Cardiac fibrosis: Difference between revisions
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===Laboratory Findings=== | ===Laboratory Findings=== | ||
Biomarkers of fibrosis can be detected in blood tests.<ref name="pmid30344312">{{cite journal| author=Espeland T, Lunde IG, H Amundsen B, Gullestad L, Aakhus S| title=Myocardial fibrosis. | journal=Tidsskr Nor Laegeforen | year= 2018 | volume= 138 | issue= 16 | pages= | pmid=30344312 | doi=10.4045/tidsskr.17.1027 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30344312 }} </ref> | |||
===Electrocardiogram=== | ===Electrocardiogram=== | ||
Revision as of 22:05, 7 February 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Niloofarsadaat Eshaghhosseiny, MD[2]
Synonyms and keywords:Davies disease
Overview
Cardiac fibrosis refers to an abnormal thickening of the heart valves due to inappropriate proliferation of cardiac fibroblasts.
Historical Perspective
First description for endomyocardial fibrosis was in 1948 by Davies in Uganda.[1] Endomyocardial fibrosis was first discovered in 1984 in Ugenda.[1]
There have been several outbreaks of endomycardial fibrosis, including Africa,Asia,and South America.[1]
Classification
Myocardial fibrosis may be classified into two groups:interstitial fibrosis (diffuse),replacement fibrosis (scar) .[2] The interstitial fibrosis divided in to two subclasses:reactive and infiltrative.[3]
Pathophysiology
It is thought that cardiac fibrosis is the result of remodeling of extracellular and deposition of extracellular matrix that causes to impaired muscles function.[3] Also cardiac fibrosis is mediated by cardial fibrosis include Eosinophilia, Infectious such as toxoplasma, malaria,helminthic parasites,rheumatic fever,Environmental exposure such as cerium ,casava ,Immunologic and Genetic.[4][5][6] [7][8][9]
Causes
The most common cause of cardiac fibrosis is cardiac fibrotic scars that usually occure after myocardial infarction . other causes of cardiac fibrotic scars include , hypertensive heart disease,diabetic hypertrophic cardiomyopathy and ,idiopathic dilated cardiomyopathy.[3]
Differentiating ((Page name)) from other Diseases
[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].
OR
[Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].
Epidemiology and Demographics
Endomyocardial fibrosis is the most cause of heart failure,that up 20% of cases are in endmic area.[10]
Recently the incidence of EMF has been decreased.[10]
In one of the researches in 2008 the prevalence of EMF was 19.8%.[11]
The incidence of EMF is approximately 10,000,000 people worldwide.[11]
The incidence of endomycardial fibrosis is more common in Africa,Asia and South America.[1]
The most cases in Uganda,Mozambique and some west of Africa are Endemic for EMF.[1] Although sporadic cases have been reported in Congo and Malawi.[1] In India the most cases are in rain forest area of Kerala State.[1] In china we can see the high frequency of EMF in Guanxi.[1] And in south of America , Brazil and Colombia are the most frequent area.[1]
Patients of all age groups may develop EMF butcommonly affects young adults between 10 to 30 years old with poor socioeconomic status.[1]
In some researches EMF affects men and women equally but prevalence of EMF in Uganda,is 2-fold higher in women of childbearing age .[1]
The majority of EMF cases are reported in Africa.[1]
Risk Factors
Common risk factors in the development of cardiac fibrosis may be occupational, environmental, genetic, and viral.[3]
Common risk factors in the development of cardiac fibrosis include Obesity, Metabolic dysfunction,DM,HTN.[12]
Screening
There is insufficient evidence to recommend routine screening for cardiac fibrosis but in high risk individuals or in endemic areas we can use echocardiography as screening.[13]
Natural History, Complications, and Prognosis
Common complications of cardiac fibrosis include stifness of left ventricle,heart failure,arrihythmias.[14]
Prognosis is very poor.[13]
Diagnosis
Diagnostic Study of Choice
The diagnosis and severity of cardiac fibrosis according to classification is made when we have 2 major criteria or 1 major criterion with 2 minor criteria.(table below)[1]
| criterion | score |
|---|---|
| MAJOR CRITERIA | |
| Endomyocardial plaques >2mm in thickness | 2 |
| Thin(<1mm) endomyocardial patches affecting >1 ventricular wall | 3 |
| Oblitration of the right ventricular or left ventricular apex | 4 |
| Thrombi or spontaneous contrast without sever ventricular dysfunction | 4 |
| Retraction of right venticular apex (right ventricular apical notch) | 4 |
| Atrioventricular valve dysfunction caused by adhession of the valvular apparatus | 1-4 |
| MINOR CRITERIA | |
| Thin endomyocardial patches localized to 1 ventricular wall | 1 |
| Restrictive flow pattern across mitral or tricuspid valve | 2 |
| Pulmonary valve diastolic opening | 2 |
| Diffuse thickening of the anterior mitral leaflet | 1 |
| Enlarged atrium with normal-sized ventricle | 2 |
| M-movment of the interventricular septum and flat posterior wall | 1 |
| Enhanced density of the moderator or other intraventricular bands | 1 |
History and Symptoms
EMF symptoms divided in to two phases:Acute , Chronic The most common symptoms of acute include febrile illness ,pancarditis,eosinophilia,dyspenea,itching, pericardial effusion. Symptoms of chronic phase deponds on biventricular or isolated right/left ventricular involvement(RV heart failure/LV heart failure).[1] In right ventricular involvement most common symptoms are :systemic venous HTN,facial edema,exophtalmos,jugular vein distention,gross hepatomegaly,splenomegaly and abdomonal swelling.[1]
Physical Examination
Patients with cardiac fibrosis usually appear ill. Common physical examination findings of cardial fibrosis causing heart failure include,facial and periorbital edema, acscites,jvp distention,fever,pericardial friction rub due to pericarditis and non specific signs in chronic phase are clubbing of digits,growth retardation ,testicular atrophy, cachexia.[1]
Laboratory Findings
Biomarkers of fibrosis can be detected in blood tests.[2]
Electrocardiogram
There are no ECG findings associated with [disease name].
OR
An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
X-ray
There are no x-ray findings associated with [disease name].
OR
An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
Echocardiography or Ultrasound
There are no echocardiography/ultrasound findings associated with [disease name].
OR
Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
CT scan
There are no CT scan findings associated with [disease name].
OR
[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
MRI
There are no MRI findings associated with [disease name].
OR
[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
Other Imaging Findings
There are no other imaging findings associated with [disease name].
OR
[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
There are no other diagnostic studies associated with [disease name].
OR
[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
There is no treatment for [disease name]; the mainstay of therapy is supportive care.
OR
Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].
OR
The majority of cases of [disease name] are self-limited and require only supportive care.
OR
[Disease name] is a medical emergency and requires prompt treatment.
OR
The mainstay of treatment for [disease name] is [therapy].
OR
The optimal therapy for [malignancy name] depends on the stage at diagnosis.
OR
[Therapy] is recommended among all patients who develop [disease name].
OR
Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].
OR
Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].
OR
Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].
OR
Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].
Surgery
Surgical intervention is not recommended for the management of [disease name].
OR
Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]
OR
The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].
OR
The feasibility of surgery depends on the stage of [malignancy] at diagnosis.
OR
Surgery is the mainstay of treatment for [disease or malignancy].
Primary Prevention
There are no established measures for the primary prevention of [disease name].
OR
There are no available vaccines against [disease name].
OR
Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
OR
[Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].
Secondary Prevention
There are no established measures for the secondary prevention of [disease name].
OR
Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 Grimaldi A, Mocumbi AO, Freers J, Lachaud M, Mirabel M, Ferreira B; et al. (2016). "Tropical Endomyocardial Fibrosis: Natural History, Challenges, and Perspectives". Circulation. 133 (24): 2503–15. doi:10.1161/CIRCULATIONAHA.115.021178. PMID 27297343.
- ↑ 2.0 2.1 Espeland T, Lunde IG, H Amundsen B, Gullestad L, Aakhus S (2018). "Myocardial fibrosis". Tidsskr Nor Laegeforen. 138 (16). doi:10.4045/tidsskr.17.1027. PMID 30344312.
- ↑ 3.0 3.1 3.2 3.3 Hinderer S, Schenke-Layland K (2019). "Cardiac fibrosis - A short review of causes and therapeutic strategies". Adv Drug Deliv Rev. 146: 77–82. doi:10.1016/j.addr.2019.05.011. PMID 31158407.
- ↑ Weller PF, Bubley GJ (1994). "The idiopathic hypereosinophilic syndrome". Blood. 83 (10): 2759–79. PMID 8180373.
- ↑ Ijaola O, Falase AO (1990). "Distribution of antibodies against Coxsackie B viruses, arboviruses and Toxoplasma gondii among patients with endomyocardial fibrosis (EMF) compared with normal subjects from EMF endemic and non-endemic zones of Nigeria". Afr J Med Med Sci. 19 (2): 93–103. PMID 2165348.
- ↑ Valiathan SM, Kartha CC (1990). "Endomyocardial fibrosis--the possible connexion with myocardial levels of magnesium and cerium". Int J Cardiol. 28 (1): 1–5. doi:10.1016/0167-5273(90)90002-m. PMID 2194985.
- ↑ Sezi CL (1996). "Effects of cassava diet on Cercopithecus aethiops livers: a case for cassava as the cause of both tropical splenomegaly syndrome (TSS) and endomyocardial fibrosis (EMF)". East Afr Med J. 73 (5 Suppl): S24–8. PMID 8756024.
- ↑ Mocumbi AO, Latif N, Yacoub MH (2010). "Presence of circulating anti-myosin antibodies in endomyocardial fibrosis". PLoS Negl Trop Dis. 4 (4): e661. doi:10.1371/journal.pntd.0000661. PMC 2857887. PMID 20422043.
- ↑ Lowenthal MN (1978). "Endomyocardial fibrosis: familial and other cases from northern Zambia". Med J Zambia. 12 (1): 2–7. PMID 757895.
- ↑ 10.0 10.1 Duraes AR, de Souza Lima Bitar Y, Roever L, Neto MG (2019). "Endomyocardial fibrosis: past, present, and future". Heart Fail Rev. doi:10.1007/s10741-019-09848-4. PMID 31414216.
- ↑ 11.0 11.1 Mocumbi AO, Ferreira MB, Sidi D, Yacoub MH (2008). "A population study of endomyocardial fibrosis in a rural area of Mozambique". N Engl J Med. 359 (1): 43–9. doi:10.1056/NEJMoa0708629. PMID 18596273.
- ↑ Cavalera M, Wang J, Frangogiannis NG (2014). "Obesity, metabolic dysfunction, and cardiac fibrosis: pathophysiological pathways, molecular mechanisms, and therapeutic opportunities". Transl Res. 164 (4): 323–35. doi:10.1016/j.trsl.2014.05.001. PMC 4180761. PMID 24880146.
- ↑ 13.0 13.1 "Correction". Circulation. 131 (24): e535. 2015. doi:10.1161/CIR.0000000000000219. PMID 26078378.
- ↑ Ma ZG, Yuan YP, Wu HM, Zhang X, Tang QZ (2018). "Cardiac fibrosis: new insights into the pathogenesis". Int J Biol Sci. 14 (12): 1645–1657. doi:10.7150/ijbs.28103. PMC 6216032. PMID 30416379.
Pathophysiology
These cells secrete collagen, and normally function to provide structural support for the heart. When over activated this process causes thickening and fibrosis, primarily on the tricuspid valve, but also occurring on the pulmonary valve, eventually leading to right-sided heart failure.
Certain diseases such as gastrointestinal carcinoid tumors, which release large amounts of serotonin into the blood, produce a characteristic pattern of mostly right sided cardiac fibrosis which can be identified at autopsy. This pathology has also been seen in certain african tribes who eat foods containing excess amounts of serotonin.
Some appetite suppressant drugs such as fenfluramine and chlorphentermine induce a similar pattern of cardiac fibrosis, by over-stimulating 5HT2B receptors on the cardiac fibroblast cells. These drugs consequently tended to cause increased risk of heart valve damage and subsequent heart failure, which eventually led to them being withdrawn from the market.
A compound found in red wine, resveratrol has been found to slow down the development of cardiac fibrosis.