Heart Failure Workup

  • Author: Ioana Dumitru, MD; Chief Editor: Henry H Ooi, MB, MRCPI   more...
 
Updated: May 21, 2012
 

Approach Considerations

Careful evaluation of the patient's history and physical examination (including signs of congestion, such as jugular venous distention [JVD]) can provide important information about the underlying cardiac abnormality in heart failure.[2] However, other studies and/or tests may be necessary to identify structural abnormalities or conditions that can lead to or exacerbate heart failure.[2]

The American College of Cardiology/American Heart Association (ACC/AHA),[2] Heart Failure Society of America (HFSA),[58, 45] and European Society of Cardiology (ESC)[51] recommend the following basic laboratory tests and studies in the initial evaluation of patients with suspected heart failure:

  • Complete blood cell (CBC) count, which may indicate anemia or infection as potential causes of heart failure
  • Urinalysis (UA), which may reveal proteinuria, which is associated with cardiovascular disease
  • Serum electrolyte levels, which may be abnormal owing to causes such as fluid retention or renal dysfunction
  • Blood urea nitrogen (BUN) and creatinine levels, which may indicate decreased renal blood flow
  • Fasting blood glucose levels, because elevated levels indicate a significantly increased risk for heart failure (diabetic and nondiabetic patients)
  • Liver function tests (LFTs), which may show elevated liver enzyme levels and indicate liver dysfunction due to heart failure
  • B-type natriuretic peptide (BNP) and N-terminal pro-B-type (NT-proBNP) natriuretic peptide levels, which are increased in heart failure; these measurements are closely correlated with the NYHA heart failure classification
  • Electrocardiogram (ECG) (12-lead), which may reveal arrhythmias, ischemia/infarction, and coronary artery disease as possible causes of heart failure

The ACC/AHA recommendations also include obtaining a lipid profile and thyroid stimulating hormone (TSH) level.[2] These tests reveal potential cardiovascular or thyroid disease as causes of heart failure. If the clinical presentation also suggests an acute coronary syndrome, the ESC recommends obtaining levels of troponin I or T[51] ; increased troponin levels indicate injury to the myocytes and the severity of heart failure.

The ACC/AHA, HFSA, and ESC also recommend the following imaging studies and procedures[2, 51, 58] :

  • Chest radiography (posterior-anterior, lateral), which may show pulmonary congestion, an enlarged cardiac silhouette, or other potential causes of the patient's symptoms
  • 2-D echocardiographic and Doppler flow ultrasonographic studies, which may reveal ventricular dysfunction and/or valvular abnormalities[59, 60]
  • Coronary arteriography in patients with a history of exertional angina or suspected ischemic LV dysfunction, which may reveal coronary artery disease
  • Maximal exercise testing with/without respiratory gas exchange and/or blood oxygen saturation, which assesses cardiac and pulmonary function with activity, the inability to walk more than short distances, and a decreased peak oxygen consumption reflect more severe disease

Other studies may be indicated in selected patients,[2] such as the following:

  • Screening for hemochromatosis, in which iron overload affects cardiac function
  • Screening for sleep-disturbed breathing, which affects neurohormonal activation
  • Screening for human immunodeficiency virus (HIV), which may result in heart failure from possible direct infectious effects, from disease treatment effects causing CAD, or from other causes
  • Testing for rheumatologic diseases, amyloidosis, or pheochromocytoma, all of which may cause cardiomyopathy
  • Serum and urine electrophoresis for light-chain disease
  • Genetic testing for at-risk patients with a first-degree relative who has been diagnosed with a cardiomyopathy leading to heart failure, which may aid in detecting early disease onset and guide treatment[23, 45]
  • Holter monitoring, which may reveal arrhythmias or abnormal electrical activity (eg, in patients with heart failure and a history of MI who are being considered for electrophysiologic study to document ventricular tachycardia [VT] inducibility)[51, 58]

The ESC indicates that pulmonary function testing is generally not helpful in the diagnosis of heart failure. However, it may demonstrate or exclude respiratory causes of dyspnea and help assess any pulmonary causes of dyspnea.[51]

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Routine Laboratory Tests

Laboratory studies should include a complete blood count (CBC), serum electrolytes (including calcium and magnesium), and renal and liver function studies. Other tests may be indicated in specific patients. The CBC aids in the assessment of severe anemia, which may cause or aggravate heart failure. Leukocytosis may signal underlying infection. Otherwise, CBCs are usually of little diagnostic help.

Serum electrolyte values are generally within reference ranges in patients with mild to moderate heart failure before treatment. In cases of severe heart failure, however, prolonged, rigid sodium restriction, coupled with intensive diuretic therapy and the inability to excrete water, may lead to dilutional hyponatremia, which occurs because of a substantial expansion of extracellular and intravascular fluid volume and a normal or increased level of total body sodium.

Potassium levels are usually within reference ranges, although the prolonged administration of diuretics may result in hypokalemia. Hyperkalemia may occur in patients with severe heart failure who show marked reductions in glomerular filtration rate (GFR) and inadequate delivery of sodium to the distal tubular sodium-potassium exchange sites of the kidney, particularly if they are receiving potassium-sparing diuretics and/or angiotensin-converting enzyme inhibitors (ACEIs).

Renal function tests

Blood urea nitrogen (BUN) and creatinine levels can be within reference ranges in patients with mild to moderate heart failure and normal renal function, although BUN levels and BUN/creatinine ratios may be elevated.

Patients with severe heart failure, particularly those on large doses of diuretics for long periods, may have elevated BUN and creatinine levels indicative of renal insufficiency because of chronic reductions of renal blood flow from reduced cardiac output. Diuresing this group of patients is complex. In some individuals, diuretics will improve renal congestion and renal function, whereas in others, overaggressive diuresis may aggravate renal insufficiency due to volume depletion.

Liver function tests

Congestive hepatomegaly and cardiac cirrhosis are often associated with impaired hepatic function, which is characterized by abnormal values of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactic dehydrogenase (LDH), and other liver enzymes. Hyperbilirubinemia secondary to an increase in the directly and indirectly reacting bilirubin is common. In severe cases of acute RV or LV failure, frank jaundice may occur.

Acute hepatic venous congestion can result in severe jaundice, with a bilirubin level as high as 15-20 mg/dL, elevation of AST to more than 10 times the upper reference range limit, elevation of the serum alkaline phosphatase level, and prolongation of the prothrombin time. The clinical and laboratory pictures may resemble viral hepatitis, but the impairment of hepatic function is rapidly resolved by successful treatment of heart failure. In patients with long-standing heart failure, albumin synthesis may be impaired, leading to hypoalbuminemia and intensifying the accumulation of fluid. Fulminant hepatic failure is an uncommon, late, and sometimes terminal complication of cardiac cirrhosis.

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Natriuretic Peptides

Clinical findings and routine diagnostic tests are not always sufficient to diagnose heart failure. In such ambiguous cases, rapid measurement of B-type natriuretic peptide (BNP) or N-terminal proBNP (NT-proBNP) levels can aid clinicians in differentiating between cardiac and noncardiac causes of dyspnea.[2, 51, 54, 55, 58, 61, 62] That is, BNP is mostly limited to the differentiation of heart failure versus other causes of dyspnea in patients with an atypical presentation.

BNP is a 32-amino-acid polypeptide containing a 17-amino-acid ring structure common to all natriuretic peptides. The major source of plasma BNP is the cardiac ventricles, and the release of BNP appears to be in direct proportion to ventricular volume and pressure overload. BNP is an independent predictor of high LV end-diastolic pressure and is more useful than atrial natriuretic peptide (ANP) or norepinephrine levels for assessing mortality risk in patients with heart failure.[63, 64, 65, 66]

Although BNP has been determined to be the strongest predictor of systolic versus nonsystolic heart failure (followed by oxygen saturation, history of myocardial infarction, and heart rate), BNP does not reliably differentiate between heart failure with preserved ejection fraction and heart failure with reduced ejection fraction.[61] Increased NT-proBNP was found to be the strongest independent predictor of a final diagnosis of acute heart failure.[67, 68, 69]

Measurement of B-type natriuretic peptide (BNP) and its precursor, N-terminal proBNP (NT-proBNP), in the urgent care setting can be used to establish the diagnosis of heart failure when the clinical presentation is ambiguous or when confounding comorbidities are present.[2, 51, 58] BNP and NT-proBNP assays have different cutoff values for ruling in and ruling out heart failure.[70, 71, 72]

The American College of Cardiology/American Heart Association (ACC/AHA),[2] the Heart Failure Society of America (HFSA),[58] and the European Society of Cardiology (ESC)[51] recommend measuring BNP or NT-proBNP in the workup of heart failure when the diagnosis is unclear. The HFSA recommends this test in all cases of suspected heart failure, particularly in ambiguous cases.[58]

BNP levels correlate closely with the NYHA classification of heart failure.[73, 74] BNP levels greater than 100 pg/mL have a specificity greater than 95% and a sensitivity greater than 98% when comparing patients without heart failure to all patients with heart failure.[75] Even BNP levels greater than 80 pg/mL have a specificity greater than 95% and a sensitivity greater than 98% in the diagnosis of heart failure.[70]

Table of cutoff values

Table 4, below, summarizes the evidence-based cutoff values of BNP and NT-proBNP for ruling in and ruling out the diagnosis of heart failure in the dyspneic patient presenting to the emergency department.

Table 4. Evidence-Based BNP and NT-proBNP Cutoff Values for Diagnosing HF (Open Table in a new window)

CriterionBNP, pg/mLNT-proBNP, pg/mL
HF Unlikely (LR-Negative)HF Likely (LR-Positive)HF Unlikely (LR-Negative)HF Likely (LR-Positive)
Age, y>17< 100 (0.13)*>500 (8.1)*--
>21--< 300 (0.02)†-
21-50--->450 (14)†
50-75--->900 (5.0)†
>75--->1800 (3.1)†
Estimated GFR, < 60 mL/min< 200 (0.13)‡>500 (9.3)‡--
BNP = B-type natriuretic peptide; GRF = glomerular filtration rate; HF = heart failure; LR = likelihood ratio; NPV = negative predictive value; NT-pro-BNP = N-terminal proBNP; PPV = positive predictive value; – = not specifically defined.



* Derived from Breathing Not Properly data (1586 emergency department [ED] patients, prevalence of HF = 47%).[54]



† Derived from PRIDE data (1256 ED patients, prevalence of HF = 57%).[55, 62]



‡ Derived from subset of Breathing Not Properly data (452 ED patients, prevalence of HF = 49%).[61]



BNP and NT-proBNP levels are higher in older patients,[76] women,[76] and patients with renal dysfunction[77] or sepsis. Atrial fibrillation has also been associated with increased BNP levels in the absence of acute heart failure. However, BNP levels may be disproportionately lower in patients who are obese due to fat metabolism or who have hypothyroidism or advanced end-stage heart failure (the latter due to increased fibrosis). NT-proBNP plasma levels are also lower in obese heart failure patients relative to nonobese patients with heart failure, regardless of whether the etiology is ischemic or nonischaemic.[78]

However, NT-proBNP may be elevated in severely obese patients (BMI >40 kg/m2) due to an increased cardiac burden in these individuals.[79] . NT-pro-BNP may be a better marker for detecting cardiac dysfunction than BNP, because its chemical stability is better in circulating blood than that of BNP, and it is a sensitive marker of cardiac function even in early cardiac decompensation.[80]

BNP measurement not indicated with nesiritide therapy

Nesiritide is a synthetic BNP analogue; therefore, the measurement of BNP is not indicated in patients who are receiving nesiritide. If BNP is used as a diagnostic marker to rule in heart failure, the level must be determined before nesiritide therapy is started.[81, 82, 83, 84]

In a study by Miller et al, levels of NT-proBNP and BNP decreased in patients with advanced heart failure after therapy with nesiritide, but the majority of the patients did not have biochemically significant decreases in these markers even with a clinical response.[85] The investigators were unable to give a definitive reason for their results, and they indicated that nesiritide therapy should not be guided by the use of levels of both markers.[85] Fitzgerald et al also found decreased levels of both natriuretic peptides following nesiritide therapy in patients with decompensated heart failure.[86]

For more information, see the Medscape Reference article Natriuretic Peptides in Congestive Heart Failure.

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Genetic Testing

Cardiomyopathy phenotypes that have known genetic cause(s) include hypertrophic (HCM), dilated (DCM), restrictive (RCM), arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C), and left ventricular noncompaction (LVNC). Because most cases of cardiomyopathy are treatable—which is not the case in many genetic diseases—and screening for genetic risk of cardiomyopathy before the onset of disease can guide the recommendations for early detection of disease and therapy (see Clinical, History),[23, 45] it is recommended that consideration be given for patients with cardiomyopathy to be referred to centers with expertise in these matters and in family-based management.[45] These specialized centers will have a better understanding of the complexities involved in genetic evaluation, testing, and counseling of patients with cardiomyopathy.

To establish specific gene testing and laboratories offering tests, please see www.genetests.org for further information and larger eviews.

Genetic testing has the highest yield in 3 types of cardiomyopathy: DCM, HCM, and autosomal dominant ARVD/C. The diagnosis must be established using the specific criteria for each type of cardiomyopathy, as the genetic testing is different for each type.

Dilated cardiomyopathy

It is thought that approximately 20-50% of idiopathic dilated cardiomyopathy (IDC) may have a genetic basis. Screening first-degree relatives of a proband with IDC by echocardiography and electrocardiography (ECG) reveals that 20-48% of probands have affected relatives, consistent with a diagnosis of familial dilated cardiomyopathy (FDC).[87, 88, 89]

Molecular genetic testing of the proband for an LMNA mutation is probably indicated, particularly if significant conduction system disease is present in the family. It should be noted that although the analytical sensitivity for detecting LMNA gene mutations is quite high, the clinical sensitivity (likelihood of identifying a mutation in a person with the disorder) is approximately 8% for FDC. Because molecular genetic testing for MYH7 has comparable clinical sensitivity, testing for mutations in MHY7 may also be considered.

Hypertrophic cardiomyopathy

HCM, caused by mutation in one of the genes currently known to encode different components of the sarcomere, is characterized by left ventricular hypertrophy (LVH) in the absence of predisposing cardiac conditions (eg, aortic stenosis) or cardiovascular conditions (eg, long-standing hypertension). Most often, the LVH of HCM becomes apparent during adolescence or young adulthood, although it may also develop late in life, in infancy, or in childhood.

Molecular genetic testing of any of the 14 genes currently known to encode different components of the sarcomere is clinically available. A detailed 3- to 4-generation family history should be obtained from relatives to assess the possibility of familial HCM. Attention should be directed to a history of any of the following in relatives: heart failure, HCM, cardiac transplantation, unexplained sudden death, unexplained cardiac conduction system disease and/or arrhythmia, or unexplained stroke or other thromboembolic disease.

Autosomal dominant arrhythmogenic right ventricular dysplasia/cardiomyopathy

ARVD/C is characterized by progressive fibrofatty replacement of the myocardium that predisposes to ventricular tachycardia and sudden death in young individuals and athletes. It primarily affects the right ventricle; with time, it may also involve the left ventricle. The presentation of disease is highly variable even within families, and affected individuals may not meet established clinical criteria. The mean age at diagnosis is 31 years (±13 y; range, 4-64 y).

Genetic testing should be considered in individuals who have a clinical diagnosis of ARVD based on the diagnostic criteria. A case can be made to offer genetic testing to all with a clinical diagnosis of ARVD with a negative family history based on the high rate of reduced penetrance thus far identified with the ARVD genes. Molecular genetic testing is available on a clinical basis for TGFB3, RYR2, TMEM43, DSP, PKP2, DSG2, DSC2, and JUP.[90]

For more information regarding genetic testing and cardiomyopathy, please see HFSA Guideline Approach to Medical Evidence for Genetic Evaluation of Cardiomyopathy), as well as Murphy RT, Starling RC. Genetics and cardiomyopathy: where are we now?. Cleve Clin J Med. Jun 2005;72(6):465-6, 469-70, 472-3 passim.[23]

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Assessment of Hypoxemia

Arterial and venous blood gases

Although arterial blood gas (ABG) measurement is more accurate than pulse oximetry for measuring oxygen saturation, it is unclear if ABG results add any clinical utility to pulse oximetry. In the setting of acute heart failure, ABG measurement is rarely performed. Indications include severe respiratory distress, documented hypoxemia by pulse oximetry not responsive to supplemental oxygen, and evidence of acidosis by serum chemistry or elevated lactate level.

In general, heart failure patients who do not have comorbid lung disease do not manifest hypoxemia except in severe acute decompensation. Patients with severe heart failure may have signs and symptoms ranging from severe hypoxemia, or even hypoxia, along with hypercapnia, to decreased vital capacity and poor ventilation.

ABG measurement helps assess the presence of hypercapnia, a potential early marker for impending respiratory failure. Hypoxemia and hypocapnia occur in stages 1 and 2 of pulmonary edema because of V/Q mismatch. In stage 3 of pulmonary edema, right-to-left intrapulmonary shunt develops secondary to alveolar flooding and further contributes to hypoxemia. In more severe cases, hypercapnia and respiratory acidosis are usually observed. The decision regarding intubation and the use of mechanical ventilation is frequently based on many clinical parameters, including oxygenation, ventilation, and mental status. ABG values in isolation are rarely useful, but they may add to the entire clinical picture.

Mixed venous oxygen saturation (obtained from the main pulmonary artery in the absence of an intracardiac shunt) is a good marker of the blood circulation time and therefore of cardiac output and cardiac performance. Patients who have advanced heart failure have low cardiac output and slower circulation time, which translate into an increased oxygen extraction by the tissue and therefore lower saturation of oxygen (< 60% saturation).

Pulse oximetry

Pulse oximetry is highly accurate at assessing the presence of hypoxemia and, therefore, the severity of acute heart failure presentations. Patients with mild to moderate acute heart failure may show modest reductions in oxygen saturation, whereas patients with severe heart failure may have severe oxygen desaturation, even at rest. Pulse oximetry is also useful for monitoring the patient's response to supplemental oxygen and other therapies.

Patients with mild to moderate heart failure may have normal oxygen saturations at rest, but they may exhibit marked reductions in oxygen saturations during physical exertion or recumbency. In general, arterial desaturation during exercise is not expected in heart failure and suggests the presence of comorbid lung disease. The use of continuous oxygen may be needed until compensation returns oxygen saturation to normal during exertion and recumbency or on a permanent basis if oxygen desaturation during exertion and/or recumbency exists during compensated severe chronic heart failure.

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Electrocardiography

A screening electrocardiogram (ECG) is reasonable in patients with symptoms suggestive of heart failure. The presence of left atrial enlargement and LVH is sensitive (although nonspecific) for chronic LV dysfunction. It is unlikely that an ECG would be completely normal in the presence of heart failure; therefore, an alternative diagnosis should be sought in such cases.[58, 51]

Electrocardiography may suggest an acute tachyarrhythmia or bradyarrhythmia as the cause of heart failure. It may also aid in the diagnosis of acute myocardial ischemia or infarction as the cause of heart failure or may suggest the likelihood of prior MI or the presence of coronary artery disease as the cause of heart failure.[2, 58]

Heart failure can have multiple and diverse presentations on ECGs (see the images below).

This electrocardiogram (ECG) is from a 32-year-oldThis electrocardiogram (ECG) is from a 32-year-old female with recent-onset congestive heart failure and syncope. The ECG demonstrates a tachycardia with a 1:1 atrial:ventricular relationship. It is not clear from this tracing whether the atria are driving the ventricles (sinus tachycardia) or the ventricles are driving the atria (ventricular tachycardia).At first glance, sinus tachycardia in this ECG might be considered with severe conduction disease manifesting as marked first-degree atrioventricular block with left bundle branch block. Looking more closely, electrocardiographic morphology gives clues to the actual diagnosis of VT. These clues include the absence of RS complexes in the precordial leads, a QS pattern in V6, and an R wave in aVR. The patient proved to have an incessant VT associated with dilated cardiomyopathy. Electrocardiogram depicting ventricular fibrillatiElectrocardiogram depicting ventricular fibrillation in a patient with a left ventricular assist device (LVAD). Ventricular fibrillation is often due to ischemic heart disease and can lead to myocardial infarction and/or sudden death. This electrocardiogram (ECG) shows evidence of sevThis electrocardiogram (ECG) shows evidence of severe left ventricular hypertrophy (LVH) with prominent precordial voltage, left atrial abnormality, lateral ST-T abnormalities, and a somewhat leftward QRS axis (–15º). The patient had malignant hypertension with acute heart failure, accounting also for the sinus tachycardia (blood pressure initially 280/180 mmHg). The ST-T changes seen here are nonspecific and could be due to, for example, LVH alone or coronary artery disease. However, the ECG is not consistent with extensive inferolateral myocardial infarction. Image courtesy of http://ecg.bidmc.harvard.edu . This electrocardiogram shows an extensive acute/evThis electrocardiogram shows an extensive acute/evolving anterolateral myocardial infarction pattern, with ST-T changes most apparent in leads V2-V6, I, and aVL. Slow R wave progression is also present in leads V1-V3. The rhythm is borderline sinus tachycardia with a single premature atrial complex (PAC) (4th beat). Note also the low limb lead voltage and probable left atrial abnormality. Left ventriculography showed diffuse hypokinesis as well as akinesis of the anterolateral and apical walls, with an ejection fraction estimated at 33%. Image courtesy of http://ecg.bidmc.harvard.edu. This electrocardiogram shows a patient is having aThis electrocardiogram shows a patient is having an evolving anteroseptal myocardial infarction secondary to cocaine. There are Q waves in leads V2-V3 with ST segment elevation in leads V2-V5 associated with T-wave inversion. Also noted are biphasic T-waves in the inferior leads. These multiple abnormalities suggest occlusion of a large left anterior descending artery that wraps around the apex of the heart (or multivessel coronary artery disease). Image courtesy of http://ecg.bidmc.harvard.edu .

Electrocardiography is of limited help when an acute valvular abnormality or LV systolic dysfunction is considered to be the cause of heart failure; however, the presence of left bundle branch block (LBBB) on an ECG is a strong marker for diminished LV systolic function.

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Chest Radiography

Chest radiographs (see the images below) are used in cases of heart failure to assess heart size, pulmonary congestion, pulmonary or thoracic causes of dyspnea, and the proper positioning of any implanted cardiac devices. Posterior-anterior and lateral views are recommended.[2, 51, 58]

This chest radiograph shows an enlarged cardiac siThis chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases, signs of acute heart failure. A 28-year-old woman presented with acute heart faiA 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).

Although up to 50% of patients with heart failure and documented elevation of PCWP do not manifest typical radiographic findings of pulmonary congestion, the following 2 principal features of chest radiographs are useful in the evaluation of patients with heart failure: (1) the size and shape of the cardiac silhouette and (2) edema at the lung bases.

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Echocardiography

Two-dimensional (2-D) echocardiography is recommended in the initial evaluation of patients with known or suspected heart failure.[2, 51, 58] Ventricular function may be evaluated, and primary and secondary valvular abnormalities may be accurately assessed.[91, 92, 93, 94, 95]

Doppler echocardiography, along with 2-D echocardiography, may play a valuable role in determining diastolic function and in establishing the diagnosis of diastolic heart failure. Approximately 30-40% of patients presenting with heart failure have normal systolic function but abnormal diastolic relaxation. The primary finding to differentiate diastolic heart failure is the presence of a normal ejection fraction; however, note that findings of diastolic dysfunction are common in the elderly and may not be associated with clinical heart failure. Because the therapy for this condition is distinctly different from that for systolic dysfunction, establishing the appropriate etiology and diagnosis is essential.

Doppler and 2-D echocardiography may also be used to determine both systolic and diastolic LV performance, cardiac output (ejection fraction), and pulmonary artery and ventricular filling pressures. In addition, echocardiography may be used to identify clinically important valvular disease.

(See the images below.)

Hypokinesis of the anteroseptal wall observed duriHypokinesis of the anteroseptal wall observed during echocardiography in a patient presenting with an acute anteroseptal myocardial infarction, which can precipitate heart failure. Cervicocephalic fibromuscular dysplasia (FMD) can Cervicocephalic fibromuscular dysplasia (FMD) can lead to complications such as hypertension and chronic kidney failure, which can lead to heart failure. In this color Doppler and spectral Doppler ultrasonographic examination of the left internal carotid artery (ICA) in a patient with cervicocephalic FMD, stenoses of about 70% is seen in the ICA. Cervicocephalic fibromuscular dysplasia (FMD) can Cervicocephalic fibromuscular dysplasia (FMD) can lead to complications such as hypertension and chronic kidney failure, which, in turn, can lead to heart failure. Nodularity in an artery is known as the string-of-beads sign, and it can be seen this color Doppler ultrasonographic image from a 51-year-old patient with low-grade stenosing FMD of the internal carotid artery (ICA). Echocardiogram of a patient with severe pulmonic sEchocardiogram of a patient with severe pulmonic stenosis. This image shows a parasternal short axis view of the thickened pulmonary valve. Pulmonic stenosis can lead to pulmonary hypertension, which can result in hepatic congestion and in right-sided heart failure.
This video is an echocardiogram of a patient with severe pulmonic stenosis. The first segment shows the parasternal short axis view of the thickened pulmonary valve. The second segment shows the presence of moderate pulmonary insufficiency (orange color flow). AV = aortic valve, PV = pulmonary valve, PA = pulmonary artery, PI = pulmonary insufficiency.

The following video and images are from patients with arrhythmogenic right ventricular dysplasia (ARVD), a congenital cardiomyopathy that can lead to heart failure.

Apical 4-chamber echocardiogram in a 37-year-old man with arrhythmogenic right ventricular dysplasia (ARVD), a congenital cardiomyopathy. Note the prominent trabeculae and abnormal wall motion of the dilated right ventricle.ARVD can result in ventricular and supraventricular arrhythmias. The most significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias. Apical long-axis echocardiogram in a young female Apical long-axis echocardiogram in a young female patient with arrhythmogenic right ventricular dysplasia (ARVD) illustrates end-diastolic measurement of a dilated right ventricular outflow tract (RVOT). Ao = aorta, LA = left atrium, LV = left ventricle, RV = right ventricle. Apical 4-chamber end-diastolic echocardiogram in aApical 4-chamber end-diastolic echocardiogram in a patient with arrhythmogenic right ventricular dysplasia (ARVD) shows dilatation of the right ventricle (RV) (arrow) and prominent trabeculae. Ao = aorta, LA = left atrium, LV = left ventricle.

Transesophageal echocardiography

Transesophageal echocardiography is particularly useful in patients who are on mechanical ventilation or are morbidly obese and in patients whose transthoracic echocardiogram is suboptimal in its imaging.[51] It is an easy and safe alternative to conventional transthoracic echocardiography and provides better imaging quality. (See the following videos and image.)

Transesophageal echocardiogram in an apical 3-chamber view with color Doppler interrogation of the mitral valve revealing aliasing, which is consistent with increased gradient across the mitral valve secondary to stenosis. Also shown in this image, a posteriorly directed jet of severe mitral regurgitation. Valvular heart disease, such as mitral stenosis and mitral regurgitation, can precipitate heart failure.
Transthoracic echocardiogram demonstrating severe mitral regurgitation with heavily calcified mitral valve and prolapse of the posterior leaflet into the left atrium.
Transesophageal echocardiogram demonstrating prolapse of both mitral valve leaflets during systole in a patient with mitral regurgitation. Transesophageal echocardiogram with continuous wavTransesophageal echocardiogram with continuous wave Doppler interrogation across the mitral valve demonstrating an increased mean gradient of 16 mm Hg consistent with severe mitral stenosis.

Stress echocardiography

Stress echocardiography, also known as dobutamine or exercise echocardiography, has several uses; however, in heart failure, this technique is used mainly to assess coronary artery disease (CAD). This imaging modality may be used to detect ventricular dysfunction caused by ischemia, evaluate myocardial viability in the presence of marked hypokinesis or akinesis, identify myocardial stunning and hibernation, and relate heart failure symptoms to valvular abnormalities.[51] However, stress echocardiography may have a lower sensitivity and specificity in heart failure patients because of LV dilatation or because of the presence of bundle branch block.[51]

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CT Scanning and MRI

Computed tomography (CT) scanning or magnetic resonance imaging (MRI) may be useful in evaluating chamber size and ventricular mass, cardiac function, and wall motion; delineating congenital and valvular abnormalities; and demonstrating the presence of pericardial disease.[2] However, cardiac CT scanning is usually not required in the routine diagnosis and management of heart failure, and echocardiography and MRI may provide similar information without exposing the patient to ionizing radiation.

The benefits of cardiac MRI (cMRI) include the ability to obtain a great deal of information with a noninvasive test. This modality provides detailed functional and morphologic information; can be used to assess ischemic versus nonischemic disease, infiltrative disease, and hypertrophic disease; and can be employed to determine viability. It is used principally for the delineation of congenital cardiac abnormalities and for the assessment of valvular heart disease, and it is the gold standard for evaluating RV function (see the image below).

This magnetic resonance image shows a scar in the This magnetic resonance image shows a scar in the anterior cardiac wall, which may be indicative of a previous myocardial infarction (MI). MIs can precipitate heart failure.
Cardiac magnetic resonance image (CMRI), short axis view. This image shows right ventricular dilatation, trabucular derangement, aneurysm formation and dyskinetic free wall in a patient with arrhythmogenic right ventricular dysplasia.

MRI has become particularly useful for evaluating abnormalities in wall motion and viable myocardium, and MRI results can help predict the success of revascularization in patients with low ejection fractions.[96] However, the detailed information obtained by MRI must be balanced by its high costs and the fact that this imaging modality cannot be performed in patients with implantable defibrillators.

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Nuclear Imaging

Radionuclide multiple-gated acquisition scanning

Radionuclide multiple-gated acquisition (MUGA) scan is a reliable imaging technique for evaluation of LV and RV function and wall motion abnormalities. Because of its reliability, LV ejection fraction (LVEF), as determined by MUGA scanning, is often used for serial assessment of postchemotherapy LV function.[97]

Electrocardiogram-gated myocardial perfusion imaging

The high photon flux of compounds labeled with technetium-99m (99m TC) makes it feasible to acquire myocardial perfusion images in an ECG-gated mode. ECG-gated single-photon emission CT (SPECT) images allow for assessment of global LVEF, regional wall motion, and regional wall thickening at rest in patients with documented stress-induced wall motion and perfusion abnormalities.

In general, LVEF from gated SPECT agrees well with resting LVEF determined by other modalities. Quality assurance is important, however, because determinations of LVEF with gated SPECT may be less accurate, even invalidated, in the presence of an irregular heart rate, low count density, intense extracardiac radiotracer uptake adjacent to the LV, or a small LV.

Combined interpretation of perfusion and function on ECG-gated images substantially increases the confidence of interpretation. Taillefer and associates reported that the interpretation of stress and rest end-diastolic section, rather than summed ungated sections, may enhance the overall sensitivity for the detection of mild coronary artery disease.[98]

ECG-gated images are useful for recognizing artifactual defects caused by attenuation (breast and diaphragm) and thus are useful in the quality control of SPECT imaging. ECG-gated SPECT imaging is currently considered the state of the art of radionuclide myocardial perfusion imaging.

There are 3 important practical issues that need to be addressed in the evaluation of patients with presumed ischemic dysfunction, as follows:

  • Assessment of the relative regional myocardial uptake of thallium-201 (201 Tl; often after rest reinjection),99m Tc-sestamibi, or99m Tc-tetrofosmin (often after rest administration of nitroglycerin); when the resting uptake of radiotracer is greater than 50% of normal, expect recovery of function after revascularization
  • Assessment of the presence of demonstrable ischemia (eg, partially reversible defect) in a myocardial segment with decreased uptake, even if the resting uptake is less than 50%
  • Data reported in 2011 from a STICH viability substudy failed to demonstrate a significant impact on survival based on the extent of viable myocardium in patients with CAD and LV dysfunction treated surgically or medically[99]

Equilibrium radionuclide angiocardiography

Equilibrium radionuclide angiocardiography (ERNA) uses ECG events to define the temporal relationship between the acquisition of nuclear data and the volumetric components of the cardiac cycle. Sampling is performed repetitively over several hundred heartbeats, with physiologic segregation of nuclear data in accordance with their occurrence within the cardiac cycle.

Data are quantified and displayed in an endless-loop, cinegraphic format for additional qualitative visual interpretation and analysis. Equilibrium blood-pool labeling is achieved by use of99m Tc. Data are analyzed by use of a computer, generally with some operator interaction.

Analysis may be obtained in either the frame or list mode. Radionuclide data are collected and segregated temporally. The process generally requires 3-10 minutes for completion of each view. Following data acquisition, data from the several hundred individual beats are summed, processed, and displayed as a single representative cardiac cycle.

Data from the left anterior oblique (LAO) view are also used for qualitative analysis of global LV function. On this view, overlap of the 2 ventricles is minimal. In a count-based approach, LVEF and other indices of filling and ejection are calculated from the LV radioactivity preset at various points throughout the cardiac cycle.

RV function is best evaluated by first-pass techniques. The LAO view provides qualitative information concerning contraction of the septal, inferoapical, and lateral walls. The anterior view provides data concerning regional motion of the anterior and apical segments. The left lateral or left posterior oblique view provides optimal qualitative information concerning contraction of the inferior wall and posterobasal segment.

ERNA may easily be combined with additional physiologic stress testing or provocation, which may be in the form of either physiologic stress, such as exercise; pharmacologic stress, with the use of positive inotropic agents, such as dobutamine or isoproterenol; or psychological stress. The degree of confidence with ERNA is moderately high. False-positive and false-negative findings are infrequent.

Radionuclide ventriculography

Radionuclide ventriculography is most often performed as part of a myocardial perfusion scan to obtain accurate measurements of LV function and right ventricular EF, but it is unable to directly assess valvular abnormalities or cardiac hypertrophy and has limited value for assessing volumes or more subtle indices of systolic or diastolic function.[2, 51]

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Catheterization and Angiography

In patients with a nonischemic cardiomyopathy, perfusion deficits and segmental wall-motion abnormalities suggestive of coronary artery disease are commonly present on noninvasive imaging.[2] Only coronary angiography, however, can reliably demonstrate or exclude the presence of obstructed coronary vessels (see the following image).[2]

A color-enhanced angiogram of the heart left showsA color-enhanced angiogram of the heart left shows a plaque-induced obstruction (top center) in a major artery, which can lead to myocardial infarction (MI). MIs can precipitate heart failure.

According to the American College of Cardiology/American Heart Association (ACC/AHA),[2] Heart Failure Society of America (HFSA),[58] and European Society of Cardiology (ESC),[51] cardiac catheterization and coronary angiography should be considered for patients with heart failure in the following situations:

  • When symptoms worsen without a clear cause in patients with heart failure, no angina, and known coronary artery disease
  • In heart failure caused by systolic dysfunction in association with angina or regional wall-motion abnormalities and/or scintigraphic evidence of reversible myocardial ischemia when revascularization is being considered
  • When pretest probability of underlying ischemic cardiomyopathy is high and surgical coronary procedures are being considered
  • Before cardiac transplantation or left ventricular assist device placement
  • In cases of heart failure secondary to postinfarction ventricular aneurysm or other mechanical complications of myocardial infarction

For these patients, the procedures are frequently indicated when systolic dysfunction of unexplained cause is present on noninvasive testing or when normal systolic function with episodic heart failure suggests ischemically mediated LV dysfunction. However, although coronary angiography may be indicated in young patients to exclude the presence of congenital coronary anomalies, this procedure may not be as useful in older patients, because revascularization has not been shown to improve clinical outcomes in patients without angina.[2] Despite this, because revascularization may improve LV function, some experts suggest that coronary artery disease should be excluded whenever possible, especially in patients with diabetes mellitus or other states associated with silent myocardial ischemia.[2] The degree of confidence is moderately high.

Right-sided heart catheterization

Right heart catheterization is useful in providing important hemodynamic information about filling pressures, vascular resistance, and cardiac output when there is doubt about the patient's fluid status; in heart failure refractory to initial therapy; in the presence of significant hypotension (systolic blood pressure typically < 90 mm Hg or symptomatic low systolic blood pressure) and/or worsening renal function during initial treatment; and when heart transplantation or placement of a mechanical circulatory support device is being considered.[2] However, it plays a limited role in the diagnosis of heart failure, as studies evaluating right heart catheterization and overall improved outcomes have been essentially neutral.[100]

Normal right-sided hemodynamics include right atrial pressure less than 7 mm Hg, RV pressure less than 30/7 mm Hg, pulmonary pressure less than 30/18, pulmonary capillary wedge pressure (PCWP) less than 18 mm Hg, and cardiac index (CI) greater than 2.2 L/min/m2.

PCWP can be measured by using a pulmonary arterial catheter (Swan-Ganz catheter). This helps differentiate cardiogenic causes of decompensated heart failure from noncardiogenic causes, such as acute respiratory distress syndrome (ARDS), which occurs secondary to injury to the alveolar-capillary membrane rather than to alteration in Starling forces. A PCWP exceeding 18 mm Hg in a patient not known to have chronically elevated left atrial pressure is indicative of cardiogenic decompensated heart failure. In patients with chronic pulmonary capillary hypertension, capillary wedge pressures exceeding 25 mm Hg are generally required to overcome the pumping capacity of the lymphatics and produce pulmonary edema.

Large V waves may be observed in the PCWP tracing in patients with significant mitral regurgitation because large volumes of blood regurgitate into a poorly compliant left atrium. This raises pulmonary venous pressure and may cause pulmonary edema.

Left-sided heart catheterization

Left-sided heart catheterization and coronary angiography should be undertaken when the etiology of heart failure cannot be determined by clinical or noninvasive imaging methods or when the etiology is likely to be due to acute myocardial ischemia or infarction. Coronary angiography is particularly helpful in patients with LV systolic dysfunction and known or suspected coronary artery disease in whom myocardial ischemia is thought to play a dominant role in the reduction of LV systolic function and the worsening of heart failure.

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Endomyocardial Biopsy

Endomyocardial biopsy is indicated only when a specific diagnosis is suspected that would influence therapy in patients presenting with heart failure (see the image below). The Heart Failure Society of America (HFSA) suggests that endomyocardial biopsy be considered in patients with rapidly progressive clinical heart failure or ventricular dysfunction, despite appropriate medical therapy, as well as in patients suspected of having myocardial infiltrative processes (eg, sarcoidosis, amyloidosis) or in patients with malignant arrhythmias out of proportion to their LV dysfunction (eg, sarcoidosis, giant cell myocarditis).[58]

Histologic section of an autopsy myocardial specimHistologic section of an autopsy myocardial specimen from a patient with long-standing hypertension and associated coronary artery disease. The slide shows myocardial hypertrophy, contraction bands (typical of left ventricular hypertrophy), and "car box" nuclei.
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Assessment of Functional Capacity

The European Society of Cardiology (ESC) indicates the 6-minute walk test is a good indicator of functional status and prognosis in patients with heart failure.[51] It evaluates distance walked, dyspnea index on a Borg scale from 0 to 10, oxygen saturation, and heart rate response to exercise. A normal value is walking more than 1500 feet. Patients who walk less than 600 feet have severe cardiac dysfunction and a worse short- and long-term prognosis.

Cardiopulmonary stress testing (maximal exercise stress testing with measurement of respiratory gas exchange) can help assess a patient’s chance of survival within the next year, as well as determine the need for referral for either cardiac transplantation or implantation of mechanical circulatory support. The ACC/AHA[2] and HFSA[58] do not recommend routine maximal exercise stress testing but indicate it may be useful in situations such as the following with measurement of gas exchange:

  • To assess the disparity between symptomatic limitation and objective indicators of disease severity
  • To distinguish non HF-related causes of functional limitation, specifically cardiac versus pulmonary
  • To consider whether patients are candidates for cardiac transplantation or mechanical circulatory support
  • To determine the prescription for cardiac rehabilitation

Values of peak oxygen consumption of less than 50% of predicted or less than 14 cc/kg/min reflect poor cardiac performance and a likelihood of 1-year survival less than 50%, facilitating referral for cardiac transplantation or mechanical circulatory device placement.[2, 3]

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Contributor Information and Disclosures
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, and International Society for Heart and Lung Transplantation

Disclosure: Nothing to disclose.

Coauthor(s)

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.

Chief Editor

Henry H Ooi, MB, 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.

Additional Contributors

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 Academy ofSciences,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; eMedicine 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

Additional Contributors

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 Academy ofSciences,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; eMedicine 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

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This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases, signs of acute heart failure.
Cardiac cirrhosis. Congestive hepatopathy with large renal vein.
Cardiac cirrhosis. Congestive hepatopathy with large inferior vena cava.
This electrocardiogram (ECG) is from a 32-year-old female with recent-onset congestive heart failure and syncope. The ECG demonstrates a tachycardia with a 1:1 atrial:ventricular relationship. It is not clear from this tracing whether the atria are driving the ventricles (sinus tachycardia) or the ventricles are driving the atria (ventricular tachycardia).At first glance, sinus tachycardia in this ECG might be considered with severe conduction disease manifesting as marked first-degree atrioventricular block with left bundle branch block. Looking more closely, electrocardiographic morphology gives clues to the actual diagnosis of VT. These clues include the absence of RS complexes in the precordial leads, a QS pattern in V6, and an R wave in aVR. The patient proved to have an incessant VT associated with dilated cardiomyopathy.
This is a posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. Earliest activation is recorded in red; late activation shows as blue to magenta. Fragmented low-amplitude diastolic local electrocardiograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
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).
Epsilon wave on an electrocardiogram in a patient with arrhythmogenic right ventricular dysplasia (ARVD). ARVD is a congenital cardiomyopathy that is characterized by infiltration of adipose and fibrous tissue into the right ventricle wall and loss of myocardial cells. Primary injuries usually are at the free wall of right ventricular and right atria, resulting in ventricular and supraventricular arrhythmias. The most significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias.
Electrocardiogram depicting ventricular fibrillation in a patient with a left ventricular assist device (LVAD). Ventricular fibrillation is often due to ischemic heart disease and can lead to myocardial infarction and/or sudden death.
Hypokinesis of the anteroseptal wall observed during echocardiography in a patient presenting with an acute anteroseptal myocardial infarction, which can precipitate heart failure.
The rhythm on this electrocardiogram (ECG) is sinus with borderline PR prolongation. There is evidence of an acute/evolving anterior ischemia/myocardial infarction (MI) superimposed on the left bundle branch block–like (LBBB) pattern. Note the primary T wave inversions in leads V2-V4, rather than the expected discordant (upright) T waves in the leads with a negative QRS. Although this finding is not particularly sensitive for ischemia/MI with LBBB, such primary T wave changes are relatively specific. The prominent voltage with left atrial abnormality and leftward axis in concert with the left ventricular intraventricular conduction delay (IVCD) are consistent with underlying left ventricular hypertrophy. This ECG is an example of "bundle branch block plus." Image courtesy of http://ecg.bidmc.harvard.edu .
This electrocardiogram (ECG) shows evidence of severe left ventricular hypertrophy (LVH) with prominent precordial voltage, left atrial abnormality, lateral ST-T abnormalities, and a somewhat leftward QRS axis (–15º). The patient had malignant hypertension with acute heart failure, accounting also for the sinus tachycardia (blood pressure initially 280/180 mmHg). The ST-T changes seen here are nonspecific and could be due to, for example, LVH alone or coronary artery disease. However, the ECG is not consistent with extensive inferolateral myocardial infarction. Image courtesy of http://ecg.bidmc.harvard.edu .
The rhythm on this electrocardiogram is atrial tachycardia (rate, 154 beats/min) with a 2:1 atrioventricular (AV) block. Note the partially hidden, nonconducted P waves on the ST segments (eg, leads I and aVL). The QRS is very wide with an atypical intraventricular conduction defect (IVCD) pattern. The rSR' type complex in the lateral leads (I, aVL) is not due to a right bundle branch block (RBBB) but to an atypical left ventricular conduction defect. These unexpected rSR' complexes in the lateral leads (El-Sherif sign) correlate with underlying extensive myocardial infarction (MI) and, occasionally, ventricular aneurysm. (El-Sherif. Br Heart J. 1970;32:440-8.) The notching on the upstroke of the S waves in lead V4 with a left bundle branch block-type pattern also suggests underlying MI (Cabrera sign). This patient had severe cardiomyopathy secondary to coronary artery disease, with extensive left ventricular wall motion abnormalities. Image courtesy of http://ecg.bidmc.harvard.edu .
On this electrocardiogram, baseline artifact is present, simulating atrial fibrillation. Such artifact may be caused by a variety of factors, including poor electrode contact, muscle tremor, and electrical interference. A single premature ventricular complex (PVC) is present with a compensatory pause such that the RR interval surrounding the PVC is twice as long as the preceding sinus RR interval. Evidence of a previous anterior myocardial infarction is present with pathologic Q waves in leads V1-V3. Borderline-low precordial voltage is a nonspecific finding. Cardiac catheterization showed a 90% stenosis in the patient's proximal portion the left anterior descending coronary artery, which was treated with angioplasty and stenting. Broad P waves in lead V1 with a prominent negative component is consistent with a left atrial abnormality. Image courtesy of http://ecg.bidmc.harvard.edu .
This electrocardiogram (ECG) is from a patient who underwent urgent cardiac catheterization, which revealed diffuse severe coronary spasm (most marked in the left circumflex system) without any fixed obstructive lesions. Severe left ventricular wall motion abnormalities were present, involving the anterior and inferior segments. A question of so-called takotsubo cardiomyopathy (left ventricular apical ballooning syndrome) is also raised (see Bybee et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Int Med 2004:141:858-65). The latter is most often reported in postmenopausal, middle-aged to elderly women in the context of acute emotional stress and may cause ST elevations acutely with subsequent T wave inversions. A cocaine-induced cardiomyopathy (possibly related to coronary vasospasm) is a consideration but was excluded here. Myocarditis may also be associated with this type of ECG and the cardiomyopathic findings shown here. No fixed obstructive epicardial coronary lesions were detected by coronary arteriography. The findings in this ECG include low-amplitude QRS complexes in the limb leads (with an indeterminate QRS axis), loss of normal precordial R wave progression (leads V1-V3), and prominent anterior/lateral T wave inversions. Image courtesy of http://ecg.bidmc.harvard.edu .
This electrocardiogram shows an extensive acute/evolving anterolateral myocardial infarction pattern, with ST-T changes most apparent in leads V2-V6, I, and aVL. Slow R wave progression is also present in leads V1-V3. The rhythm is borderline sinus tachycardia with a single premature atrial complex (PAC) (4th beat). Note also the low limb lead voltage and probable left atrial abnormality. Left ventriculography showed diffuse hypokinesis as well as akinesis of the anterolateral and apical walls, with an ejection fraction estimated at 33%. Image courtesy of http://ecg.bidmc.harvard.edu.
This electrocardiogram shows a patient is having an evolving anteroseptal myocardial infarction secondary to cocaine. There are Q waves in leads V2-V3 with ST segment elevation in leads V2-V5 associated with T-wave inversion. Also noted are biphasic T-waves in the inferior leads. These multiple abnormalities suggest occlusion of a large left anterior descending artery that wraps around the apex of the heart (or multivessel coronary artery disease). Image courtesy of http://ecg.bidmc.harvard.edu .
A color-enhanced angiogram of the heart left shows a plaque-induced obstruction (top center) in a major artery, which can lead to myocardial infarction (MI). MIs can precipitate heart failure.
Emphysema is included in the differential diagnosis of heart failure. In this radiograph, emphysema bubbles are noted in the left lung; these can severely impede breathing capacity.
Cervicocephalic fibromuscular dysplasia (FMD) can lead to complications such as hypertension and chronic kidney failure, which can lead to heart failure. In this color Doppler and spectral Doppler ultrasonographic examination of the left internal carotid artery (ICA) in a patient with cervicocephalic FMD, stenoses of about 70% is seen in the ICA.
Cervicocephalic fibromuscular dysplasia (FMD) can lead to complications such as hypertension and chronic kidney failure, which, in turn, can lead to heart failure. Nodularity in an artery is known as the string-of-beads sign, and it can be seen this color Doppler ultrasonographic image from a 51-year-old patient with low-grade stenosing FMD of the internal carotid artery (ICA).
Electrocardiogram from a 46-year-old man with long-standing hypertension showing left atrial abnormality and left ventricular hypertrophy with strain.
Electrocardiogram from a 46-year-old man with long-standing hypertension showing left atrial abnormality and left ventricular hypertrophy with strain.
Histologic section of an autopsy myocardial specimen from a patient with long-standing hypertension and associated coronary artery disease. The slide shows myocardial hypertrophy, contraction bands (typical of left ventricular hypertrophy), and "car box" nuclei.
Apical 4-chamber echocardiogram in a 37-year-old man with arrhythmogenic right ventricular dysplasia (ARVD), a congenital cardiomyopathy. Note the prominent trabeculae and abnormal wall motion of the dilated right ventricle.ARVD can result in ventricular and supraventricular arrhythmias. The most significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias.
Apical long-axis echocardiogram in a young female patient with arrhythmogenic right ventricular dysplasia (ARVD) illustrates end-diastolic measurement of a dilated right ventricular outflow tract (RVOT). Ao = aorta, LA = left atrium, LV = left ventricle, RV = right ventricle.
Apical 4-chamber end-diastolic echocardiogram in a patient with arrhythmogenic right ventricular dysplasia (ARVD) shows dilatation of the right ventricle (RV) (arrow) and prominent trabeculae. Ao = aorta, LA = left atrium, LV = left ventricle.
Cardiac magnetic resonance image (CMRI), short axis view. This image shows right ventricular dilatation, trabucular derangement, aneurysm formation and dyskinetic free wall in a patient with arrhythmogenic right ventricular dysplasia.
This magnetic resonance image shows a scar in the anterior cardiac wall, which may be indicative of a previous myocardial infarction (MI). MIs can precipitate heart failure.
Transthoracic echocardiogram demonstrating severe mitral regurgitation with heavily calcified mitral valve and prolapse of the posterior leaflet into the left atrium.
Transesophageal echocardiogram demonstrating prolapse of both mitral valve leaflets during systole in a patient with mitral regurgitation.
Apical 4-chamber view demonstrating restricted opening of the anterior and posterior mitral valve leaflet with diastolic doming of anterior leaflet with left atrial enlargement. This patient has mitral stenosis.
Transesophageal echocardiogram with continuous wave Doppler interrogation across the mitral valve demonstrating an increased mean gradient of 16 mm Hg consistent with severe mitral stenosis.
Transesophageal echocardiogram in an apical 3-chamber view showing calcification and doming of the anterior mitral leaflet and restricted opening of both leaflets in a patient with mitral stenosis.
Transesophageal echocardiogram in an apical 3-chamber view with color Doppler interrogation of the mitral valve revealing aliasing, which is consistent with increased gradient across the mitral valve secondary to stenosis. Also shown in this image, a posteriorly directed jet of severe mitral regurgitation. Valvular heart disease, such as mitral stenosis and mitral regurgitation, can precipitate heart failure.
Echocardiogram of a patient with severe pulmonic stenosis. This image shows a parasternal short axis view of the thickened pulmonary valve. Pulmonic stenosis can lead to pulmonary hypertension, which can result in hepatic congestion and in right-sided heart failure.
Echocardiogram of a patient with severe pulmonic stenosis. This image shows a Doppler scan of the peak velocity (5.2 m/s) and gradients (peak 109 mm Hg, mean 65 mm Hg) across the valve.
Echocardiogram of a patient with severe pulmonic stenosis. This image shows that moderately severe pulmonary insufficiency (orange color flow) is also present.
This video is an echocardiogram of a patient with severe pulmonic stenosis. The first segment shows the parasternal short axis view of the thickened pulmonary valve. The second segment shows the presence of moderate pulmonary insufficiency (orange color flow). AV = aortic valve, PV = pulmonary valve, PA = pulmonary artery, PI = pulmonary insufficiency.
Table 1. Framingham Diagnostic Criteria for Heart Failure
Major CriteriaMinor Criteria
Paroxysmal nocturnal dyspneaNocturnal cough
Weight loss of 4.5 kg in 5 days in response to treatmentDyspnea on ordinary exertion
Neck vein distentionA decrease in vital capacity by one third the maximal value recorded
RalesPleural effusion
Acute pulmonary edemaTachycardia (rate of 120 bpm)
Hepatojugular refluxHepatomegaly
S3 gallopBilateral ankle edema
Central venous pressure > 16 cm water
Circulation time of 25 sec
Radiographic cardiomegaly
Pulmonary edema, visceral congestion, or cardiomegaly at autopsy
Source:  Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol. 1993 Oct;22(4 suppl A):6A-13A.[49]
Table 2. NYHA Functional Classification of Heart Failure
ClassFunctional Capacity
IPatients without limitation of physical activity
IIPatients with slight limitation of physical activity, in which ordinary physical activity leads to fatigue, palpitation, dyspnea, or anginal pain; they are comfortable at rest
IIIPatients with marked limitation of physical activity, in which less than ordinary activity results in fatigue, palpitation, dyspnea, or anginal pain; they are comfortable at rest
IVPatients who are not only unable to carry on any physical activity without discomfort but who also have symptoms of heart failure or the anginal syndrome even at rest; the patient's discomfort increases if any physical activity is undertaken
Source:  American Heart Association. Classes of heart failure. Available at: http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Classes-of-Heart-Failure_UCM_306328_Article.jsp. Accessed: September 6, 2011.[1]
Table 3. ACC/AHA Stages of Heart Failure Development
levelDescriptionExamplesNotes
AAt high risk for heart failure but without structural heart disease or symptoms of heart failurePatients with coronary artery disease, hypertension, or diabetes mellitus without impaired LV function, hypertrophy, or geometric chamber distortion
  • Patients with predisposing risk factors for developing heart failure
  • Corresponds with patients with NYHA class I heart failure
BStructural heart disease but without signs/symptoms of heart failurePatients who are asymptomatic but who have LVH and/or impaired LV function
CStructural heart disease with current or past symptoms of heart failurePatients with known structural heart disease and shortness of breath and fatigue, reduced exercise tolerance
  • The majority of patients with heart failure are in this stage
  • Corresponds with patients with NYHA class II and III heart failure
DRefractory heart failure requiring specialized interventionsPatients who have marked symptoms at rest despite maximal medical therapy
  • Patients in this stage may be eligible to receive mechanical circulatory support, receive continuous inotropic infusions, undergo procedures to facilitate fluid removal, or undergo heart transplantation or other procedures
  • Corresponds with patients with NYHA class IV heart failure
Sources:  (1) Hunt SA, American College of Cardiology, and the American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2005 Sep 20;46(6):e1-82.[3] ; and (2) Hunt SA, Abraham WT, Chin MH, et al. 2009 Focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation. J Am Coll Cardiol. Apr 14 2009;53(15):e1-e90.[2]
Table 4. Evidence-Based BNP and NT-proBNP Cutoff Values for Diagnosing HF
CriterionBNP, pg/mLNT-proBNP, pg/mL
HF Unlikely (LR-Negative)HF Likely (LR-Positive)HF Unlikely (LR-Negative)HF Likely (LR-Positive)
Age, y>17< 100 (0.13)*>500 (8.1)*--
>21--< 300 (0.02)†-
21-50--->450 (14)†
50-75--->900 (5.0)†
>75--->1800 (3.1)†
Estimated GFR, < 60 mL/min< 200 (0.13)‡>500 (9.3)‡--
BNP = B-type natriuretic peptide; GRF = glomerular filtration rate; HF = heart failure; LR = likelihood ratio; NPV = negative predictive value; NT-pro-BNP = N-terminal proBNP; PPV = positive predictive value; – = not specifically defined.



* Derived from Breathing Not Properly data (1586 emergency department [ED] patients, prevalence of HF = 47%).[54]



† Derived from PRIDE data (1256 ED patients, prevalence of HF = 57%).[55, 62]



‡ Derived from subset of Breathing Not Properly data (452 ED patients, prevalence of HF = 49%).[61]



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