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Media Gallery

Heart Failure. This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases, signs of acute heart failure.
Heart Failure. Cardiac cirrhosis. Congestive hepatopathy with large renal vein.
Heart Failure. Cardiac cirrhosis. Congestive hepatopathy with large inferior vena cava.
Heart Failure. 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 [VT]). 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. On closer examination, the ECG 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.
Heart Failure. This is a posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. The earliest activation is recorded in red; late activation displays 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.
Heart Failure. A 28-year-old woman presented with acute heart failure secondary to chronic hypertension. The enlarged cardiac silhouette on this anteroposterior (AP) radiograph is caused by acute heart failure due to the effects of chronic high blood pressure on the left ventricle. The heart then becomes enlarged, and fluid accumulates in the lungs (ie, pulmonary congestion).
Heart Failure. 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 RV wall and loss of myocardial cells. Primary injuries usually are at the free wall of the RV 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.
Heart Failure. 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.
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 (LBBB)–like 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.
Heart Failure. 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.
Heart Failure. 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.
Heart Failure. 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.
Heart Failure. 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.
Heart Failure. 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) (fourth 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.
Heart Failure. 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.
Heart Failure. A color-enhanced angiogram of the left heart shows a plaque-induced obstruction (top center) in a major artery, which can lead to myocardial infarction (MI). MIs can precipitate heart failure.
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.
Heart Failure. 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.
Heart Failure. 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).
Heart Failure. Electrocardiogram from a 46-year-old man with long-standing hypertension. Note the left atrial abnormality and left ventricular hypertrophy with strain.
Heart Failure. Electrocardiogram from a 46-year-old man with long-standing hypertension. Left atrial abnormality and left ventricular hypertrophy with strain is revealed.
Heart Failure. Apical four-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 RV. ARVD can result in ventricular and supraventricular arrhythmias. The most significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias.
Heart Failure. Cardiac magnetic resonance image (CMRI), short-axis view. This image shows right ventricular (RV) dilatation, trabucular derangement, aneurysm formation, and dyskinetic free wall in a patient with arrhythmogenic RV dysplasia.
Heart Failure. This transthoracic echocardiogram demonstrates severe mitral regurgitation with a heavily calcified mitral valve and prolapse of the posterior leaflet into the left atrium.
Heart Failure. Echocardiogram of a patient with severe pulmonic stenosis. This image shows a parasternal short-axis view of a thickened pulmonary valve. Pulmonic stenosis can lead to pulmonary hypertension, which can result in hepatic congestion and in right-sided heart failure.
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 mmHg, mean 65 mmHg) across the valve.
Heart Failure. Echocardiogram of a patient with severe pulmonic stenosis. This image shows moderately severe pulmonary insufficiency (orange color flow) is also present.
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, PA = pulmonary artery, PI = pulmonary insufficiency, PV = pulmonary valve.
Heart Failure. Transesophageal echocardiogram with continuous wave Doppler interrogation across the mitral valve. An increased mean gradient of 16 mmHg is revealed, consistent with severe mitral stenosis.

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Table 1. Framingham Diagnostic Criteria for Heart Failure

Major Criteria	Minor Criteria
Paroxysmal nocturnal dyspnea	Nocturnal cough
Weight loss of 4.5 kg in 5 days in response to treatment	Dyspnea on ordinary exertion
Neck vein distention	A decrease in vital capacity by one third the maximal value recorded
Rales	Pleural effusion
Acute pulmonary edema	Tachycardia (rate of 120 bpm)
Hepatojugular reflux	Hepatomegaly
S₃ gallop	Bilateral ankle edema
Central venous pressure >16 cm water
Circulation time of ≥25 seconds
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.

Table 2. Evidence-Based BNP and NT-proBNP Cutoff Values for Diagnosing HF

Criterion		BNP, pg/mL		NT-proBNP, pg/mL
Criterion		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%).^[65] ^† Derived from PRIDE data (1256 ED patients, prevalence of HF = 57%).^{[66, 75]} ^‡ Derived from subset of Breathing Not Properly data (452 ED patients, prevalence of HF = 49%).^[74]

Table 3. 2013 American College of Cardiology Foundation/American Heart Association (ACCF/AHA) Heart Failure Staging System

Stage	Description	Examples	Notes
A	At high risk for heart failure but without structural heart disease or symptoms of heart failure	Patients with coronary artery disease, hypertension, or diabetes mellitus without impaired left ventricular (LV) function, LV hypertrophy (LVH), or geometric chamber distortion	Patients with predisposing risk factors for developing heart failure No corresponding New York Heart Association (NYHA) functional classification
B	Structural heart disease but without signs/symptoms of heart failure	Patients who are asymptomatic but who have LVH and/or impaired LV function	Corresponds with patients with NYHA class I
C	Structural heart disease with current or past symptoms of heart failure	Patients with known structural heart disease and shortness of breath and fatigue, as well as reduced exercise tolerance	The majority of patients with heart failure are in this stage Corresponds with NYHA classes I, II, III and IV
D	Refractory heart failure requiring specialized interventions	Patients 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

Table 4. 2022 ACC/AHA/Heart Failure Society of America (HFSA) Heart Failure Staging System

Proposed Terminology	Stage	Definition and Criteria
At risk for HF	A	At risk of HF; asymptomatic, no structural heart disease nor cardiac biomarkers of stretch injury (eg, patients with hypertension, atherosclerotic cardiovascular disease, diabetes, metabolic syndrome and obesity, exposure to cardiotoxic agents, genetic variant for cardiomyopathy, or positive family history of cardiomyopathy)
Pre-HF	B	No signs/symptoms of HF and evidence of one of the following: Structural heart disease Reduced left or right ventricular systolic function Reduced ejection fraction, reduced strain Ventricular hypertrophy Enlarged chamber Wall motion anomalies Valvular heart disease Evidence for raised filling pressures by invasive hemodynamic measurements or by noninvasive imaging that suggests elevated filling pressures (eg, Doppler echocardiography) Patients with risk factors and raised levels of B-type natriuretic peptides or persistently elevated cardiac troponin in the absence of competing diagnoses that result in such biomarker elevations (eg, acute coronary syndrome, chronic kidney disease, pulmonary embolus, or myopericarditis)
Symptomatic HF	C	Structural heart disease with current or previous symptoms of HF
Advanced HF	D	Marked HF symptoms that interfere with daily life and with repeated hospitalizations despite attempts to optimize guideline-directed medical therapy
HF = heart failure

Table 5. 2022 ACC/AHA/HFSA Classification of Heart Failure (HF) by Left Ventricular Ejection Fraction (LVEF)

HF Type by LVEF

Criteria

HF with reduced EF

(HFrEF)

LVEF ≤40%

HF with improved EF

(HFimpEF)

Previous LVEF ≤40% and a followup LVEF >40%

HF with mildly reduced EF

(HFmrEF)

LVEF of 41%-49%

Evidence of spontaneous/provokable increased LV filling pressures (eg, elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement)

HF with preserved EF

(HFpEF)

LVEF ≥50%

Evidence of spontaneous/provokable increased LV filling pressures (eg, elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement)

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Author

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

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Nothing to disclose.

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

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

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

Chief Editor

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

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

Disclosure: Nothing to disclose.

Additional Contributors

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

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

Mariclaire Cloutier Freelance editor, Medscape Drugs & Diseases

Disclosure: Nothing to disclose.

Acknowledgements

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

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