U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Reduced left ventricular ejection fraction

MedGen UID:
868398
Concept ID:
C4022792
Finding
Synonym: Reduced ejection fraction
 
HPO: HP:0012664

Definition

A diminution of the volumetric fraction of blood pumped out of the ventricle with each cardiac cycle. [from HPO]

Conditions with this feature

Emery-Dreifuss muscular dystrophy 2, autosomal dominant
MedGen UID:
98048
Concept ID:
C0410190
Disease or Syndrome
Emery-Dreifuss muscular dystrophy (EDMD) is characterized by the clinical triad of: joint contractures that begin in early childhood; slowly progressive muscle weakness and wasting initially in a humero-peroneal distribution that later extends to the scapular and pelvic girdle muscles; and cardiac involvement that may manifest as palpitations, presyncope and syncope, poor exercise tolerance, and congestive heart failure along with variable cardiac rhythm disturbances. Age of onset, severity, and progression of muscle and cardiac involvement demonstrate both inter- and intrafamilial variability. Clinical variability ranges from early onset with severe presentation in childhood to late onset with slow progression in adulthood. In general, joint contractures appear during the first two decades, followed by muscle weakness and wasting. Cardiac involvement usually occurs after the second decade and respiratory function may be impaired in some individuals.
Dilated cardiomyopathy 1D
MedGen UID:
316943
Concept ID:
C1832243
Disease or Syndrome
Left ventricular noncompaction is a heart (cardiac) muscle disorder that occurs when the lower left chamber of the heart (left ventricle), which helps the heart pump blood, does not develop correctly. Instead of the muscle being smooth and firm, the cardiac muscle in the left ventricle is thick and appears spongy. The abnormal cardiac muscle is weak and has an impaired ability to pump blood because it either cannot completely contract or it cannot completely relax. For the heart to pump blood normally, cardiac muscle must contract and relax fully.\n\nSome individuals with left ventricular noncompaction experience no symptoms at all; others have heart problems that can include sudden cardiac death. Additional signs and symptoms include abnormal blood clots, irregular heart rhythm (arrhythmia), a sensation of fluttering or pounding in the chest (palpitations), extreme fatigue during exercise (exercise intolerance), shortness of breath (dyspnea), fainting (syncope), swelling of the legs (lymphedema), and trouble laying down flat. Some affected individuals have features of other heart defects. Left ventricular noncompaction can be diagnosed at any age, from birth to late adulthood. Approximately two-thirds of individuals with left ventricular noncompaction develop heart failure.
Dilated cardiomyopathy 1E
MedGen UID:
331341
Concept ID:
C1832680
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the SCN5A gene.
Dilated cardiomyopathy 1S
MedGen UID:
371831
Concept ID:
C1834481
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the MYH7 gene.
Hypertrophic cardiomyopathy 8
MedGen UID:
324806
Concept ID:
C1837471
Disease or Syndrome
Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the MYL3 gene.
Dilated cardiomyopathy 1M
MedGen UID:
334498
Concept ID:
C1843808
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the CSRP3 gene.
Dilated cardiomyopathy 1L
MedGen UID:
335735
Concept ID:
C1847667
Disease or Syndrome
Dilated cardiomyopathy, a disorder characterized by cardiac dilation and reduced systolic function, represents an outcome of a heterogeneous group of inherited and acquired disorders. For background and phenotypic information on dilated cardiomyopathy, see CMD1A (115200).
Dilated cardiomyopathy 1I
MedGen UID:
387998
Concept ID:
C1858154
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the DES gene.
Dilated cardiomyopathy 1G
MedGen UID:
347714
Concept ID:
C1858763
Disease or Syndrome
Dilated cardiomyopathy-1G (CMD1G) is an autosomal dominant disorder characterized by ventricular dilatation and systolic contractile dysfunction (Siu et al., 1999). For a general phenotypic description and a discussion of genetic heterogeneity of dilated cardiomyopathy (CMD), see CMD1A (115200).
Hypertrophic cardiomyopathy 4
MedGen UID:
350526
Concept ID:
C1861862
Disease or Syndrome
While most people with familial hypertrophic cardiomyopathy are symptom-free or have only mild symptoms, this condition can have serious consequences. It can cause abnormal heart rhythms (arrhythmias) that may be life threatening. People with familial hypertrophic cardiomyopathy have an increased risk of sudden death, even if they have no other symptoms of the condition. A small number of affected individuals develop potentially fatal heart failure, which may require heart transplantation.\n\nThe symptoms of familial hypertrophic cardiomyopathy are variable, even within the same family. Many affected individuals have no symptoms. Other people with familial hypertrophic cardiomyopathy may experience chest pain; shortness of breath, especially with physical exertion; a sensation of fluttering or pounding in the chest (palpitations); lightheadedness; dizziness; and fainting.\n\nNonfamilial hypertrophic cardiomyopathy tends to be milder. This form typically begins later in life than familial hypertrophic cardiomyopathy, and affected individuals have a lower risk of serious cardiac events and sudden death than people with the familial form.\n\nIn familial hypertrophic cardiomyopathy, cardiac thickening usually occurs in the interventricular septum, which is the muscular wall that separates the lower left chamber of the heart (the left ventricle) from the lower right chamber (the right ventricle). In some people, thickening of the interventricular septum impedes the flow of oxygen-rich blood from the heart, which may lead to an abnormal heart sound during a heartbeat (heart murmur) and other signs and symptoms of the condition. Other affected individuals do not have physical obstruction of blood flow, but the pumping of blood is less efficient, which can also lead to symptoms of the condition. Familial hypertrophic cardiomyopathy often begins in adolescence or young adulthood, although it can develop at any time throughout life.\n\nHypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. When multiple members of a family have the condition, it is known as familial hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy also occurs in people with no family history; these cases are considered nonfamilial hypertrophic cardiomyopathy. 
Hypertrophic cardiomyopathy 2
MedGen UID:
349383
Concept ID:
C1861864
Disease or Syndrome
Hypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. When multiple members of a family have the condition, it is known as familial hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy also occurs in people with no family history; these cases are considered nonfamilial hypertrophic cardiomyopathy. \n\nIn familial hypertrophic cardiomyopathy, cardiac thickening usually occurs in the interventricular septum, which is the muscular wall that separates the lower left chamber of the heart (the left ventricle) from the lower right chamber (the right ventricle). In some people, thickening of the interventricular septum impedes the flow of oxygen-rich blood from the heart, which may lead to an abnormal heart sound during a heartbeat (heart murmur) and other signs and symptoms of the condition. Other affected individuals do not have physical obstruction of blood flow, but the pumping of blood is less efficient, which can also lead to symptoms of the condition. Familial hypertrophic cardiomyopathy often begins in adolescence or young adulthood, although it can develop at any time throughout life.\n\nNonfamilial hypertrophic cardiomyopathy tends to be milder. This form typically begins later in life than familial hypertrophic cardiomyopathy, and affected individuals have a lower risk of serious cardiac events and sudden death than people with the familial form.\n\nThe symptoms of familial hypertrophic cardiomyopathy are variable, even within the same family. Many affected individuals have no symptoms. Other people with familial hypertrophic cardiomyopathy may experience chest pain; shortness of breath, especially with physical exertion; a sensation of fluttering or pounding in the chest (palpitations); lightheadedness; dizziness; and fainting.\n\nWhile most people with familial hypertrophic cardiomyopathy are symptom-free or have only mild symptoms, this condition can have serious consequences. It can cause abnormal heart rhythms (arrhythmias) that may be life threatening. People with familial hypertrophic cardiomyopathy have an increased risk of sudden death, even if they have no other symptoms of the condition. A small number of affected individuals develop potentially fatal heart failure, which may require heart transplantation.
Dilated cardiomyopathy 1X
MedGen UID:
370583
Concept ID:
C1969024
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the FKTN gene.
Dilated cardiomyopathy 1W
MedGen UID:
370063
Concept ID:
C1969639
Disease or Syndrome
An genetic condition that is a subtype of dilated cardiomyopathy caused by mutation(s) in the VCL gene, encoding vinculin.
Cardiomyopathy, familial restrictive, 3
MedGen UID:
382807
Concept ID:
C2676271
Disease or Syndrome
Familial restrictive cardiomyopathy is a genetic form of heart disease. For the heart to beat normally, the heart (cardiac) muscle must contract and relax in a coordinated way. Oxygen-rich blood from the lungs travels first through the upper chambers of the heart (the atria), and then to the lower chambers of the heart (the ventricles).\n\nAdults with familial restrictive cardiomyopathy typically first develop shortness of breath, fatigue, and a reduced ability to exercise. Some individuals have an irregular heart beat (arrhythmia) and may also experience a sensation of fluttering or pounding in the chest (palpitations) and dizziness. Abnormal blood clots are commonly seen in adults with this condition. Without treatment, approximately one-third of adults with familial restrictive cardiomyopathy do not survive more than five years after diagnosis.\n\nIn people with familial restrictive cardiomyopathy, the heart muscle is stiff and cannot fully relax after each contraction. Impaired muscle relaxation causes blood to back up in the atria and lungs, which reduces the amount of blood in the ventricles.\n\nFamilial restrictive cardiomyopathy can appear anytime from childhood to adulthood. The first signs and symptoms of this condition in children are failure to gain weight and grow at the expected rate (failure to thrive), extreme tiredness (fatigue), and fainting. Children who are severely affected may also have abnormal swelling or puffiness (edema), increased blood pressure, an enlarged liver, an abnormal buildup of fluid in the abdominal cavity (ascites), and lung congestion. Some children with familial restrictive cardiomyopathy do not have any obvious signs or symptoms, but they may die suddenly due to heart failure. Without treatment, the majority of affected children survive only a few years after they are diagnosed.
Atrial fibrillation, familial, 6
MedGen UID:
394252
Concept ID:
C2677294
Disease or Syndrome
Atrial fibrillation (AF) is the most common sustained cardiac rhythm disturbance, affecting more than 2 million Americans, with an overall prevalence of 0.89%. The prevalence increases rapidly with age, to 2.3% between the ages of 40 and 60 years, and to 5.9% over the age of 65. The most dreaded complication is thromboembolic stroke (Brugada et al., 1997). For a discussion of genetic heterogeneity of atrial fibrillation, see 608583.
Dilated cardiomyopathy 1EE
MedGen UID:
412965
Concept ID:
C2750466
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the MYH6 gene.
Hypertrophic cardiomyopathy 13
MedGen UID:
442487
Concept ID:
C2750472
Disease or Syndrome
Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the TNNC1 gene.
Dilated cardiomyopathy 1CC
MedGen UID:
413929
Concept ID:
C2751084
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the NEXN gene.
Long QT syndrome 13
MedGen UID:
462083
Concept ID:
C3150733
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the EKG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7); hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8); and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Dilated cardiomyopathy 1GG
MedGen UID:
462248
Concept ID:
C3150898
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the SDHA gene.
Dilated cardiomyopathy 1V
MedGen UID:
462308
Concept ID:
C3150958
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the PSEN2 gene.
Hypertrophic cardiomyopathy 16
MedGen UID:
462554
Concept ID:
C3151204
Disease or Syndrome
Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the MYOZ2 gene.
Hypertrophic cardiomyopathy 20
MedGen UID:
462617
Concept ID:
C3151267
Disease or Syndrome
Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the NEXN gene.
Arterial calcification, generalized, of infancy, 2
MedGen UID:
477791
Concept ID:
C3276161
Disease or Syndrome
Generalized arterial calcification of infancy (GACI) is characterized by infantile onset of widespread arterial calcification and/or narrowing of large and medium-sized vessels resulting in cardiovascular findings (which can include heart failure, respiratory distress, edema, cyanosis, hypertension, and/or cardiomegaly). Additional findings can include typical skin and retinal manifestations of pseudoxanthoma elasticum (PXE), periarticular calcifications, development of rickets after infancy, cervical spine fusion, and hearing loss. While mortality in infancy is high, survival into the third and fourth decades has occurred.
Atrial fibrillation, familial, 11
MedGen UID:
481323
Concept ID:
C3279693
Disease or Syndrome
Atrial fibrillation is the most common sustained cardiac rhythm disturbance, affecting more than 2 million Americans, with an overall prevalence of 0.89%. The prevalence increases rapidly with age, to 2.3% between the ages of 40 and 60 years, and to 5.9% over the age of 65. The most dreaded complication is thromboembolic stroke (Brugada et al., 1997). For a discussion of genetic heterogeneity of familial atrial fibrillation, see ATFB1 (608583).
Dilated cardiomyopathy 2B
MedGen UID:
766323
Concept ID:
C3553409
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the GATAD1 gene.
Dilated cardiomyopathy 1JJ
MedGen UID:
815265
Concept ID:
C3808935
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the LAMA4 gene.
Very long chain acyl-CoA dehydrogenase deficiency
MedGen UID:
854382
Concept ID:
C3887523
Disease or Syndrome
Deficiency of very long-chain acyl-coenzyme A dehydrogenase (VLCAD), which catalyzes the initial step of mitochondrial beta-oxidation of long-chain fatty acids with a chain length of 14 to 20 carbons, is associated with three phenotypes. The severe early-onset cardiac and multiorgan failure form typically presents in the first months of life with hypertrophic or dilated cardiomyopathy, pericardial effusion, and arrhythmias, as well as hypotonia, hepatomegaly, and intermittent hypoglycemia. The hepatic or hypoketotic hypoglycemic form typically presents during early childhood with hypoketotic hypoglycemia and hepatomegaly, but without cardiomyopathy. The later-onset episodic myopathic form presents with intermittent rhabdomyolysis provoked by exercise, muscle cramps and/or pain, and/or exercise intolerance. Hypoglycemia typically is not present at the time of symptoms.
Dilated cardiomyopathy 1NN
MedGen UID:
863093
Concept ID:
C4014656
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the RAF1 gene.
Cardioencephalomyopathy, fatal infantile, due to cytochrome c oxidase deficiency 4
MedGen UID:
905398
Concept ID:
C4225304
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 13 (MC4DN13) is an autosomal recessive metabolic disorder characterized by the onset of hypertrophic cardiomyopathy soon after birth. Affected individuals have hypotonia, weakness, and failure to thrive, resulting in death in infancy. Laboratory studies show increased serum lactate and decreased levels and activity of mitochondrial respiratory complex IV (summary by Baertling et al., 2015). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Combined oxidative phosphorylation defect type 8
MedGen UID:
1377817
Concept ID:
C4518839
Disease or Syndrome
Combined oxidative phosphorylation deficiency-8 (COXPD8) is an autosomal recessive disorder caused by dysfunction of the mitochondrial respiratory chain. The main clinical manifestation is a lethal infantile hypertrophic cardiomyopathy, but there may also be subtle skeletal muscle and brain involvement. Biochemical studies show combined respiratory chain complex deficiencies in complexes I, III, and IV in cardiac muscle, skeletal muscle, and brain. The liver is not affected (summary by Gotz et al., 2011). For a discussion of genetic heterogeneity of combined oxidative phosphorylation deficiency, see COXPD1 (609060).
Cardiomyopathy, dilated, 2c
MedGen UID:
1648379
Concept ID:
C4748647
Disease or Syndrome
CMD2C is characterized by dilated cardiomyopathy of variable severity, with age of onset ranging from 2 to 20 years. Affected individuals exhibit reduction in coenzyme A (CoA) levels. Some severely affected children die in the first few years of life (Iuso et al., 2018). For a general phenotypic description and a discussion of genetic heterogeneity of dilated cardiomyopathy (CMD), see 115200.
Cardiomyopathy, dilated, 2D
MedGen UID:
1782612
Concept ID:
C5543535
Disease or Syndrome
Dilated cardiomyopathy-2D (CMD2D) is characterized by neonatal onset of severe cardiomyopathy, with rapid progression to cardiac decompensation and death unless the patient undergoes heart transplantation (Ganapathi et al., 2020). For a general phenotypic description and a discussion of genetic heterogeneity of dilated cardiomyopathy, see 115200.
Cardiomyopathy, familial hypertrophic, 28
MedGen UID:
1779612
Concept ID:
C5543616
Disease or Syndrome
Familial hypertrophic cardiomyopathy-28 (CMH28) is characterized by asymmetric septal hypertrophy, atrial fibrillation and nonsustained ventricular tachycardia, and risk of sudden death. Dyspnea is the most common symptom, but more than half of affected individuals are asymptomatic. Hypertrabeculation of the left ventricle with noncompaction has been observed in some patients (Ochoa et al., 2018). For a general phenotypic description and discussion of genetic heterogeneity of familial hypertrophic cardiomyopathy, see CMH1 (192600).
Hypomagnesemia 7, renal, with or without dilated cardiomyopathy
MedGen UID:
1824039
Concept ID:
C5774266
Disease or Syndrome
Renal hypomagnesemia-7 with or without dilated cardiomyopathy (HOMG7) is characterized primarily by renal salt wasting resulting in hypomagnesemia with secondary effects such as hypokalemia or hypocalcemia. Many patients develop nephrocalcinosis, although renal function is generally well-preserved. The age at onset is highly variable, ranging from infancy to young adulthood. A subset of patients develop severe dilated cardiomyopathy as early as in infancy, which may require heart transplant (Schlingmann et al., 2021). For a discussion of genetic heterogeneity of hypomagnesemia, see 602014.
Cardiomyopathy, dilated, 2H
MedGen UID:
1824069
Concept ID:
C5774296
Disease or Syndrome
CMD2H is an autosomal recessive disorder characterized by rapidly progressive dilated cardiomyopathy and death in early infancy (Verhagen et al., 2019). For a general phenotypic description and a discussion of genetic heterogeneity of dilated cardiomyopathy, see 115200.
Cardiomyopathy, dilated, 100
MedGen UID:
1840927
Concept ID:
C5830291
Disease or Syndrome
Dilated cardiomyopathy-1OO (CMD1OO) is characterized by enlarged left ventricular end-diastolic diameter and reduced left ventricular ejection fraction, resulting in cardiac failure that may result in premature death. Some patients also exhibit second-degree atrioventricular block and premature ventricular beats (Shi et al., 2023). For a general phenotypic description and discussion of genetic heterogeneity of dilated cardiomyopathy, see CMD1A (115200).

Professional guidelines

PubMed

Masini G, Graham FJ, Pellicori P, Cleland JGF, Cuthbert JJ, Kazmi S, Inciardi RM, Clark AL
J Am Coll Cardiol 2022 Feb 1;79(4):341-351. doi: 10.1016/j.jacc.2021.11.039. PMID: 35086656
Praz F, Muraru D, Kreidel F, Lurz P, Hahn RT, Delgado V, Senni M, von Bardeleben RS, Nickenig G, Hausleiter J, Mangieri A, Zamorano JL, Prendergast BD, Maisano F
EuroIntervention 2021 Nov 19;17(10):791-808. doi: 10.4244/EIJ-D-21-00695. PMID: 34796878Free PMC Article
Marcus GM
Circulation 2020 Apr 28;141(17):1404-1418. Epub 2020 Apr 27 doi: 10.1161/CIRCULATIONAHA.119.042434. PMID: 32339046

Recent clinical studies

Etiology

Marcus GM
Circulation 2020 Apr 28;141(17):1404-1418. Epub 2020 Apr 27 doi: 10.1161/CIRCULATIONAHA.119.042434. PMID: 32339046
Sun LY, Gaudino M, Chen RJ, Bader Eddeen A, Ruel M
JAMA Cardiol 2020 Jun 1;5(6):631-641. doi: 10.1001/jamacardio.2020.0239. PMID: 32267465Free PMC Article
Bjarnason-Wehrens B, Nebel R, Jensen K, Hackbusch M, Grilli M, Gielen S, Schwaab B, Rauch B; German Society of Cardiovascular Prevention and Rehabilitation (DGPR)
Eur J Prev Cardiol 2020 Jun;27(9):929-952. Epub 2019 Jun 8 doi: 10.1177/2047487319854140. PMID: 31177833Free PMC Article
Metra M, Teerlink JR
Lancet 2017 Oct 28;390(10106):1981-1995. Epub 2017 Apr 28 doi: 10.1016/S0140-6736(17)31071-1. PMID: 28460827
Gasparini M
Card Electrophysiol Clin 2015 Dec;7(4):749-54. Epub 2015 Sep 12 doi: 10.1016/j.ccep.2015.08.006. PMID: 26596816

Diagnosis

Kalra PR, Cleland JGF, Petrie MC, Thomson EA, Kalra PA, Squire IB, Ahmed FZ, Al-Mohammad A, Cowburn PJ, Foley PWX, Graham FJ, Japp AG, Lane RE, Lang NN, Ludman AJ, Macdougall IC, Pellicori P, Ray R, Robertson M, Seed A, Ford I; IRONMAN Study Group
Lancet 2022 Dec 17;400(10369):2199-2209. Epub 2022 Nov 5 doi: 10.1016/S0140-6736(22)02083-9. PMID: 36347265
Masini G, Graham FJ, Pellicori P, Cleland JGF, Cuthbert JJ, Kazmi S, Inciardi RM, Clark AL
J Am Coll Cardiol 2022 Feb 1;79(4):341-351. doi: 10.1016/j.jacc.2021.11.039. PMID: 35086656
Marcus GM
Circulation 2020 Apr 28;141(17):1404-1418. Epub 2020 Apr 27 doi: 10.1161/CIRCULATIONAHA.119.042434. PMID: 32339046
Bjarnason-Wehrens B, Nebel R, Jensen K, Hackbusch M, Grilli M, Gielen S, Schwaab B, Rauch B; German Society of Cardiovascular Prevention and Rehabilitation (DGPR)
Eur J Prev Cardiol 2020 Jun;27(9):929-952. Epub 2019 Jun 8 doi: 10.1177/2047487319854140. PMID: 31177833Free PMC Article
Metra M, Teerlink JR
Lancet 2017 Oct 28;390(10106):1981-1995. Epub 2017 Apr 28 doi: 10.1016/S0140-6736(17)31071-1. PMID: 28460827

Therapy

Kalra PR, Cleland JGF, Petrie MC, Thomson EA, Kalra PA, Squire IB, Ahmed FZ, Al-Mohammad A, Cowburn PJ, Foley PWX, Graham FJ, Japp AG, Lane RE, Lang NN, Ludman AJ, Macdougall IC, Pellicori P, Ray R, Robertson M, Seed A, Ford I; IRONMAN Study Group
Lancet 2022 Dec 17;400(10369):2199-2209. Epub 2022 Nov 5 doi: 10.1016/S0140-6736(22)02083-9. PMID: 36347265
Marcus GM
Circulation 2020 Apr 28;141(17):1404-1418. Epub 2020 Apr 27 doi: 10.1161/CIRCULATIONAHA.119.042434. PMID: 32339046
McMurray JJV, DeMets DL, Inzucchi SE, Køber L, Kosiborod MN, Langkilde AM, Martinez FA, Bengtsson O, Ponikowski P, Sabatine MS, Sjöstrand M, Solomon SD; DAPA-HF Committees and Investigators
Eur J Heart Fail 2019 May;21(5):665-675. Epub 2019 Mar 21 doi: 10.1002/ejhf.1432. PMID: 30895697Free PMC Article
Metra M, Teerlink JR
Lancet 2017 Oct 28;390(10106):1981-1995. Epub 2017 Apr 28 doi: 10.1016/S0140-6736(17)31071-1. PMID: 28460827
Pitt B, Pfeffer MA, Assmann SF, Boineau R, Anand IS, Claggett B, Clausell N, Desai AS, Diaz R, Fleg JL, Gordeev I, Harty B, Heitner JF, Kenwood CT, Lewis EF, O'Meara E, Probstfield JL, Shaburishvili T, Shah SJ, Solomon SD, Sweitzer NK, Yang S, McKinlay SM; TOPCAT Investigators
N Engl J Med 2014 Apr 10;370(15):1383-92. doi: 10.1056/NEJMoa1313731. PMID: 24716680

Prognosis

Marcus GM
Circulation 2020 Apr 28;141(17):1404-1418. Epub 2020 Apr 27 doi: 10.1161/CIRCULATIONAHA.119.042434. PMID: 32339046
Sun LY, Gaudino M, Chen RJ, Bader Eddeen A, Ruel M
JAMA Cardiol 2020 Jun 1;5(6):631-641. doi: 10.1001/jamacardio.2020.0239. PMID: 32267465Free PMC Article
Metra M, Teerlink JR
Lancet 2017 Oct 28;390(10106):1981-1995. Epub 2017 Apr 28 doi: 10.1016/S0140-6736(17)31071-1. PMID: 28460827
Pitt B, Pfeffer MA, Assmann SF, Boineau R, Anand IS, Claggett B, Clausell N, Desai AS, Diaz R, Fleg JL, Gordeev I, Harty B, Heitner JF, Kenwood CT, Lewis EF, O'Meara E, Probstfield JL, Shaburishvili T, Shah SJ, Solomon SD, Sweitzer NK, Yang S, McKinlay SM; TOPCAT Investigators
N Engl J Med 2014 Apr 10;370(15):1383-92. doi: 10.1056/NEJMoa1313731. PMID: 24716680
Anker SD, Comin Colet J, Filippatos G, Willenheimer R, Dickstein K, Drexler H, Lüscher TF, Bart B, Banasiak W, Niegowska J, Kirwan BA, Mori C, von Eisenhart Rothe B, Pocock SJ, Poole-Wilson PA, Ponikowski P; FAIR-HF Trial Investigators
N Engl J Med 2009 Dec 17;361(25):2436-48. Epub 2009 Nov 17 doi: 10.1056/NEJMoa0908355. PMID: 19920054

Clinical prediction guides

Vijayaraman P, Zalavadia D, Haseeb A, Dye C, Madan N, Skeete JR, Vipparthy SC, Young W, Ravi V, Rajakumar C, Pokharel P, Larsen T, Huang HD, Storm RH, Oren JW, Batul SA, Trohman RG, Subzposh FA, Sharma PS
Heart Rhythm 2022 Aug;19(8):1263-1271. Epub 2022 Apr 29 doi: 10.1016/j.hrthm.2022.04.023. PMID: 35500791
Marcus GM
Circulation 2020 Apr 28;141(17):1404-1418. Epub 2020 Apr 27 doi: 10.1161/CIRCULATIONAHA.119.042434. PMID: 32339046
Sun LY, Gaudino M, Chen RJ, Bader Eddeen A, Ruel M
JAMA Cardiol 2020 Jun 1;5(6):631-641. doi: 10.1001/jamacardio.2020.0239. PMID: 32267465Free PMC Article
Bjarnason-Wehrens B, Nebel R, Jensen K, Hackbusch M, Grilli M, Gielen S, Schwaab B, Rauch B; German Society of Cardiovascular Prevention and Rehabilitation (DGPR)
Eur J Prev Cardiol 2020 Jun;27(9):929-952. Epub 2019 Jun 8 doi: 10.1177/2047487319854140. PMID: 31177833Free PMC Article
Lewis GD, Malhotra R, Hernandez AF, McNulty SE, Smith A, Felker GM, Tang WHW, LaRue SJ, Redfield MM, Semigran MJ, Givertz MM, Van Buren P, Whellan D, Anstrom KJ, Shah MR, Desvigne-Nickens P, Butler J, Braunwald E; NHLBI Heart Failure Clinical Research Network
JAMA 2017 May 16;317(19):1958-1966. doi: 10.1001/jama.2017.5427. PMID: 28510680Free PMC Article

Recent systematic reviews

Taha AM, Hendi NI, Elwekel AB, Atia A, Taha NA, Shrestha AB, Elbanna M
Clin Cardiol 2024 Jan;47(1):e24177. Epub 2023 Oct 25 doi: 10.1002/clc.24177. PMID: 37877802Free PMC Article
Bjerkén LV, Rønborg SN, Jensen MT, Ørting SN, Nielsen OW
Heart Fail Rev 2023 Mar;28(2):419-430. Epub 2022 Nov 8 doi: 10.1007/s10741-022-10283-1. PMID: 36344908Free PMC Article
Goyal M, Ray I, Mascarenhas D, Kunal S, Sachdeva RA, Ish P
QJM 2023 Feb 14;116(1):7-25. doi: 10.1093/qjmed/hcac064. PMID: 35238384Free PMC Article
Qu Q, Sun JY, Zhang ZY, Kan JY, Wu LD, Li F, Wang RX
J Cardiovasc Electrophysiol 2021 Dec;32(12):3245-3258. Epub 2021 Oct 25 doi: 10.1111/jce.15269. PMID: 34664764
Bjarnason-Wehrens B, Nebel R, Jensen K, Hackbusch M, Grilli M, Gielen S, Schwaab B, Rauch B; German Society of Cardiovascular Prevention and Rehabilitation (DGPR)
Eur J Prev Cardiol 2020 Jun;27(9):929-952. Epub 2019 Jun 8 doi: 10.1177/2047487319854140. PMID: 31177833Free PMC Article

Supplemental Content

Table of contents

    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.
    • Bookshelf
      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Consumer resources

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...