Back To Search Results


Editor: Waqas J. Siddiqui Updated: 11/20/2022 10:39:33 PM


Cardiomegaly means enlargement of the heart. The definition is when the transverse diameter of the cardiac silhouette is greater than or equal to 50% of the transverse diameter of the chest (increased cardiothoracic ratio) on a posterior-anterior projection of a chest radiograph or a computed tomography. It should not be confused with an enlargement of the cardiomediastinal outline. Cardiomegaly is usually a manifestation of another pathologic process and presents with several forms of primary or acquired cardiomyopathies. It may involve enlargement of the right, left, or both ventricles or the atria. Many types of cardiomyopathy, such as dilated cardiomyopathy, are characterized by left ventricular dilation and systolic dysfunction, although right ventricular impairment and diastolic dysfunction can also develop.[1]


Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care


Several etiologies have been attributed to the development of cardiomegaly resulting in either dilated or hypertrophic cardiomyopathy.[2][3][4] These include the following:

  • Coronary artery disease, including myocardial infarction and ischemia (most common cause)[5]
  • Hypertensive heart disease[6]
  • Valvular heart diseases, including stenosis or regurgitation of the aortic, mitral, pulmonary, or tricuspid valves and sub-acute bacterial endocarditis[7]
  • Congenital heart disorders, including atrial septal defect, ventricular septal defect, patent ductus arteriosus, tetralogy of Fallot, Ebstein anomaly, and coarctation of the aorta
  • Pulmonary diseases such as primary pulmonary hypertension, chronic obstructive pulmonary disease (COPD), obesity hypoventilation syndrome, and pulmonary embolism with cor-pulmonale[8]
  • Infectious myocarditis secondary to viral infection (most common), HIV, Chaga disease[9]
  • Infiltrative/deposition diseases, such as amyloidosis, sarcoidosis, hypothyroidism, acromegaly, and hemochromatosis[10]
  • Toxin-induced cardiomyopathy (alcohol, cocaine, chemotherapeutic agents such as doxorubicin, cyclophosphamide, trastuzumab, and radiation)[11]
  • Autoimmune cardiomyopathy, including eosinophilic myocarditis, idiopathic giant cell myocarditis, and collagen vascular disease
  • Arrhythmia, including atrial fibrillation and flutter leading to tachycardia-induced cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC) with the fibro-fatty replacement of RV
  • Systemic diseases leading to a high output state, including anemia, hyperthyroidism, vitamin B1 deficiency (“beriberi”), and AV fistula[12]
  • Physiologic conditions include stress cardiomyopathy, exercise-induced cardiomegaly or “athletic” heart, and pregnancy
  • Familial cardiomyopathy, hypertrophic obstructive cardiomyopathy (HOCM)[13]
  • Peripartum cardiomyopathy[14]
  • Idiopathic cardiomyopathy


Enlargement of the heart, both in the form of dilatation or hypertrophy, leads to a spectrum of clinical heart failure syndrome, with a prevalence of nearly 5.8 million people in the United States. Heart failure with preserved ejection fraction (HFpEF) represents more than half of these cases. The incidence of heart failure increases with age, male gender, and African American race. About half of the people diagnosed with heart failure die within five years of diagnosis.[15]

In adults, dilated cardiomyopathy is more prevalent in men than in women. In the pediatric population, the annual incidence is 0.57 cases per 100,000 per year (higher in boys than girls, in Blacks than Whites, and in babies less than one year than in children). Two-thirds of children have idiopathic disease.[16]

Hypertrophic cardiomyopathy is a global disease, with cases in over 50 countries on all continents affecting both sexes and of several ethnic and racial origins.[17] In diverse regions, such as the USA, Europe, China, Japan, and east Africa, hypertrophic cardiomyopathy is a common genetic cardiac disease, having a prevalence of around 1 in 500 in the general population.[18]


The development of cardiac remodeling and hypertrophy is complex, with genetic and non-genetic components. The most critical pathophysiological changes leading to cardiomegaly include dilated hypertrophy, fibrosis, and contractile malfunction. Contractile dysfunction and abnormal myocardial remodeling can lead to hypertrophic cardiomyopathy or dilated cardiomyopathy. Mechanical stretching, circulating neurohormones, and oxidative stress are significant stimuli for the signal transduction of inflammatory cytokines and MAP kinase in cardiomyocytes. Signal transduction leads to changes in structural proteins and proteins that regulate excitation-contraction. Dilated cardiomyopathy mutations result in a reduced force of the sarcomere contraction and a reduction in sarcomere content. Hypertrophic cardiomyopathy mutations result in a molecular phenotype of hyperdynamic contractility, poor relaxation, and increased energy consumption.[19][20]

Pathophysiological mechanisms can vary with the underlying cause of cardiomyopathy. For instance, in diabetic cardiomyopathy, fatty acid metabolism is enhanced, glucose oxidation is suppressed, and intracellular signaling is modified, causing impairment in multiple steps of inefficient energy production, excitation-contraction coupling, and increased potential for ischemia/reperfusion injury. In alcohol-induced cardiomyopathy, cell death due to apoptosis ultimately leads to changes in various aspects of myocyte function.[21] In mitochondrial cardiomyopathy, multiple biochemical pathways involving mitochondria result in impaired oxidative phosphorylation.[22] 

Peripartum cardiomyopathy is associated with genetic alterations, angiogenic imbalance, oxidative stress, and the production of a prolactin fragment.[23] In hypertrophic cardiomyopathy, ventricular hypertrophy results in a dynamic pressure gradient across the left ventricular outflow tract (LVOT), which is associated with further narrowing during systole. During this cardiac cycle, the mitral valve is pulled towards the septum by several proposed mechanisms: contraction of the papillary muscles, abnormal location in the outflow tract, and low pressure that occurs as blood is ejected at high velocity through a narrowed outflow tract (Venturi effect).[24]

History and Physical

Many patients with cardiomegaly are asymptomatic, and the presence of symptoms alone is neither sensitive nor specific to diagnosis. The diagnosis of cardiomegaly is based on imaging, and history is only helpful in determining the cause of heart failure symptoms, resulting in systemic congestion and impaired organ perfusion.[25]

A detailed history should elicit the presence or absence of the following:

  • Shortness of breath on exertion or rest, orthopnea, and paroxysmal nocturnal dyspnea
  • Peripheral edema and abdominal distension
  • Fatigue and poor exercise tolerance
  • Palpitations, lightheadedness, and/or syncope[26]
  • Angina
  • Anorexia, nausea, and early satiety
  • Family history of cardiomyopathy
  • Recent pregnancy/childbirth
  • Comorbid illnesses, such as hypertension and diabetes mellitus

It is worth mentioning that cardiac function is adequate during rest and may become inadequate with exertion. Hence it is not uncommon for patients to be asymptomatic at rest and experience symptoms on exertion only. The New York Heart Association classifies the severity of disease based on symptoms, where class I disease is asymptomatic with ordinary physical activity, and class IV denotes symptoms with rest. 

Perhaps the most specific sign of cardiomegaly is a displaced point of maximal impulse (PMI).[27] The precordial examination will reveal a displaced PMI, usually below the 5th intercostal space, lateral to the midclavicular line, and palpable across two intercostal spaces. Sustained PMI is a sign of severe left ventricular hypertrophy. A sustained and prolonged left parasternal heave is indicative of right ventricular hypertrophy. Another physical finding observed in cardiomegaly is the holosystolic murmur of mitral and/or tricuspid regurgitation resulting from dilatation of the mitral annulus and displacement of papillary muscles with abnormal myocardial remodeling. Other exam findings may be seen depending on the presence or absence of decompensated heart failure. In such cases, a detailed physical exam may reveal the following abnormalities: 

  • Sinus tachycardia resulting from increased sympathetic drive
  • Diminished pulse pressure reflecting reduced stroke volume
  • Varying degrees of respiratory distress based on the severity of the disease
  • Cool, cyanotic extremities secondary to peripheral vasoconstriction
  • Jugular venous distension and/or positive abdominojugular reflex indicating elevated right-sided filling pressures
  • Ascites, hepatomegaly, and peripheral edema result from increased pressure in the hepatic veins and systemic veins[28]
  • Pulmonary crackles resulting from elevated left-sided filling pressure and transudation of fluid into alveoli
  • S3 gallop in early diastole resulting from volume overload and systolic dysfunction; S4 gallop in late diastole resulting from diastolic dysfunction


Diagnosis of cardiomegaly is primarily through imaging techniques that assess the heart's size and function. Diagnostic testing includes one of the following:

  • A chest X-ray with an enlarged cardiac silhouette and a cardiothoracic ratio of more than 50% suggests cardiomegaly.[29] Further delineation of specific chamber enlargement is also possible. Right ventricle (RV) enlargement produces an upward deviation of the left apical margin, while left ventricle (LV) enlargement leads to a leftward displacement of the left heart border. Right atrial (RA) enlargement increases the right heart border convexity. Left atrial (LA) enlargement and its extension to the right leads to a "double density" sign.[30] Also, in heart failure, cephalization of the pulmonary vessels, Kerley B-lines, pulmonary edema, and pleural effusions are present.
  • A transthoracic echocardiogram can be used to assess LV, RV, atrial size, and systolic/diastolic function. It can also determine valve structure and function and wall motion changes that suggest ischemia.
  • Cardiac MRI is an emerging diagnostic modality for accurately evaluating LV and RV mass, size, and function. It can also characterize ischemic and non-ischemic causes such as myocarditis.
  • An electrocardiogram (ECG) can reveal non-specific changes, including LV/RV hypertrophy, low voltage QRS in case of fibrosis/dilated cardiomyopathy, conduction abnormality, arrhythmia, premature ventricular complexes (PVCs), ST-T wave changes, and Q waves suggestive of prior myocardial infarction (MI).
  • Serum levels of brain natriuretic peptide (pro-BNP), troponin I and T, renal function, and liver function tests are helpful in the setting of heart failure.[31]
  • Stress test and/or coronary angiogram to evaluate for coronary artery disease.
  • Often the etiology of cardiomegaly is unclear despite standard workup. In such cases, additional testing may be pursued to determine the underlying etiology.

Treatment / Management

Treatment of mild cardiomegaly centers upon the treatment of the underlying condition. Standard heart failure (HF) treatment guidelines also apply in moderate to severe cardiomegaly associated with heart failure. 

  • Patients at risk of cardiomyopathy benefit from risk factor modification such as smoking cessation, limiting alcohol intake, weight loss, exercise, and consuming a healthy diet. Recommendations include treating underlying risk factors such as hypertension, dyslipidemia, and diabetes. Other underlying conditions, including obstructive sleep apnea, arrhythmias, anemia, and thyroid disorders, also require treatment.[32]
  • Patients with early onset cardiomyopathy who are asymptomatic are managed with risk factor modification and the addition of an angiotensin-converting enzyme (ACE) inhibitor or ARB (if intolerant to ACE) and beta-blocker if there is a history of MI or reduced ejection fraction (EF).[33]
  • Patients with cardiomyopathy and symptoms of heart failure are managed with diuretics and salt restriction in addition to the above therapies.[34] All such patients should receive an ACE inhibitor or ARB (if intolerant to ACE) and a beta-blocker if they have reduced EF. An ARNI (ARB plus neprilysin inhibitor) is occasionally used instead of ACE/ARB to reduce hospitalization in heart failure and mortality. For patients with moderate to severe symptoms and reduced EF, the addition of aldosterone antagonists further reduces mortality. A hydralazine/nitrate combination, when added to ACE inhibitor, beta blocker, and diuretics, improve outcomes in Black patients. Digoxin is added in some patients to reduce the rate of hospitalization with heart failure; however, it does not impact outcomes. An ICD (implantable cardioverter defibrillator) is placed in patients with EF 35% or less to reduce mortality from sudden cardiac death. CRT (cardiac resynchronization) is performed with or without ICD in patients with EF 35% or less and moderate to severe symptoms with evidence of left bundle branch block.
  • Patients with refractory heart failure should receive optimal medical management. Also, eligible patients can be considered for cardiac transplantation and bridge therapy, such as ventricle assist devices.[35] 
  • (A1)

Of special consideration, no pharmacologic agent has shown benefit in HFpEF. The mainstay of treatment is controlling underlying conditions such as hypertension, heart rate in patients with atrial fibrillation, ischemia with medication and/or coronary intervention, and diuretics for fluid overload. Patients with asymptomatic HOCM (hypertrophic obstructive cardiomyopathy) can be safely monitored. Patients with symptoms of HF and left ventricular outflow tract obstruction may benefit from negative inotropes such as beta-blockers, calcium channel blockers, or dipyridamole. Vasodilators and diuretics should be avoided in such patients.

Some novel treatment strategies are being studied through recent evidence favoring the supplementation of endogenous antioxidants for managing diabetic cardiomyopathy. These strategies include gene therapy targeting the phosphoinositide 3-kinase signaling pathway and miRNA dysregulation. A future strategy could be to target redox stress and protective protein signaling pathways for combating the ever-rising incidence of heart failure in patients with diabetes.[36]

Differential Diagnosis

Differentials of cardiomegaly include disorders that can result in an enlarged cardiomediastinal silhouette on a frontal (or posteroanterior) chest X-ray. These include: 

  • Pericardial effusion
  • Anterior mediastinal mass
  • Prominent epicardial fat pad
  • Mediastinal widening secondary to pulmonary/aortic pathology
  • Expiratory radiograph
  • AP projection
  • Thymus tumor[37]
  • Cardiac neoplasms
  • Myocarditis


Despite the advent of new therapies, mortality remains high in patients with symptomatic HF. Roughly, 1-year mortality is 30%, while 5-year mortality is 50%. The severity of symptoms, advanced age, and HF hospitalization are significant predictors of mortality in HF.[38] Overall, the prognosis of patients with dilated cardiomyopathy is guarded. Most patients eventually end up with chronic heart failure. Many become candidates for a heart transplant or an assist device which also adds morbidity.

Almost 50% of patients are dead within five years. Mortality rates of 1% to 4% have been reported in patients with hypertrophic cardiomyopathy, but these numbers have greatly improved in the past two decades. Even though most patients have no symptoms, the first clinical presentation is often sudden death from malignant arrhythmias. The highest mortality is in young people.


As cardiomegaly can be secondary to various underlying pathologies, resulting complications tend to vary a great deal as well. The following are a few important complications to be aware of:

  • Decompensated heart failure
  • Sudden cardiac death and malignant ventricular arrhythmias[39]
  • Thromboembolism secondary to mural thrombi

Deterrence and Patient Education

Patient education regarding medication compliance, dietary restrictions, and regular follow-up is critical to achieving the best outcomes. In addition, families should go through an investigative procedure when someone is found to have hypertrophic obstructive cardiomyopathy.

Pearls and Other Issues

Cardiac transplantation is an emerging treatment for patients with refractory end-stage heart failure. Patients undergo cardiopulmonary assessment and prognostication using specific scoring systems to determine their candidacy for transplant. Patients with systemic illness, life expectancy under two years, active substance and alcohol abuse, and non-compliance with medical therapy are considered poor candidates for cardiac transplantation. Patients should have a robust psychosocial support system to qualify. A risk-benefit assessment is necessary before the patient is a candidate for the transplant list. Patients who are not candidates for a cardiac transplant can qualify for a durable ventricular assist device.[40]

Enhancing Healthcare Team Outcomes

Heart failure readmissions account for a majority of national healthcare expenditures. Support programs are operating nationwide to minimize the number of CHF-related hospitalizations and thereby reduce the economic strain. These programs utilize a collaborative approach with many integrated disciplines and providers. Some inpatient strategies include guideline-based care, discharge support by nurses, patient education, medication reconciliation by the pharmacist, and early post-discharge follow-up. A board-certified cardiology pharmacist can assist clinicians in selecting medications for blood pressure control and other factors where medication can provide ancillary benefits. Cardiology-specialized nurses are also valuable members of the interprofessional team, coordinating activities between various specialists and other clinicians and providing patient counseling. Promising outpatient strategies include interprofessional team engagement in HF clinics and disease management programs that make in-person contact with patients and provide individualized education.[41]

Cardiomegaly and HF require an interprofessional team approach that includes physicians and specialists, specialty-trained nurses, pharmacists, and therapists, all working collaboratively to bring about optimal therapeutic choices that lead to the best possible patient outcomes. This interprofessional approach requires open communication between all members of the care team and accurate, updated documentation to be effective. [Level 5]



Jefferies JL,Towbin JA, Dilated cardiomyopathy. Lancet (London, England). 2010 Feb 27;     [PubMed PMID: 20189027]


Felker GM,Thompson RE,Hare JM,Hruban RH,Clemetson DE,Howard DL,Baughman KL,Kasper EK, Underlying causes and long-term survival in patients with initially unexplained cardiomyopathy. The New England journal of medicine. 2000 Apr 13     [PubMed PMID: 10760308]


Goff ZD,Calkins H, Sudden death related cardiomyopathies - Hypertrophic cardiomyopathy. Progress in cardiovascular diseases. 2019 May - Jun     [PubMed PMID: 31004609]


Vischer AS,Castelletti S,Syrris P,McKenna WJ,Pantazis A, Heart failure in patients with arrhythmogenic right ventricular cardiomyopathy: Genetic characteristics. International journal of cardiology. 2019 Jul 1     [PubMed PMID: 30765282]


Heusch G,Libby P,Gersh B,Yellon D,Böhm M,Lopaschuk G,Opie L, Cardiovascular remodelling in coronary artery disease and heart failure. Lancet (London, England). 2014 May 31;     [PubMed PMID: 24831770]


Berk BC,Fujiwara K,Lehoux S, ECM remodeling in hypertensive heart disease. The Journal of clinical investigation. 2007 Mar;     [PubMed PMID: 17332884]


Chin CWL,Everett RJ,Kwiecinski J,Vesey AT,Yeung E,Esson G,Jenkins W,Koo M,Mirsadraee S,White AC,Japp AG,Prasad SK,Semple S,Newby DE,Dweck MR, Myocardial Fibrosis and Cardiac Decompensation in Aortic Stenosis. JACC. Cardiovascular imaging. 2017 Nov;     [PubMed PMID: 28017384]


Baguet JP,Barone-Rochette G,Tamisier R,Levy P,Pépin JL, Mechanisms of cardiac dysfunction in obstructive sleep apnea. Nature reviews. Cardiology. 2012 Dec;     [PubMed PMID: 23007221]


Cunha-Neto E,Chevillard C, Chagas disease cardiomyopathy: immunopathology and genetics. Mediators of inflammation. 2014;     [PubMed PMID: 25210230]

Level 3 (low-level) evidence


Mohty D,Damy T,Cosnay P,Echahidi N,Casset-Senon D,Virot P,Jaccard A, Cardiac amyloidosis: updates in diagnosis and management. Archives of cardiovascular diseases. 2013 Oct;     [PubMed PMID: 24070600]


Renu K,V G A,P B TP,Arunachalam S, Molecular mechanism of doxorubicin-induced cardiomyopathy - An update. European journal of pharmacology. 2018 Jan 5;     [PubMed PMID: 29074412]


Helali J,Park S,Ziaeian B,Han JK,Lankarani-Fard A, Thiamine and Heart Failure: Challenging Cases of Modern-Day Cardiac Beriberi. Mayo Clinic proceedings. Innovations, quality     [PubMed PMID: 31193878]

Level 2 (mid-level) evidence


Prinz C,Farr M,Hering D,Horstkotte D,Faber L, The diagnosis and treatment of hypertrophic cardiomyopathy. Deutsches Arzteblatt international. 2011 Apr;     [PubMed PMID: 21505608]


Hilfiker-Kleiner D,Sliwa K,Drexler H, Peripartum cardiomyopathy: recent insights in its pathophysiology. Trends in cardiovascular medicine. 2008 Jul;     [PubMed PMID: 18790387]

Level 3 (low-level) evidence


Bui AL,Horwich TB,Fonarow GC, Epidemiology and risk profile of heart failure. Nature reviews. Cardiology. 2011 Jan;     [PubMed PMID: 21060326]


Towbin JA,Lowe AM,Colan SD,Sleeper LA,Orav EJ,Clunie S,Messere J,Cox GF,Lurie PR,Hsu D,Canter C,Wilkinson JD,Lipshultz SE, Incidence, causes, and outcomes of dilated cardiomyopathy in children. JAMA. 2006 Oct 18;     [PubMed PMID: 17047217]


Maron BJ, Hypertrophic cardiomyopathy: an important global disease. The American journal of medicine. 2004 Jan 1;     [PubMed PMID: 14706671]

Level 2 (mid-level) evidence


Richard P,Charron P,Carrier L,Ledeuil C,Cheav T,Pichereau C,Benaiche A,Isnard R,Dubourg O,Burban M,Gueffet JP,Millaire A,Desnos M,Schwartz K,Hainque B,Komajda M,EUROGENE Heart Failure Project., Hypertrophic cardiomyopathy: distribution of disease genes, spectrum of mutations, and implications for a molecular diagnosis strategy. Circulation. 2003 May 6;     [PubMed PMID: 12707239]


Garfinkel AC,Seidman JG,Seidman CE, Genetic Pathogenesis of Hypertrophic and Dilated Cardiomyopathy. Heart failure clinics. 2018 Apr;     [PubMed PMID: 29525643]


Rababa'h AM,Guillory AN,Mustafa R,Hijjawi T, Oxidative Stress and Cardiac Remodeling: An Updated Edge. Current cardiology reviews. 2018 Mar 14;     [PubMed PMID: 29332590]


Piano MR, Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology. Chest. 2002 May;     [PubMed PMID: 12006456]

Level 3 (low-level) evidence


Meyers DE,Basha HI,Koenig MK, Mitochondrial cardiomyopathy: pathophysiology, diagnosis, and management. Texas Heart Institute journal. 2013     [PubMed PMID: 24082366]

Level 3 (low-level) evidence


Hilfiker-Kleiner D,Sliwa K, Pathophysiology and epidemiology of peripartum cardiomyopathy. Nature reviews. Cardiology. 2014 Jun     [PubMed PMID: 24686946]


Poliac LC,Barron ME,Maron BJ, Hypertrophic cardiomyopathy. Anesthesiology. 2006 Jan     [PubMed PMID: 16394705]


Rocklin DM, The Role of the Clinical Examination in Patients With Heart Failure: E-Z CVP. JACC. Heart failure. 2018 Nov;     [PubMed PMID: 30384921]


Williams L,Frenneaux M, Syncope in hypertrophic cardiomyopathy: mechanisms and consequences for treatment. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2007 Sep;     [PubMed PMID: 17522079]


Razi R,Estrada JR,Doll J,Spencer KT, Bedside hand-carried ultrasound by internal medicine residents versus traditional clinical assessment for the identification of systolic dysfunction in patients admitted with decompensated heart failure. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography. 2011 Dec     [PubMed PMID: 21885245]


Chinnaiyan KM,Leff CB,Marsalese DL, Constrictive pericarditis versus restrictive cardiomyopathy: challenges in diagnosis and management. Cardiology in review. 2004 Nov-Dec     [PubMed PMID: 15476569]

Level 3 (low-level) evidence


Mensah YB,Mensah K,Asiamah S,Gbadamosi H,Idun EA,Brakohiapa W,Oddoye A, Establishing the Cardiothoracic Ratio Using Chest Radiographs in an Indigenous Ghanaian Population: A Simple Tool for Cardiomegaly Screening. Ghana medical journal. 2015 Sep     [PubMed PMID: 26693191]


Sethi T,Singh AP,Singla V,Singh Y, Biatrial enlargement: an unusual cause of massive cardiomegaly. BMJ case reports. 2013 Jan 31;     [PubMed PMID: 23376674]

Level 3 (low-level) evidence


Knudsen CW,Omland T,Clopton P,Westheim A,Abraham WT,Storrow AB,McCord J,Nowak RM,Aumont MC,Duc P,Hollander JE,Wu AH,McCullough PA,Maisel AS, Diagnostic value of B-Type natriuretic peptide and chest radiographic findings in patients with acute dyspnea. The American journal of medicine. 2004 Mar 15;     [PubMed PMID: 15006584]


Oliveros-Ruiz L,Vallejo M,Diez Canseco LF,Cárdenas M,Hermosillo JA, Determinants of thyrotoxic cardiomyopathy recovery. BioMed research international. 2013     [PubMed PMID: 24106705]


McMurray J,Cohen-Solal A,Dietz R,Eichhorn E,Erhardt L,Hobbs FD,Krum H,Maggioni A,McKelvie RS,Piña IL,Soler-Soler J,Swedberg K, Practical recommendations for the use of ACE inhibitors, beta-blockers, aldosterone antagonists and angiotensin receptor blockers in heart failure: putting guidelines into practice. European journal of heart failure. 2005 Aug     [PubMed PMID: 16087129]


Philipson H,Ekman I,Forslund HB,Swedberg K,Schaufelberger M, Salt and fluid restriction is effective in patients with chronic heart failure. European journal of heart failure. 2013 Nov     [PubMed PMID: 23787719]

Level 1 (high-level) evidence


Yancy CW,Jessup M,Bozkurt B,Butler J,Casey DE Jr,Colvin MM,Drazner MH,Filippatos G,Fonarow GC,Givertz MM,Hollenberg SM,Lindenfeld J,Masoudi FA,McBride PE,Peterson PN,Stevenson LW,Westlake C, 2016 ACC/AHA/HFSA Focused Update on New Pharmacological Therapy for Heart Failure: An Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Circulation. 2016 Sep 27;     [PubMed PMID: 27208050]

Level 3 (low-level) evidence


Huynh K,Bernardo BC,McMullen JR,Ritchie RH, Diabetic cardiomyopathy: mechanisms and new treatment strategies targeting antioxidant signaling pathways. Pharmacology     [PubMed PMID: 24462787]


Calderon AM,Merchan JA,Rozo JC,Guerrero CI,Treistman B,Sulak LE,Cheong BY,Rodríguez G,Mesa A, Intrapericardial primary thymic carcinoma in a 73-year-old man. Texas Heart Institute journal. 2008;     [PubMed PMID: 19156242]

Level 3 (low-level) evidence


Ho KK,Pinsky JL,Kannel WB,Levy D, The epidemiology of heart failure: the Framingham Study. Journal of the American College of Cardiology. 1993 Oct;     [PubMed PMID: 8376698]


McKenna WJ,Behr ER, Hypertrophic cardiomyopathy: management, risk stratification, and prevention of sudden death. Heart (British Cardiac Society). 2002 Feb     [PubMed PMID: 11796562]


Mehra MR,Canter CE,Hannan MM,Semigran MJ,Uber PA,Baran DA,Danziger-Isakov L,Kirklin JK,Kirk R,Kushwaha SS,Lund LH,Potena L,Ross HJ,Taylor DO,Verschuuren EAM,Zuckermann A,International Society for Heart Lung Transplantation (ISHLT) Infectious Diseases, Pediatric and Heart Failure and Transplantation Councils., The 2016 International Society for Heart Lung Transplantation listing criteria for heart transplantation: A 10-year update. The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation. 2016 Jan     [PubMed PMID: 26776864]


Feltner C,Jones CD,Cené CW,Zheng ZJ,Sueta CA,Coker-Schwimmer EJ,Arvanitis M,Lohr KN,Middleton JC,Jonas DE, Transitional care interventions to prevent readmissions for persons with heart failure: a systematic review and meta-analysis. Annals of internal medicine. 2014 Jun 3     [PubMed PMID: 24862840]

Level 1 (high-level) evidence