- The clinical syndrome of heart failure (HF) may result from disorders of the pericardium, myocardium, endocardium, heart valves, or great vessels or from certain metabolic abnormalities, but most patients with HF have symptoms due to impaired left ventricular (LV) myocardial function.
- Because some patients present without signs or symptoms of volume overload, the term “heart failure” is preferred over “congestive heart failure.”
- HF is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood.
- It should be emphasized that HF is not synonymous with either cardiomyopathy or LV dysfunction; these latter terms describe possible structural or functional reasons for the development of HF.
- HF may be associated with a wide spectrum of LV functional abnormalities, which may range from patients with normal LV size and preserved ejection fraction (EF) to those with severe dilatation and/or markedly reduced EF.
- In most patients, abnormalities of systolic and diastolic dysfunction coexist, irrespective of EF.
- The EF is considered important in classification of patients with HF because of differing patient demographics, comorbid conditions, prognosis, and response to therapies and because most clinical trials have selected patients based on EF.
- EF values are dependent on the imaging technique employed, method of analysis, and operator. Because other techniques may indicate abnormalities in systolic function among patients with a preserved EF, it is preferable to use the terms “preserved EF” (HFpEF) or “reduced EF” (HFrEF) over preserved or reduced “systolic function.”
- In view of the advances in medical therapy across the spectrum of cardiovascular diseases, the American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guideline task force has designated the term “guideline-directed medical therapy” (GDMT) to represent optimal medical therapy—a combination of lifestyle modifications and medications—as defined by their guideline-directed therapies (primarily Class I)(see Figure 1).
- This guideline outlines a comprehensive approach to the management of HF by ACCF/AHA stage of HF development (see algorithmic summary in Figure 3).
- The definition of HFrEF has been variable, but to date efficacious therapies have been demonstrated only in patients with an EF of ≤35% or ≤40%.
- Approximately half of patients with HFrEF may also have variable degrees of LV enlargement.
- Although coronary artery disease (CAD) with antecedent myocardial infarction (MI) is a major cause of HFrEF, many other risk factors may lead to LV enlargement and HFrEF.
- In patients with clinical HF, studies estimate that the prevalence of HFpEF ranges from 40% to 71% because the EF cutoff has varied between >40% and ≥55%.
- Proposed criteria to define HFpEF include:
- Clinical signs or symptoms of HF
- Evidence of preserved or normal left ventricular ejection fraction (LVEF) and
- Evidence of abnormal LV diastolic dysfunction that can be determined by Doppler echocardiography or cardiac catheterization.
- Prevalent associated conditions include:
- Hypertension (60%–89%)
- Older age, female
- Diabetes mellitus
- Atrial fibrillation (AF)
Table 1. Definitions of HFrEF and HFpEF
|I. Heart failure with reduced ejection fraction (HFrEF)||≤40%||Also referred to as “systolic HF.” Randomized clinical trials have mainly enrolled patients with HFrEF, and it is only in these patients that efficacious therapies have been demonstrated to date.|
|II. Heart failure with preserved ejection fraction (HFpEF)||≥50%||Also referred to as “diastolic HF.” Several different criteria have been used to further define HFpEF. The diagnosis of HFpEF is challenging because it is largely one of excluding other potential noncardiac causes of symptoms suggestive of HF. To date, efficacious therapies have not been identified.|
|IIa. HFpEF, borderline||41%–49%||These patients fall into a borderline or intermediate group. Their characteristics, treatment patterns, and outcomes appear similar to those of patients with HFpEF.|
|IIb. HFpEF, improved||>40%||It has been recognized that a subset of patients with HFpEF previously had HFrEF. These patients with improvement or recovery in EF may be clinically distinct from those with persistently preserved or reduced EF. Further research is needed to better characterize these patients.|
Table 2. Comparison of ACCF/AHA Stages of HF and NYHA Functional Classifications
|ACCF/AHA Stages of HF||NYHA Functional Classification|
- A thorough history and physical examination should be obtained/performed in patients presenting with HF to identify cardiac and noncardiac disorders or behaviors that might cause or accelerate the development or progression of HF. (I-C)
- In patients with idiopathic dilated cardiomyopathy (DCM), a 3-generational family history should be obtained to aid in establishing the diagnosis of familial DCM. (I-C)
- Volume status and vital signs should be assessed at each patient encounter. This includes serial assessment of weight, as well as estimates of jugular venous pressure and the presence of peripheral edema or orthopnea. (I-B)
- Validated multivariable risk scores can be useful to estimate subsequent risk of mortality in ambulatory or hospitalized patients with HF. (IIa-B)
Table 3. History and Physical Examination in HF
|Potential clues suggesting etiology of HF||A careful family history may identify an underlying familial cardiomyopathy in patients with idiopathic DCM. Other etiologies should be considered as well.|
|Duration of illness||A patient with recent-onset systolic HF may recover over time.|
|Severity and triggers of dyspnea and fatigue, presence of chest pain, exercise capacity, physical activity, sexual activity||To determine NYHA class, identify potential symptoms of coronary ischemia.|
|Anorexia and early satiety, weight loss||Gastrointestinal symptoms are common in patients with HF. Cardiac cachexia is associated with adverse prognosis.|
|Weight gain||Rapid weight gain suggests volume overload.|
|Palpitations, (pre)syncope, ICD shocks||Palpitations may be indications of paroxysmal AF or ventricular tachycardia. ICD shocks are associated with adverse prognosis.|
|Symptoms suggesting transient ischemic attack or thromboembolism||Affects consideration of the need for anticoagulation.|
|Development of peripheral edema or ascites||Suggests volume overload.|
|Disordered breathing at night, sleep problems||Treatment for sleep apnea may improve cardiac function and decrease pulmonary hypertension.|
|Recent or frequent prior hospitalizations for HF||Associated with adverse prognosis.|
|History of discontinuation of medications for HF||Determine whether lack of GDMT in patients with HFrEF reflects intolerance, an adverse event, or perceived contraindication to use. Withdrawal of these medications has been associated with adverse prognosis.|
|Medications that may exacerbate HF||Removal of such medications may represent a therapeutic opportunity.|
|Diet||Awareness and restriction of sodium and fluid intake should be assessed.|
|Adherence to medical regimen||Access to medications; family support; access to follow-up; cultural sensitivity.|
|BMI and evidence of weight loss||Obesity may be a contributing cause of HF; cachexia may correspond with poor prognosis.|
|Blood pressure (supine and upright)||Assess for hypertension or hypotension. Width of pulse pressure may reflect adequacy of cardiac output. Response of blood pressure to Valsalva maneuver may reflect LV filling pressures.|
|Pulse||Manual palpation will reveal strength and regularity of pulse rate.|
|Examination for orthostatic changes in blood pressure and heart rate||Consistent with volume depletion or excess vasodilation from medications.|
|Jugular venous pressure at rest and following abdominal compression (http://wn.com/Jugular_Venous_Distension_Example)||Most useful finding on physical examination to identify congestion.|
|Presence of extra heart sounds and murmurs||S3 is associated with adverse prognosis in HFrEF. Murmurs may be suggestive of valvular heart disease.|
|Size and location of point of maximal impulse||Enlarged and displaced point of maximal impulse suggests ventricular enlargement.|
|Presence of RV heave||Suggests significant RV dysfunction and/or pulmonary hypertension.|
|Pulmonary status: respiratory rate, rales, pleural effusion||In advanced chronic HF, rales are often absent despite major pulmonary congestion.|
|Hepatomegaly and/or ascites||Usually markers of volume overload.|
|Peripheral edema||Many patients, particularly those who are young, may not be edematous despite intravascular volume overload. In obese patients and elderly patients, edema may reflect peripheral rather than cardiac causes.|
|Temperature of lower extremities||Cool lower extremities may reflect inadequate cardiac output.|
Table 4. Selected Multivariable Risk Scores to Predict Outcome in HF
All patients with chronic HF
|Seattle Heart Failure Model||http://SeattleHeartFailureModel.org|
|Heart Failure Survival Score||http://handheld.softpedia.com/get/Health/Calculator/HFSS-Calc-37354.shtml|
|CHARM risk score||Pocock SJ, et al. Eur Heart J. 2006;27:65-75.|
|CORONA risk score||Wedel H, et al. Eur J Heart Fail. 2009;11:281-291.|
Specific to chronic HFpEF
|I-PRESERVE score||Komajda M, et al. Circ Heart Fail. 2011;4:27-35.|
Acute Decompensated HF
|ADHERE classification and regression tree (CART) model||Fonarow GC, et al. JAMA. 2005;293:572-580.|
|American Heart Association Get With The Guidelines-HF score||http://www.heart.org/HEARTORG/HealthcareProfessional/GetWithTheGuidelinesHFStroke/GetWithTheGuidelinesHeartFailureHomePage/Get-With-The-Guidelines-Heart-Failure-Home- Page_UCM_306087_SubHomePage.jsp|
|EFFECT risk score||http://www.ccort.ca/Research/CHFRiskModel.aspx|
|ESCAPE risk model and discharge score||O'Connor CM, et al. J Am Coll Cardiol. 2010;55:872-878.|
|OPTIMIZE-HF risk-prediction nomogram||Kociol RD, Horton JR, Fonarow GC, et al. Circ Heart Fail. 2011;4:628-636.|
- Initial laboratory evaluation of patients presenting with HF should include a complete blood cell count, urinalysis, measurement of serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, glucose, and thyroid-stimulating hormone, a fasting lipid profile, and liver function tests. (I-C)
- Serial monitoring, when indicated, should include serum electrolyte levels and renal function. (I-C)
- A 12-lead electrocardiogram (ECG) should be performed initially on all patients presenting with HF. (I-C)
- Screening for hemochromatosis or HIV is reasonable in selected patients who present with HF. (IIa-C)
- Diagnostic tests for rheumatological diseases, amyloidosis, or pheochromocytoma are reasonable in patients presenting with HF in whom there is a clinical suspicion of these diseases. (IIa-C)
Table 5. Biomarkers for Prevention (2017)
For patients at risk of developing HF, natriuretic peptide biomarker–based screening followed by team-based care, including a cardiovascular specialist optimizing GDMT, can be useful to prevent the development of left ventricular dysfunction (systolic or diastolic) or new-onset HF.
Table 6. Biomarkers for Diagnosis (2017)
In patients presenting with dyspnea, measurement of natriuretic peptide biomarkers is useful to support a diagnosis or exclusion of HF.
Table 7. Biomarkers for Prognosis or Added Stratification (2017)
Measurement of BNP or NT-proBNP is useful for establishing prognosis or disease severity in chronic HF.
Measurement of baseline levels of natriuretic peptide biomarkers and/or cardiac troponin on admission to the hospital is useful to establish a prognosis in acutely decompensated HF.
During a HF hospitalization, a predischarge natriuretic peptide level can be useful to establish a postdischarge prognosis.
In patients with chronic HF, measurement of other clinically available tests, such as biomarkers of myocardial injury or fibrosis, may be considered for additive risk stratification.
Table 8. Selected Potential Causes of Elevated Natriuretic Peptide Levels (2017)
Noninvasive Cardiac Imaging (see Table 9)
- Patients with suspected or new-onset HF, or those presenting with acute decompensated HF, should undergo a chest x-ray to assess heart size and pulmonary congestion and to detect alternative cardiac, pulmonary, and other diseases that may cause or contribute to the patient’s symptoms. (I-C)
- A 2-dimensional echocardiogram with Doppler should be performed during initial evaluation of patients presenting with HF to assess ventricular function, size, wall thickness, wall motion, and valve function. (I-C)
- Repeat measurement of EF and measurement of the severity of structural remodeling are useful to provide information in patients with HF who have had a significant change in clinical status; who have experienced or recovered from a clinical event; or who have received treatment, including GDMT, that might have had a significant effect on cardiac function; or who may be candidates for device therapy. (I-C)
- Noninvasive imaging to detect myocardial ischemia and viability is reasonable in patients presenting with de novo HF, who have known CAD and no angina, unless the patient is not eligible for revascularization of any kind. (IIa-C)
- Viability assessment is reasonable in select situations when planning revascularization in HF patients with CAD. (IIa-B)
- Radionuclide ventriculography or magnetic resonance imaging can be useful to assess LVEF and volume when echocardiography is inadequate. (IIa-C)
- Magnetic resonance imaging is reasonable when assessing myocardial infiltrative processes or scar burden. (IIa-B)
- Routine repeat measurement of LV function assessment in the absence of clinical status change or treatment interventions should NOT be performed. (III-B: No Benefit)
Table 9. Recommendations for Noninvasive Imaging
|Patients with suspected, acute, or new-onset HF should undergo a chest x-ray||I||C|
|A 2-dimensional echocardiogram with Doppler should be obtained for initial evaluation of HF||I||C|
|Repeat measurement of EF is useful in patients with HF who have had a significant change in clinical status or received treatment that might affect cardiac function, or for consideration of device therapy||I||C|
|Noninvasive imaging to detect myocardial ischemia and viability is reasonable in HF and CAD||IIa||C|
|Viability assessment is reasonable before revascularization in HF patients with CAD||IIa||B|
|Radionuclide ventriculography or MRI can be useful to assess LVEF and volume||IIa||C|
|MRI is reasonable when assessing myocardial infiltration or scar||IIa||B|
|Routine repeat measurement of LV function assessment should NOT be performed||III: No Benefit||B|
Invasive Evaluation (see Table 10)
- Invasive hemodynamic monitoring with a pulmonary artery catheter should be performed to guide therapy in patients who have respiratory distress or clinical evidence of impaired perfusion in whom the adequacy or excess of intracardiac filling pressures cannot be determined from clinical assessment. (I-C)
- Invasive hemodynamic monitoring can be useful for carefully selected patients with acute HF who have persistent symptoms despite empiric adjustment of standard therapies, and (IIa-C):
- Whose fluid status, perfusion, or systemic or pulmonary vascular resistance is uncertain;
- Whose systolic pressure remains low, or is associated with symptoms, despite initial therapy;
- Whose renal function is worsening with therapy;
- Who require parenteral vasoactive agents; or
- Who may need consideration for mechanical circulatory support (MCS) or transplantation.
- When ischemia may be contributing to HF, coronary arteriography is reasonable for patients eligible for revascularization. (IIa-C)
- Endomyocardial biopsy can be useful in patients presenting with HF when a specific diagnosis is suspected that would influence therapy. (IIa-C)
- Routine use of invasive hemodynamic monitoring is NOT recommended in normotensive patients with acute decompensated HF and congestion with symptomatic response to diuretics and vasodilators. (III-B: No Benefit)
- Endomyocardial biopsy should NOT be performed in the routine evaluation of patients with HF. (III-C: Harm)
Table 10. Recommendations for Invasive Evaluation
|Monitoring with a pulmonary artery catheter should be performed in patients with respiratory distress or impaired systemic perfusion when clinical assessment is inadequate||I||C|
|Invasive hemodynamic monitoring can be useful for carefully selected patients with acute HF with persistent symptoms and/or when hemodynamics are uncertain||IIa||C|
|When ischemia may be contributing to HF, coronary arteriography is reasonable||IIa||C|
|Endomyocardial biopsy can be useful in patients with HF when a specific diagnosis is suspected that would influence therapy||IIa||C|
|Routine use of invasive hemodynamic monitoring is NOT recommended in normotensive patients with acute HF||III: No Benefit||B|
|Endomyocardial biopsy should NOT be performed in the routine evaluation of HF||III: Harm||C|
- Hypertension and lipid disorders should be controlled in accordance with contemporary guidelines to lower the risk of HF. (I-A)
- Other conditions that may lead to or contribute to HF, such as obesity, diabetes mellitus, tobacco use, and known cardiotoxic agents, should be controlled or avoided. (I-C)
Stage B (see Table 11)
- In all patients with a recent or remote history of MI or acute coronary syndrome (ACS) and reduced EF, angiotensin-converting enzyme (ACE) inhibitors should be used to prevent symptomatic HF and reduce mortality. In patients intolerant of ACE inhibitors, angiotensin-receptor blockers (ARBs) are appropriate unless contraindicated. (I-A)
- In all patients with a recent or remote history of MI or ACS and reduced EF, evidence-based beta blockers should be used to reduce mortality. (I-B)
- In all patients with a recent or remote history of MI or ACS, statins should be used to prevent symptomatic HF and cardiovascular events. (I-A)
- In patients with structural cardiac abnormalities, including LV hypertrophy, in the absence of a history of MI or ACS, blood pressure should be controlled in accordance with clinical practice guidelines for hypertension to prevent symptomatic HF. (I-A)
- ACE inhibitors should be used in all patients with a reduced EF to prevent symptomatic HF, even if they do not have a history of MI. (I-A)
- Beta blockers should be used in all patients with a reduced EF to prevent symptomatic HF, even if they do not have a history of MI. (I-C)
- To prevent sudden death, placement of an implantable cardioverter-defibrillator (ICD) is reasonable in patients with asymptomatic ischemic cardiomyopathy who are ≥40 days post-MI, have an LVEF of ≤30%, are on appropriate medical therapy, and have a reasonable expectation of survival with a good functional status for
>1 year. (IIa-B)
- Nondihydropyridine calcium channel blockers with negative inotropic effects may be harmful in asymptomatic patients with low LVEF and no symptoms of HF after MI. (III-C: Harm)