic processes that affect the subendocardial layer of the LV and, to a lesser extent, with RV pressure overload. It may play a role in the symptomatology of patients with HFpEF. [28]

LV chamber stiffness

An increase in LV chamber stiffness occurs secondary to any one, or any combination, of the following three mechanisms:

A rise in filling pressure is the movement of the ventricle up along its pressure-volume curve to a steeper portion, as may occur in conditions such as volume overload secondary to acute valvular regurgitation or acute LV failure due to myocarditis.

A shift to a steeper ventricular pressure-volume curve results, most commonly, not only from increased ventricular mass and wall thickness (as observed in aortic stenosis and long-standing hypertension) but also from infiltrative disorders (eg, amyloidosis), endomyocardial fibrosis, and myocardial ischemia.

Parallel upward displacement of the diastolic pressure-volume curve is generally referred to as a decrease in ventricular distensibility. This is usually caused by extrinsic compression of the ventricles.

Concentric LV hypertrophy

Pressure overload that leads to concentric LV hypertrophy (LVH), as occurs in aortic stenosis, hypertension, and hypertrophic cardiomyopathy, shifts the diastolic pressure-volume curve to the left along its volume axis. As a result, ventricular diastolic pressure is abnormally elevated, although chamber stiffness may or may not be altered.

Increases in diastolic pressure lead to an increased myocardial energy expenditure, remodeling of the ventricle, increased myocardial oxygen demand, myocardial ischemia, and eventual progression of the maladaptive mechanisms of the heart that lead to decompensated heart failure.

Arrhythmias

Although life-threatening rhythms are more common in ischemic cardiomyopathy, arrhythmia imparts a significant burden in all forms of heart failure. In fact, some arrhythmias even perpetuate heart failure. The most significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias. Structural substrates for ventricular arrhythmias that are common in heart failure, regardless of the underlying cause, include ventricular dilatatation, myocardial hypertrophy, and myocardial fibrosis.

At the cellular level, myocytes may be exposed to increased stretch, wall tension, catecholamines, ischemia, and electrolyte imbalance. The combination of these factors contributes to an increased incidence of arrhythmogenic sudden cardiac death in patients with heart failure.

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Etiology

Most patients who present with significant heart failure do so because of an inability to provide adequate cardiac output in that scenario. This is often a combination of the causes listed below in the setting of an abnormal myocardium. The list of causes responsible for presentation of a patient with heart failure exacerbation is very long, and searching for the proximate cause to optimize therapeutic interventions is important.

From a clinical standpoint, classifying the causes of heart failure into the following four broad categories is useful:

Underlying causes

Specific underlying factors cause various forms of heart failure, such as systolic heart failure (most commonly, left vetricular [LV] systolic dysfunction), heart failure with preserved LV ejection fraction (LVEF), acute heart failure, high-output heart failure, and right heart failure.

Underlying causes of systolic heart failure include the following:

Underlying causes of diastolic heart failure include the following:

Underlying causes of acute heart failure include the following:

Underlying causes of high-output heart failure include the following:

Underlying causes of right heart failure include the following:

Precipitating causes of heart failure

A previously stable, compensated patient may develop heart failure that is clinically apparent for the first time when the intrinsic process has advanced to a critical point, such as with further narrowing of a stenotic aortic valve or mitral valve. Alternatively, decompensation may occur as a result of the failure or exhaustion of the compensatory mechanisms but without any change in the load on the heart in patients with persistent, severe pressure or volume overload. In particular, consider whether the patient has underlying coronary artery disease or valvular heart disease.

The most common cause of decompensation in a previously compensated patient with heart failure is inappropriate reduction in the intensity of treatment, such as dietary sodium restriction, physical activity reduction, or drug regimen reduction. Uncontrolled hypertension is the second most common cause of decompensation, followed closely by cardiac arrhythmias (most commonly, atrial fibrillation). Arrhythmias, particularly ventricular arrhythmias, can be life threatening. Also, patients with one form of underlying heart disease that may be well compensated can develop heart failure when a second form of heart disease ensues. For example, a patient with chronic hypertension and asymptomatic LV hypertrophy (LVH) may be asymptomatic until an MI develops and precipitates heart failure.

Systemic infection or the development of unrelated illness can also lead to heart failure. Systemic infection precipitates heart failure by increasing total metabolism as a consequence of fever, discomfort, and cough, increasing the hemodynamic burden on the heart. Septic shock, in particular, can precipitate heart failure by the release of endotoxin-induced factors that can depress myocardial contractility.

Cardiac infection and inflammation can also endanger the heart. Myocarditis or infective endocarditis may directly impair myocardial function and exacerbate existing heart disease. The anemia, fever, and tachycardia that frequently accompany these processes are also deleterious. In the case of infective endocarditis, the additional valvular damage that ensues may precipitate cardiac decompensation.

Patients with heart failure, particularly when confined to bed, are at high risk of developing pulmonary emboli, which can increase the hemodynamic burden on the right ventricle (RV) by further elevating RV systolic pressure, possibly causing fever, tachypnea, and tachycardia.

Intense, prolonged physical exertion or severe fatigue, such as may result from prolonged travel or emotional crisis, is a relatively common precipitant of cardiac decompensation. The same is true of exposure to severe climate change (ie, the individual comes in contact with a hot, humid environment or a bitterly cold one).

Excessive intake of water and/or salt and the administration of cardiac depressants or drugs that cause salt retention are other factors that can lead to heart failure. At the European Society of Cardiology 2017 Congress, investigators presented a study comprising more than 4630 people that indicated high daily salt intake (>13.7 g) is associated with a substantial increased risk of developing heart failure, independent of other risk factors. [29, 30]

Because of increased myocardial oxygen consumption and demand beyond a critical level, the following high-output states can precipitate the clinical presentation of heart failure:

Longitudinal data from the Framingham Heart Study has suggested that antecedent subclinical LV systolic or diastolic dysfunction is associated with an increased incidence of heart failure, supporting the notion that heart failure is a progressive syndrome. [31, 32] Another analysis of over 36,000 patients undergoing outpatient echocardiography reported that moderate or severe diastolic dysfunction, but not mild diastolic dysfunction, is an independent predictor of mortality. [33]

Genetics of cardiomyopathy

Autosomal dominant inheritance has been demonstrated in dilated cardiomyopathy and in arrhythmic right ventricular cardiomyopathy. Restrictive cardiomyopathies are usually sporadic and associated with the gene for cardiac troponin I. Genetic tests are available at major genetic centers for cardiomyopathies. [34]

In families with a first-degree relative who has been diagnosed with a cardiomyopathy leading to heart failure, the at-risk patient should be screened and followed. [34] The recommended screening consists of an electrocardiogram and an echocardiogram. If the patient has an asymptomatic LV dysfunction, it should be documented and treated. [34]

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Epidemiology

United States statistics

According to 2017 American Heart Association (AHA) data, heart failure affects an estimated 6.5 million Americans aged 20 years and older. [35] With improved survival of patients with acute myocardial infarction and with a population that continues to age, heart failure will continue to increase in prominence as a major health problem in the United States. The AHA projects a 46% increase of heart failure prevalence from year 2012 to year 2030, resulting in 8 million or more Americans aged 18 years or older with heart failure. [35]

Despite a more than decade-long decrease (2000-2012) in the the incidence of heart failure–related deaths in the United States, such deaths are on the rise again, particularly among men and non-Hispanic black populations, according to 2000-2014 data (the most recent data available) released by the Centers for Disease Control and Prevention (CDC) in December 2015. [36, 37] The crude rate for heart failure-related deaths decreased from 103.1 deaths per 100,000 population in 2000 to 89.5 in 2009; it then increased to 96.9 in 2014. The age-adjusted rate for heart failure-related deaths decreased from 105.4 deaths per 100,000 standard population in 2000 to 81.4 in 2012; it then increased to 83.4 in 2013 and to 84.0 in 2014. [36] The trend appears to represent a shift from coronary heart disease as the underlying cause of heart failure deaths toward other cardiovascular and noncardiovascular causes, including malignancies, diabetes, chronic lower respiratory diseases, and renal disease.

Analysis of national and regional trends in hospitalization and mortality among Medicare beneficiaries from 1998-2008 showed a relative decline of 29.5% in heart failure hospitalizations [35, 38] ; however, wide variations were noted between states and races, with black men having the slowest rate of decline. A relative decline of 6.6% in mortality was also observed, although the rate was uneven across states. The length of stay decreased from 6.8 days to 6.4 days, despite an overall increase in the comorbid conditions. [38]

Heart failure statistics for the United States are as follows [35] :

The incidence and prevalence of heart failure are higher in black persons, Hispanics, Native Americans, and recent immigrants from developing nations, Russia, and the former Soviet republics. The higher prevalence of heart failure in blacks, Hispanics, and Native Americans is directly related to the higher incidence and prevalence of hypertension and diabetes. This problem is particularly exacerbated by a lack of access to health care and by substandard preventive health care available to the most indigent of individuals in these and other groups; in addition, many persons in these groups do not have adequate health insurance.

The higher incidence and prevalence of heart failure in recent immigrants from developing nations are largely due to a lack of prior preventive health care, a lack of treatment, or substandard treatment for common conditions, such as hypertension, diabetes, rheumatic fever, and ischemic heart disease.

Men and women have a similar incidence and prevalence of heart failure. However, many differences remain between men and women with heart failure, such as the following:

The prevalence of heart failure increases with age. [40] The prevalence is 1-2% of the population younger than 55 years and increases to a rate of 10% for persons older than 75 years. Nonetheless, heart failure can occur at any age, depending on the cause.

International statistics

Heart failure is a worldwide problem. The most common cause of heart failure in industrialized countries is ischemic cardiomyopathy, with other causes, including Chagas disease and valvular cardiomyopathy, assuming a more important role in developing countries. However, in developing nations that have become more urbanized and more affluent, eating a more processed diet and leading a more sedentary lifestyle have resulted in an increased rate of heart failure, along with increased rates of diabetes and hypertension. This change was illustrated in a population study in Soweto, South Africa, where the community transformed into a more urban and westernized city, followed by an increase in diabetes, hypertension, and heart failure. [42]

In terms of treatment, one study showed few important differences in uptake of key therapies in European countries with widely differing cultures and varying economic status for patients with heart failure. In contrast, studies of sub-Saharan Africa, where healthcare resources are more limited, have shown poor outcomes in specific populations. [43, 44] For example, in some countries, hypertensive heart failure carries a 25% 1-year mortality, and human immunodeficiency virus (HIV)–associated cardiomyopathy generally progresses to death within 100 days of diagnosis in patients who are not treated with antiretroviral drugs.

Although data regarding developing nations are not as robust as studies of Western society, the following trends in developing nations are apparent:

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Prognosis

In general, the mortality following hospitalization for patients with heart failure is 10.4% at 30 days, 22% at 1 year, and 42.3% at 5 years, despite marked improvement in medical and device therapy. [35, 45, 46, 47, 48, 49]

Mortality is greater than 50% for patients with New York Heart Association (NYHA) class IV, American College of Cardiology/American Heart Association (ACC/AHA) stage D heart failure. Heart failure associated with acute myocardial infarction (MI) has an inpatient mortality of 20-40%; mortality approaches 80% in patients who are also hypotensive (eg, cardiogenic shock). (See Heart Failure Criteria, Classification, and Staging).

Heart failure related to systolic dysfunction has an associated mortality of 50% after 5 years. [24]

Numerous demographic, clinical and biochemical variables have been reported to provide important prognostic value in patients with heart failure, and several predictive models have been developed. [50]

A study by van Diepen et al suggested that patients with heart failure or atrial fibrillation have a significantly higher risk of noncardiac postoperative mortality than patients with coronary artery disease; this risk should be considered even if a minor procedure is planned. [51]

Bursi et al found that among community patients with heart failure, pulmonary artery systolic pressure (PASP), as assessed by Doppler echocardiography, can strongly predict death and can provide incremental and clinically significant prognostic information independent of known outcome predictors. [52]

In the Framingham Offspring Cohort, higher concentrations of galectin-3, a marker of cardiac fibrosis, were associated with an increased risk for incident heart failure (hazard ratio: 1.28 per 1 standard deviation increase in log galectin-3). Galectin-3 was also associated with an increased risk for all-cause mortality (multivariable-adjusted hazard ratio: 1.15). [53]

A more recent, retrospective study that evaluated data from the 2010 Nebraska Hospital Discharge files for 4319 hospitalizations of 3521 heart failure patients admitted to 79 in-state hospitals reported that risk factors for in-hospital mortality in these patients were increasing age, the presence of comordities, and length of hospital day. [54]

In a 2024 prospective, two-center observational study in 350 adults hospitalized for acute heart failure, Espersen et al found four significant independent predictors of the composite of heart failure hospitalization or all-cause mortality in acute heart failure were an admission NT-proBNP (N-terminal pro B-type natriuretic peptide) level of 2000 pg/mL or above, a baseline systolic blood pressure below 120 mmHg, a baseline left atrial volume index of 60 mL/m2 or greater, and 9 or more B-lines on predischarge 4-zone lung ultrasound score (LUS). [55] The investigators noted similar results in a subset of patients (n = 176) with 8-zone LUS data.

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Patient Education

To help prevent recurrence of heart failure in patients in whom heart failure was caused by dietary factors or medication noncompliance, counsel and educate such patients about the importance of proper diet and the necessity of medication compliance.

Dunlay et al examined medication use and adherence among community-dwelling patients with heart failure and found that medication adherence was suboptimal in many patients, often because of cost. [56] A randomized controlled trial of 605 patients with heart failure reported that the incidence of all-cause hospitalization or death was not reduced in patients receiving multisession self-care training compared to those receiving a single-session intervention. [57] The optimum method for patient education remains to be established. It appears that more intensive interventions are not necessarily better. [57]

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Author

Ioana Dumitru, MD Associate Professor of Medicine, Division of Cardiology, Founder and Medical Director, Heart Failure and Cardiac Transplant Program, University of Nebraska Medical Center; Associate Professor of Medicine, Division of Cardiology, Veterans Affairs Medical Center

Ioana Dumitru, MD is a member of the following medical societies: American College of Cardiology, Heart Failure Society of America, International Society for Heart and Lung Transplantation

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Yasmine S Ali, MD, MSCI, FACC, FACP Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine; President, LastSky Writing, LLC

Yasmine S Ali, MD, MSCI, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Medical Writers Association, National Lipid Association, Tennessee Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: LastSky Writing;Philips Healthcare;M Health;Verywell Health; MedStudy;WellnessVerge;Prose Media; AKH, Inc.; LearnRoll, LLC; Eradigm; RxCe.com; M3 USA; M3 EU; Future US Inc.; Edanz Group; ChesterPA511
Serve(d) as a speaker or a member of a speakers bureau for: RxCe.com.

Chief Editor

Gyanendra K Sharma, MD, FACC, FASE Professor of Medicine and Radiology, Director, Adult Echocardiography Laboratory, Section of Cardiology, Medical College of Georgia at Augusta University

Gyanendra K Sharma, MD, FACC, FASE is a member of the following medical societies: American Association of Cardiologists of Indian Origin, American Association of Physicians of Indian Origin, American College of Cardiology, American Society of Echocardiography, Society for Cardiovascular Magnetic Resonance, Society of Cardiovascular Computed Tomography

Disclosure: Nothing to disclose.

Additional Contributors

Mathue M Baker, MD Cardiologist, BryanLGH Heart Institute and Saint Elizabeth Regional Medical Center

Mathue M Baker, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.

Mariclaire Cloutier Freelance editor, Medscape Drugs & Diseases

Disclosure: Nothing to disclose.

Acknowledgements

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York AcademyofSciences,and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center

William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Joseph Cornelius Cleveland Jr, MD Associate Professor, Division of Cardiothoracic Surgery, University of Colorado Health Sciences Center

Joseph Cornelius Cleveland Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American College of Cardiology, American College of Chest Physicians, American College of Surgeons, American Geriatrics Society, American Physiological Society, American Society of Transplant Surgeons, Association for Academic Surgery, Heart Failure Society of America, International Society for Heart and Lung Transplantation, Phi Beta Kappa, Society of Critical Care Medicine, Society of Thoracic Surgeons, and Western Thoracic Surgical Association

Disclosure: Thoratec Heartmate II Pivotal Tria; Grant/research funds Principal Investigator - Colorado; Abbott Vascular E-Valve E-clip Honoraria Consulting; Baxter Healthcare Corp Consulting fee Board membership; Heartware Advance BTT Trial Grant/research funds Principal Investigator- Colorado; Heartware Endurance DT trial Grant/research funds Principal Investigator-Colorado

Shamai Grossman, MD, MS Assistant Professor, Department of Emergency Medicine, Harvard Medical School; Director, The Clinical Decision Unit and Cardiac Emergency Center, Beth Israel Deaconess Medical Center

Shamai Grossman, MD, MS is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

John D Newell Jr, MD Professor of Radiology, Head, Division of Radiology, National Jewish Health; Professor, Department of Radiology, University of Colorado School of Medicine

John D Newell Jr, MD is a member of the following medical societies: American College of Chest Physicians, American College of Radiology, American Roentgen Ray Society, American Thoracic Society, Association of University Radiologists, Radiological Society of North America, and Society of Thoracic Radiology

Disclosure: Siemens Medical Grant/research funds Consulting; Vida Corporation Ownership interest Board membership; TeraRecon Grant/research funds Consulting; Medscape Reference Honoraria Consulting; Humana Press Honoraria Other

Craig H Selzman, MD, FACS Associate Professor of Surgery, Surgical Director, Cardiac Mechanical Support and Heart Transplant, Division of Cardiothoracic Surgery, University of Utah School of Medicine

Craig H Selzman, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American College of Surgeons, American Physiological Society, Association for Academic Surgery, International Society for Heart and Lung Transplantation, Society of Thoracic Surgeons, Southern Thoracic Surgical Association, and Western Thoracic Surgical Association

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Brett C Sheridan, MD, FACS Associate Professor of Surgery, University of North Carolina at Chapel Hill School of Medicine

Disclosure: Nothing to disclose.

George A Stouffer III, MD Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center

George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment