Difference between revisions of "Restrictive cardiomyopathy"

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{{SK}} Infiltrative cardiomyopathy; RCM; stiff heart; stiffening of the heart; heart stiffening; stiffened heart
 
{{SK}} Infiltrative cardiomyopathy; RCM; stiff heart; stiffening of the heart; heart stiffening; stiffened heart
 
==Overview==
 
==Overview==
Restrictive cardiomyopathy (RCMP) is a rare form among other cardiomyopathies, characterized by increased stiffness of the ventricles in the presence of normal diastolic volume and normal ventricular wall thickness. It may be classified into primary i.e EMF([[endomyocardial fibrosis]]),[[Loffler's|Loffler’s endocarditis]], Idiopathic restrictive cardiomyopathy and secondary i.e, infiltrative diseases(e.g., [[amyloidosis]], [[Sarcoidosis-related myocarditis|sarcoidosis]], and [[Radiation-induced pericarditis|radiation carditis]]) and storage diseases (e.g., [[hemochromatosis]], [[Glycogen storage disorder|glycogen storage disorders]], and [[Fabry’s disease]]). Cardiac amyloidosis is the most common cause of restrictive cardiomyopathy. Mainly due to deposition of amyloid fibrils in the extracellular space and misfolding into β-pleated sheets which are antiparallel to each other making them resistant to proteolysis, and also cause oxidative stress as a result leading to myocardial damage. Sarcoidosis characterised by noncaseating granulomas formation in various tissues including heart and hemochromatosis due to excessive accumulation of iron within the cells of various organs liver, pancreas, heart, and several endocrine glands leading to cirrhosis, diabetes, heart failure, skin pigmentation are also the common causes. [[Cardiac]] [[genes]] for [[desmin]], [[Actin, alpha 1|α-actin]], [[troponin I]] and [[troponin T]] are involved in the pathogenesis of restrictive cardiomyopathy. Restrictive cardiomyopathy should be differentiated from dilated cardiomyopathy, hypertrophic cardiomyopathy, congestive heart failure. Restrictive cardiomyopathy is very rare among all other types and accounts for approximately 5% of all cases. Its prevalence varies depending on regionality, ethnicity, age, and gender. Amyloidosis affects men and women equally. The wild-type transthyretin amyloidosis is most often found in the elderly population.Common complications of restrictive cardiomyopathy include thromboembolism, rhythm abnormalities(dysrhythmias), cardiac cirrhosis, heart failure, pulmonary hypertension.Common symptoms of include dyspnea, fatigue, palpitations, syncope. [[Jugular venous distension]] is noted sometimes with kussmaul sign and [[Hepatojugular reflux]].S3 and S4 gallops seen. ECG shows [[Low QRS voltage|Low QRS voltages]], [[Conduction disorders|conduction disturbances]], [[Nonspecific ST-Segment and T-Wave Changes|nonspecific ST abnormalities]]. Transmitral spectral [[Doppler]] often shows restrictive filling pattern and [[Ejection fraction]] ([[Ejection fraction|EF]]) is normal. The main purpose of treatment in restrictive cardiomyopathy (RCM) is to reduce [[symptoms]] by decreasing the elevated filling pressures without significantly lowering the [[cardiac output]].[[Pharmacologic]] therapy may include [[Beta blockers]], [[Amiodarone]], Cardioselective [[calcium channel blockers], [[Diuretics]], [[Anticoagulants]] for [[patients]] with [[atrial fibrillation]], [[Melphalan]] (for antiplasma cell therapy in systemic [[amyloidosis]]), [[Chemotherapy]] (in [[amyloidosis]]). Other approaches like [[Pacemaker]] implantation and endomyocardectomy are also available.
+
Restrictive cardiomyopathy (RCMP) is a rare form among other cardiomyopathies, characterized by increased stiffness of the ventricles in the presence of normal diastolic volume and normal ventricular wall thickness. It may be classified into primary i.e EMF([[endomyocardial fibrosis]]),[[Loffler's|Loffler’s endocarditis]], Idiopathic restrictive cardiomyopathy and secondary i.e, infiltrative diseases(e.g., [[amyloidosis]], [[Sarcoidosis-related myocarditis|sarcoidosis]], and [[Radiation-induced pericarditis|radiation carditis]]) and storage diseases (e.g., [[hemochromatosis]], [[Glycogen storage disorder|glycogen storage disorders]], and [[Fabry’s disease]]). Cardiac amyloidosis is the most common cause of restrictive cardiomyopathy. Mainly due to deposition of amyloid fibrils in the extracellular space and misfolding into β-pleated sheets which are antiparallel to each other making them resistant to proteolysis, and also cause oxidative stress as a result leading to myocardial damage. Sarcoidosis characterized by noncaseating granulomas formation in various tissues including heart and hemochromatosis due to excessive accumulation of iron within the cells of various organs liver, pancreas, heart, and several endocrine glands leading to cirrhosis, diabetes, heart failure, skin pigmentation is also the common causes. [[Cardiac]] [[genes]] for [[desmin]], [[Actin, alpha 1|α-actin]], [[troponin I]] and [[troponin T]] are involved in the pathogenesis of restrictive cardiomyopathy. Restrictive cardiomyopathy should be differentiated from dilated cardiomyopathy, hypertrophic cardiomyopathy, congestive heart failure. Restrictive cardiomyopathy is very rare among all other types and accounts for approximately 5% of all cases. Its prevalence varies depending on regionality, ethnicity, age, and gender. Amyloidosis affects men and women equally. The wild-type transthyretin amyloidosis is most often found in the elderly population. Common complications of restrictive cardiomyopathy include thromboembolism, rhythm abnormalities(dysrhythmias), cardiac cirrhosis, heart failure, pulmonary hypertension. Common symptoms include dyspnea, fatigue, palpitations, syncope. [[Jugular venous distension]] is noted sometimes with Kussmaul sign and [[Hepatojugular reflux]].S3 and S4 gallops seen. ECG shows [[Low QRS voltage|Low QRS voltages]], [[Conduction disorders|conduction disturbances]], [[Nonspecific ST-Segment and T-Wave Changes|nonspecific ST abnormalities]]. Transmitral spectral [[Doppler]] often shows restrictive filling pattern and [[Ejection fraction]] ([[Ejection fraction|EF]]) is normal. The main purpose of treatment in restrictive cardiomyopathy (RCM) is to reduce [[symptoms]] by decreasing the elevated filling pressures without significantly lowering the [[cardiac output]].[[Pharmacologic]] therapy may include [[Beta blockers]], [[Amiodarone]], Cardioselective [[calcium channel blockers], [[Diuretics]], [[Anticoagulants]] for [[patients]] with [[atrial fibrillation]], [[Melphalan]] (for antiplasma cell therapy in systemic [[amyloidosis]]), [[Chemotherapy]] (in [[amyloidosis]]). Other approaches like [[Pacemaker]] implantation and endomyocardectomy are also available.
  
 
==Historical Perspective==
 
==Historical Perspective==
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==Gross Pathology==
 
==Gross Pathology==
 
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
[[File:Restrictive cardiomyopathy.png|400px|none|thumb|Left side of the heart from a 3-year-old castrated male domestic short-haired catwith the endomyocardial form of restrictive cardiomyopathy (RCM), showing extensiveendocardial fibrosis involving substantial portions of the left ventricular cavity,Affiliation: Laboratory of Veterinary Clinical Oncology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu, Tokyo 183-8509, Japan.https://openi.nlm.nih.gov/detailedresult?img=PMC4905831_jvms-78-781-g001&query=restrictive%20cardiomyopathy&it=xg&req=4&npos=2]]
+
[[File:Restrictive cardiomyopathy.png|400px|none|thumb|Left side of the heart from a 3-year-old castrated male domestic short-haired catwith the endomyocardial form of restrictive cardiomyopathy (RCM), showing extensiveendocardial fibrosis involving substantial portions of the left ventricular cavity, Affiliation: Laboratory of Veterinary Clinical Oncology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu, Tokyo 183-8509, Japan.https://openi.nlm.nih.gov/detailedresult?img=PMC4905831_jvms-78-781-g001&query=restrictive%20cardiomyopathy&it=xg&req=4&npos=2]]
  
 
==Microscopic Pathology==
 
==Microscopic Pathology==
On microscopic histopathological analysis restrictive cardiomyopathy will show features suggestive of the cause.
+
On microscopic histopathological analysis, restrictive cardiomyopathy will show features suggestive of the cause.
 
*Cardiac Amyloidosis:
 
*Cardiac Amyloidosis:
**On H&E stain it shows pink color and demonstrates apple-green birefringence when viewed under polarized light.  
+
**On H&E stain it shows the pink color and demonstrates apple-green birefringence when viewed under polarized light.  
 
[[File:Cardiac amyloidosis very high mag he.jpg|400px|none|thumb|The micrograph shows amyloid (extracellular fluffy pink material) and abundant lipofuscin (yellow granular material), Nephron [CC BY-SA 3.0 (https://creativecommons.org/licenses/bysa/3.0)],https://upload.wikimedia.org/wikipedia/commons/1/16/Cardiac_amyloidosis_very_high_mag_he.jpg,|https://commons.wikimedia.org/wiki/File:Cardiac_amyloidosis_very_high_mag_he.jpg]]
 
[[File:Cardiac amyloidosis very high mag he.jpg|400px|none|thumb|The micrograph shows amyloid (extracellular fluffy pink material) and abundant lipofuscin (yellow granular material), Nephron [CC BY-SA 3.0 (https://creativecommons.org/licenses/bysa/3.0)],https://upload.wikimedia.org/wikipedia/commons/1/16/Cardiac_amyloidosis_very_high_mag_he.jpg,|https://commons.wikimedia.org/wiki/File:Cardiac_amyloidosis_very_high_mag_he.jpg]]
 
*Sarcoidosis:
 
*Sarcoidosis:

Latest revision as of 18:11, 22 January 2020


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Synonyms and Keywords: Infiltrative cardiomyopathy; RCM; stiff heart; stiffening of the heart; heart stiffening; stiffened heart

Overview

Restrictive cardiomyopathy (RCMP) is a rare form among other cardiomyopathies, characterized by increased stiffness of the ventricles in the presence of normal diastolic volume and normal ventricular wall thickness. It may be classified into primary i.e EMF(endomyocardial fibrosis),Loffler’s endocarditis, Idiopathic restrictive cardiomyopathy and secondary i.e, infiltrative diseases(e.g., amyloidosis, sarcoidosis, and radiation carditis) and storage diseases (e.g., hemochromatosis, glycogen storage disorders, and Fabry’s disease). Cardiac amyloidosis is the most common cause of restrictive cardiomyopathy. Mainly due to deposition of amyloid fibrils in the extracellular space and misfolding into β-pleated sheets which are antiparallel to each other making them resistant to proteolysis, and also cause oxidative stress as a result leading to myocardial damage. Sarcoidosis characterized by noncaseating granulomas formation in various tissues including heart and hemochromatosis due to excessive accumulation of iron within the cells of various organs liver, pancreas, heart, and several endocrine glands leading to cirrhosis, diabetes, heart failure, skin pigmentation is also the common causes. Cardiac genes for desmin, α-actin, troponin I and troponin T are involved in the pathogenesis of restrictive cardiomyopathy. Restrictive cardiomyopathy should be differentiated from dilated cardiomyopathy, hypertrophic cardiomyopathy, congestive heart failure. Restrictive cardiomyopathy is very rare among all other types and accounts for approximately 5% of all cases. Its prevalence varies depending on regionality, ethnicity, age, and gender. Amyloidosis affects men and women equally. The wild-type transthyretin amyloidosis is most often found in the elderly population. Common complications of restrictive cardiomyopathy include thromboembolism, rhythm abnormalities(dysrhythmias), cardiac cirrhosis, heart failure, pulmonary hypertension. Common symptoms include dyspnea, fatigue, palpitations, syncope. Jugular venous distension is noted sometimes with Kussmaul sign and Hepatojugular reflux.S3 and S4 gallops seen. ECG shows Low QRS voltages, conduction disturbances, nonspecific ST abnormalities. Transmitral spectral Doppler often shows restrictive filling pattern and Ejection fraction (EF) is normal. The main purpose of treatment in restrictive cardiomyopathy (RCM) is to reduce symptoms by decreasing the elevated filling pressures without significantly lowering the cardiac output.Pharmacologic therapy may include Beta blockers, Amiodarone, Cardioselective [[calcium channel blockers], Diuretics, Anticoagulants for patients with atrial fibrillation, Melphalan (for antiplasma cell therapy in systemic amyloidosis), Chemotherapy (in amyloidosis). Other approaches like Pacemaker implantation and endomyocardectomy are also available.

Historical Perspective

Classification

Pathophysiology

Pathogenesis

Cardiac Amyloidosis

  • It is the most common cause of restrictive cardiomyopathy(RCM).
  • Mainly due to deposition of amyloid fibrils in the extracellular space and misfolding into β-pleated sheets which are antiparallel to each other making them resistant to proteolysis, and also cause oxidative stress as a result leading to myocardial damage.

Sarcoidosis

  • Characterised by noncaseating granulomas formation in various tissues including heart.
  • The usual location is basal septum, AV node, bundle of His, the ventricular free walls, and papillary muscles.
  • Formation of granuloma includes 3 histological stages: edema, granulomatous infiltration, and fibrosis.

Hemochromatosis

  • Due to excessive accumulation of iron within the cells of various organs liver, pancreas, heart, and several endocrine glands leading to cirrhosis, diabetes, heart failure, skin pigmentation.

Genetics

Genes involved in the pathogenesis of restrictive cardiomyopathy include[9][10][11][12]:

Gross Pathology

On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Left side of the heart from a 3-year-old castrated male domestic short-haired catwith the endomyocardial form of restrictive cardiomyopathy (RCM), showing extensiveendocardial fibrosis involving substantial portions of the left ventricular cavity, Affiliation: Laboratory of Veterinary Clinical Oncology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu, Tokyo 183-8509, Japan.https://openi.nlm.nih.gov/detailedresult?img=PMC4905831_jvms-78-781-g001&query=restrictive%20cardiomyopathy&it=xg&req=4&npos=2

Microscopic Pathology

On microscopic histopathological analysis, restrictive cardiomyopathy will show features suggestive of the cause.

  • Cardiac Amyloidosis:
    • On H&E stain it shows the pink color and demonstrates apple-green birefringence when viewed under polarized light.
  • Sarcoidosis:
    • Consists of granulomas with macrophages and epithelioid histiocytes and lymphocytes.
  • Niemann-Pick: foam cells are seen
  • Mucopolysaccharidosis type II: glycosaminoglycans
  • Hereditary hemochromatosis: Deposition of iron is seen
  • Gaucher disease: Gaucher cells (lipid-laden macrophages) are seen

Causes

The main Causes of restrictive cardiomyopathy are enlisted below:[13][14]

Differentiating restrictive cardiomyopathy from Other Diseases

Restrictive cardiomyopathy should be differentiated from dilated cardiomyopathy, hypertrophic cardiomyopathy, congestive heart failure ect [14],[13]


Differentiating restrictive cardiomyopathy from Other Diseases
Type of disease History Physical examination Chest X-ray ECG 2D echo Doppler echo CT MRI Catheterization hemodynamics Biopsy
Restrictive cardiomyopathy[14][9][13] Systemic disease (e.g., sarcoidosis, hemochromatosis). Atrial dilatation Low QRS voltages (mainly amyloidosis), conduction disturbances, nonspecific ST abnormalities ± Wall and valvular thickening, sparkling myocardium Decreased variation in mitral and/or tricuspid inflow E velocity, increased hepatic vein inspiratory diastolic flow reversal, presence of mitral and tricuspid regurgitation Normal pericardium Measurement of iron overload, various types of LGE (late gadolinium enhancement) LVEDP – RVEDP ≥ 5 mmHg

RVSP ≥ 55 mmHg

RVEDP/RVSP ≤ 0.33

May reveal underlying cause.
Constrictive pericarditis[15][16][16]
  • Thickened pericardium
  • LVEDP – RVEDP < 5 mmHg
  • RVSP < 55 mmHg
  • RVEDP/RVSP > 0.33
  • Inspiratory decrease in RAP < 5 mmHg
  • Systolic area index > 1.1 (Ref CP in the modern era)
  • Left ventricular height of rapid filling wave > 7 mmHg
  • Normal myocardium
Hypertrophic cardiomyopathy(HCM)[17][18]
Dilated Cardiomyopathy[19][20][21][22]
  • LV dilation with diffuse hypokinetic walls

Epidemiology and Demographics

Incidence

Restrictive cardiomyopathy is very rare among all other types and accounts for approximately 5% of all cases.[23][24]

Prevalance

  • Its prevalence varies depending on regionality, ethnicity, age, and gender.
  • Amyloidosis: It affects men and women equally. The wild-type transthyretin amyloidosis is most often found in the elderly population.
  • Sarcoidosis: More common in women than men. The highest prevalence is among black women. The highest incidence worldwide is in Japan.
  • Hemochromatosis: Affects both men and women equally.
  • Loffler endocarditis: More Common in tropical climates and sub-Saharan Africa.

Risk Factors

  • Any family history of restrictive cardiomyopathy[25][26]
  • Inherited diseases (such as hereditary hemochromatosis, Fabry disease, mutant-type [hereditary] TTR amyloidosis, etc.)
  • Increased number of blood transfusions leading to secondary hemochromatosis.
  • Prior anthracycline use in childhood, exposure to other toxic agents.
  • Eosinophilic syndrome or chronic parasitic infection
  • Exposure to any radiation to the chest.

Screening

Natural History, Complications, and Prognosis

Natural History

  • The symptoms of (disease name) usually develop in the first/ second/ third decade of life, and start with symptoms such as ___.
  • The symptoms of (disease name) typically develop ___ years after exposure to ___.
  • If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].

Complications

  • Common complications of restrictive cardiomyopathy include:
    • Thromboembolism
    • Rhythm abnormalities(dysrhythmias)
    • Cardiac cirrhosis
    • Heart failure
    • Pulmonary hypertension

Prognosis

  • Restrictive cardiomyopathy (RCM) has the worst prognosis among all types of cardiomyopathies.
  • Prognosis is generally poor, and the 2/5-year mortality rate of patients is approximately 50% and 70%, respectively.
  • There is an estimated 2-5 year survival rate after diagnosis.

Diagnosis

Diagnostic Study of Choice

History and Symptoms

  • The majority of patients with [disease name] are asymptomatic.

OR

  • The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].
  • Symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. 

History

Patients with [disease name]] may have a positive history of:

  • [History finding 1]
  • [History finding 2]
  • [History finding 3]

Common Symptoms

Common symptoms of include:

  • Dyspnea
  • Fatigue
  • Limited exercise capacity
  • Palpitations
  • Syncope

Less Common Symptoms

Less common symptoms of restrictive cardiomyopathy include

  • Angina

Physical Examination

Physical examination of patients with restrictive cardiomyopathy is usually abnormal with characteristic findings in cardiovascular and pulmonary systems.

Appearance of the Patient

  • Patients with restrictive cardiomyopathy usually appear normal.

Vital Signs

They are usually with in normal limitis.

Skin

  • Skin examination of patients with restrictive cardiomyopathy is usually normal except in hemochromatosis which may show classic bronze skin

HEENT

  • HEENT examination of patients with restrictive cardiomyopathy is usually normal.

Neck

Lungs

  • Fine/coarse crackles upon auscultation of the lung bases/apices unilaterally/bilaterally
  • Rhonchi

Heart

Abdomen

Back

  • Back examination of patients with restrictive cardiomyopathy is usually normal.

Genitourinary

  • Genitourinary examination of patients with restrictive cardiomyopathy is usually normal.

Neuromuscular

  • Neuromuscular examination of patients with restrictive cardiomyopathy is usually normal.

Extremities

  • Peripheral edema of the lower extremities

Laboratory Findings

Electrocardiogram

Shown below is an example of restrictive cardiomyopathy with low voltage and flipped anterior T waves.

Restrictive Cardiomyopathy.jpg

X-ray

A chest X-ray may show atrial dilatation most of the times.

Echocardiography and Ultrasound

Echocardiography may be helpful in the diagnosis of restrictive cardiomyopathy. Findings on an echocardiography suggestive of restrictive cardiomyopathy include:

CT scan

MRI

Other Imaging Findings

  • Radionuclide imaging using single-photon emission computed tomography (SPECT), or positron emission tomography (PET), is also used for the diagnostic work-up of amyloidosis.[31][32][33][34]
  • An increased myocardial uptake of Tc-99m pyrophosphate or Tc-99m 3,3-diphosphono-1,2-propanodicarboxylic acid helps to identify patients with familial transthyretin-related amyloidosis(ATTR) and also it can differentiate them from those with light chain amyloid(AL).
  • Radionuclide imaging with 18fluorodeoxyglucose- (FDG-) PET is recently being used to assist in the diagnosis of cardiac sarcoidosis.
  • Decrease in myocardial perfusion with enhanced 18FDG uptake is consistent with inflammation, while decreased perfusion with reduced 18FDG uptake is associated with scarring.

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

References

  1. GOODWIN JF, GORDON H, HOLLMAN A, BISHOP MB (January 1961). "Clinical aspects of cardiomyopathy". Br Med J. 1 (5219): 69–79. doi:10.1136/bmj.1.5219.69. PMC 1952892. PMID 13707066.
  2. BRIGDEN W (December 1957). "Uncommon myocardial diseases: the non-coronary cardiomyopathies". Lancet. 273 (7008): 1243–9. doi:10.1016/s0140-6736(57)91537-4. PMID 13492617.
  3. "Report of the WHO/ISFC task force on the definition and classification of cardiomyopathies". Br Heart J. 44 (6): 672–3. December 1980. doi:10.1136/hrt.44.6.672. PMC 482464. PMID 7459150.
  4. 4.0 4.1 4.2 Sisakian H (June 2014). "Cardiomyopathies: Evolution of pathogenesis concepts and potential for new therapies". World J Cardiol. 6 (6): 478–94. doi:10.4330/wjc.v6.i6.478. PMC 4072838. PMID 24976920.
  5. McCartan C, Mason R, Jayasinghe SR, Griffiths LR (2012). "Cardiomyopathy classification: ongoing debate in the genomics era". Biochem Res Int. 2012: 796926. doi:10.1155/2012/796926. PMC 3423823. PMID 22924131.
  6. Nakata M, Koga Y (January 2000). "[Definition and classification of cardiomyopathies and specific cardiomyopathies]". Nippon Rinsho (in Japanese). 58 (1): 7–11. PMID 10885280.
  7. Thiene G, Corrado D, Basso C (October 2004). "Cardiomyopathies: is it time for a molecular classification?". Eur. Heart J. 25 (20): 1772–5. doi:10.1016/j.ehj.2004.07.026. PMID 15474691.
  8. Cecchi F, Tomberli B, Olivotto I (2012). "Clinical and molecular classification of cardiomyopathies". Glob Cardiol Sci Pract. 2012 (1): 4. doi:10.5339/gcsp.2012.4. PMC 4239818. PMID 25610835.
  9. 9.0 9.1 Mogensen J, Kubo T, Duque M, Uribe W, Shaw A, Murphy R, Gimeno JR, Elliott P, McKenna WJ (January 2003). "Idiopathic restrictive cardiomyopathy is part of the clinical expression of cardiac troponin I mutations". J. Clin. Invest. 111 (2): 209–16. doi:10.1172/JCI16336. PMC 151864. PMID 12531876.
  10. Burke MA, Cook SA, Seidman JG, Seidman CE (December 2016). "Clinical and Mechanistic Insights Into the Genetics of Cardiomyopathy". J. Am. Coll. Cardiol. 68 (25): 2871–2886. doi:10.1016/j.jacc.2016.08.079. PMC 5843375. PMID 28007147.
  11. Parvatiyar MS, Pinto JR, Dweck D, Potter JD (2010). "Cardiac troponin mutations and restrictive cardiomyopathy". J. Biomed. Biotechnol. 2010: 350706. doi:10.1155/2010/350706. PMC 2896668. PMID 20617149.
  12. Kostareva A, Gudkova A, Sjöberg G, Mörner S, Semernin E, Krutikov A, Shlyakhto E, Sejersen T (January 2009). "Deletion in TNNI3 gene is associated with restrictive cardiomyopathy". Int. J. Cardiol. 131 (3): 410–2. doi:10.1016/j.ijcard.2007.07.108. PMID 18006163.
  13. 13.0 13.1 13.2 Hong JA, Kim MS, Cho MS, Choi HI, Kang DH, Lee SE, Lee GY, Jeon ES, Cho JY, Kim KH, Yoo BS, Lee JY, Kim WJ, Kim KH, Chung WJ, Lee JH, Cho MC, Kim JJ (September 2017). "Clinical features of idiopathic restrictive cardiomyopathy: A retrospective multicenter cohort study over 2 decades". Medicine (Baltimore). 96 (36): e7886. doi:10.1097/MD.0000000000007886. PMC 6393124. PMID 28885342.
  14. 14.0 14.1 14.2 14.3 Rammos A, Meladinis V, Vovas G, Patsouras D (2017). "Restrictive Cardiomyopathies: The Importance of Noninvasive Cardiac Imaging Modalities in Diagnosis and Treatment-A Systematic Review". Radiol Res Pract. 2017: 2874902. doi:10.1155/2017/2874902. PMC 5705874. PMID 29270320.
  15. Ramasamy V, Mayosi BM, Sturrock ED, Ntsekhe M (September 2018). "Established and novel pathophysiological mechanisms of pericardial injury and constrictive pericarditis". World J Cardiol. 10 (9): 87–96. doi:10.4330/wjc.v10.i9.87. PMC 6189073. PMID 30344956.
  16. 16.0 16.1 Biçer M, Özdemir B, Kan İ, Yüksel A, Tok M, Şenkaya I (November 2015). "Long-term outcomes of pericardiectomy for constrictive pericarditis". J Cardiothorac Surg. 10: 177. doi:10.1186/s13019-015-0385-8. PMC 4662820. PMID 26613929.
  17. Kubo T, Gimeno JR, Bahl A, Steffensen U, Steffensen M, Osman E, Thaman R, Mogensen J, Elliott PM, Doi Y, McKenna WJ (June 2007). "Prevalence, clinical significance, and genetic basis of hypertrophic cardiomyopathy with restrictive phenotype". J. Am. Coll. Cardiol. 49 (25): 2419–26. doi:10.1016/j.jacc.2007.02.061. PMID 17599605.
  18. Marian AJ, Braunwald E (September 2017). "Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Clinical Manifestations, Diagnosis, and Therapy". Circ. Res. 121 (7): 749–770. doi:10.1161/CIRCRESAHA.117.311059. PMC 5654557. PMID 28912181.
  19. Francone M (2014). "Role of cardiac magnetic resonance in the evaluation of dilated cardiomyopathy: diagnostic contribution and prognostic significance". ISRN Radiol. 2014: 365404. doi:10.1155/2014/365404. PMC 4045555. PMID 24967294.
  20. McNally EM, Mestroni L (September 2017). "Dilated Cardiomyopathy: Genetic Determinants and Mechanisms". Circ. Res. 121 (7): 731–748. doi:10.1161/CIRCRESAHA.116.309396. PMC 5626020. PMID 28912180.
  21. Tayal U, Prasad S, Cook SA (February 2017). "Genetics and genomics of dilated cardiomyopathy and systolic heart failure". Genome Med. 9 (1): 20. doi:10.1186/s13073-017-0410-8. PMC 5322656. PMID 28228157.
  22. Mitrut R, Stepan AE, Pirici D (2018). "Histopathological Aspects of the Myocardium in Dilated Cardiomyopathy". Curr Health Sci J. 44 (3): 243–249. doi:10.12865/CHSJ.44.03.07. PMC 6311227. PMID 30647944.
  23. Costabel U, Wessendorf TE, Bonella F (June 2017). "[Epidemiology and Clinical Presentation of Sarcoidosis]". Klin Monbl Augenheilkd (in German). 234 (6): 790–795. doi:10.1055/s-0042-105569. PMID 27454307.
  24. Connor DH, Somers K, Hutt MS, Manion WC, D'Arbela PG (November 1967). "Endomyocardial fibrosis in Uganda (Davies' disease). 1. An epidemiologic, clinical, and pathologic study". Am. Heart J. 74 (5): 687–709. doi:10.1016/0002-8703(67)90509-1. PMID 4861733.
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