Tricuspid stenosis: Difference between revisions
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Surgical [[tricuspid valve]] replacement in TS is recommended among patients undergoing surgical intervention for left valvular disease as well as among patients with severe symptomatic isolated TS.<ref name="pmid24589852">{{cite journal| author=Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA et al.| title=2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2014 | volume= | issue= | pages= | pmid=24589852 | doi=10.1161/CIR.0000000000000029 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24589852 }} </ref> | Surgical [[tricuspid valve]] replacement in TS is recommended among patients undergoing surgical intervention for left valvular disease as well as among patients with severe symptomatic isolated TS.<ref name="pmid24589852">{{cite journal| author=Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA et al.| title=2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2014 | volume= | issue= | pages= | pmid=24589852 | doi=10.1161/CIR.0000000000000029 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24589852 }} </ref> | ||
==2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary<ref name="pmid24589852">{{cite journal| author=Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA et al.| title=2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2014 | volume= | issue= | pages= | pmid=24589852 | doi=10.1161/CIR.0000000000000029 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24589852 }} </ref>== | |||
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| colspan="1" style="text-align:center; background:LightGreen"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]] | |||
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| bgcolor="lightgreen" |<nowiki>"</nowiki>'''1.'''Tricuspid valve surgery is recommended for patients with severe TS at the time of operation for left-sided valve disease. ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: C'']])<nowiki>"</nowiki> | |||
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==References== | ==References== | ||
Revision as of 22:54, 15 December 2016
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Tricuspid stenosis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Tricuspid stenosis On the Web |
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American Roentgen Ray Society Images of Tricuspid stenosis |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2] Fatimo Biobaku M.B.B.S [3]
Overview
Tricuspid stenosis (TS) is a type of valvular heart disease where there is narrowing of the orifice of the tricuspid valve of the heart. Tricuspid stenosis is quite uncommon, it is usually caused by rheumatic heart disease and generally accompanies mitral and/or aortic valve involvement.[1] A majority of stenotic tricuspid valves are associated with evidence of regurgiation that has been clinically documented through a physicial examination (murmur), echocardiogram, or angiogram. Stenotic tricuspid valves are anatomically abnormal and usually take years to develop, with few exceptions such as congenital causes, active infective endocarditis.
Classification
Tricuspid stenosis is staged based on the valve anatomy and hemodynamics, and the hemodynamic consequences.[2]
| Stage | Definition | Valve anatomy | Valve hemodynamics | Hemodynamic consequences | Symptoms |
|---|---|---|---|---|---|
| C, D | Severe TS | Thickened, distorted, calcified leaflets |
|
Right atrial / Inferior vena cava enlargement |
|
Pathophysiology
TS is characterized by structural changes in the tricuspid valve. The pathophysiology of the tricuspid valve stenosis depends on the underlying etiology. In rheumatic heart disease which is the most common cause of TS, there is diffuse scarring and fibrosis of the valve leaflets, fusion of the commissures, and shortening of the chordae tendineae as a result of inflammation.[3] These abnormalities limit leaflet mobility and reduce the size of the tricuspid orifice, increasing the transtricuspid diastolic gradient, which can eventually result in systemic venous hypertension and congestion.[2]
The pathophysiology of tricuspid stenosis depends on the underlying etiology:[3]
- Rheumatic tricuspid stenosis:
- Diffuse scarring and fibrosis of the valve leaflets from inflammation. Fusion of the commissures may or may not occur.
- Chordae tendineae may become thickened and shortened.
- As a result of the dense collagen and elastic fibers that make up leaflet tissue, the normal leaflet layers become significantly distorted.
- Carcinoid heart disease:
- Fibrous white plaques located on the valvular and mural endocardium are characteristic presentations of carcinoid valve lesions.
- Valve leaflets become thick, rigid and smaller in area.
- Atrial and ventricular surfaces of the valve structure contain fibrous tissue proliferation.
- Congenital tricuspid stenosis:
- More common in infants
- Lesions may present in a number of different ways, either singularly or in any combination of the following:
- Incompletely developed leaflets
- Shortened or malformed chordae
- Small annuli
- Papillary muscles of abnormal size and number
- Infective endocarditis:
- Stenosis may develop as a result of large infected vegetations obstructing the opening of the tricuspid valve.
- Other conditions may mimic tricuspid stenosis by the mechanical obstruction of flow through the tricuspid valve:
- Supravalvular obstruction from congenital diaphragms
- Intracardiac or extracardiac tumors
- Thrombosis or emboli
- Large endocarditis vegetations
- Other conditions that impair right-sided filling
Causes
The most common cause of TS is rheumatic heart disease. Other causes of TS include carcinoid syndrome, congenital abnormalities, endocarditis, lupus, and mechanical obstruction by a tumor.[3][4]
Common Causes[3]
- Rheumatic heart disease (majority of the cases)
- Carcinoid syndrome
- Congenital
Study showing the etiology of Tricuspid stenosis in operatively excised valves in patients >15years[3]
| Etiology of tricuspid stenosis in 97 operatively excised stenotic tricuspid valves | ||||
|---|---|---|---|---|
| Rheumatic | Carcinoid | Congenital | ||
| Ebstein's anomaly | Complex heart disease | Shortened chordae and/or fused commissure | ||
| 90 | 3 | 1 | 2 | 1 |
Causes by Organ System
| Cardiovascular | Congenital heart disease, cardiac tumor, saphenous vein bypass graft aneurysm,[5] Ebstein's anomaly, endomyocardial fibrosis, infective endocarditis, myxoma, rheumatic heart disease |
| Chemical/Poisoning | No underlying causes |
| Dental | No underlying causes |
| Dermatologic | No underlying causes |
| Drug Side Effect | Methysergide |
| Ear Nose Throat | No underlying causes |
| Endocrine | Carcinoid syndrome |
| Environmental | No underlying causes |
| Gastroenterologic | No underlying causes |
| Genetic | No underlying causes |
| Hematologic | No underlying causes |
| Iatrogenic | Pacemaker infection, pacemaker leads[6], device closure of right coronary arteriovenous fistula.[7] |
| Infectious Disease | Infective endocarditis |
| Musculoskeletal/Orthopedic | No underlying causes |
| Neurologic | No underlying causes |
| Nutritional/Metabolic | Fabry disease, Whipple's disease |
| Obstetric/Gynecologic | No underlying causes |
| Oncologic | Carcinoid syndrome, cardiac tumor, intravenous leiomyomatous tumor,[8] metastatic tumor, myxoma |
| Ophthalmologic | No underlying causes |
| Overdose/Toxicity | No underlying causes |
| Psychiatric | No underlying causes |
| Pulmonary | No underlying causes |
| Renal/Electrolyte | No underlying causes |
| Rheumatology/Immunology/Allergy | Amyloidosis,[9] systemic lupus erythematosus |
| Sexual | No underlying causes |
| Trauma | No underlying causes |
| Urologic | No underlying causes |
| Miscellaneous | Giant blood cyst |
Causes by Alphabetical Order
- Amyloidosis[9]
- Carcinoid syndrome
- Cardiac tumor
- Congenital heart disease
- Ebstein's anomaly
- Endomyocardial fibrosis
- Fabry disease
- Giant blood cyst
- Infective endocarditis
- Intravenous leiomyomatous tumor[8]
- Metastatic tumor
- Myxoma
- Pacemaker infection
- Pacemaker leads
- Rheumatic heart disease
- Systemic lupus erythematosus
- Whipple's disease
Differential Diagnosis
The differential diagnosis of tricuspid stenosis include valvular abnormalities causing a similar clinical presentation, and other causes of systemic venous congestion. The heart murmur of tricuspid stenosis must be differentiated from that of other valvular diseases. However, it should be noted that tricuspid stenosis often co-exist with other valvular pathologies such as tricuspid regurgitation, mitral valve and aortic valve abnormalities.[3] Tricuspid stenosis is characterized by a mid diastolic murmur best heard over the left sternal border. It has a rumbling character, a tricuspid opening snap with wide splitting of S1. The differential diagnosis of tricuspid stenosis includes:
- Aortic regurgitation: The diastolic murmur of aortic regurgitation decreases with respiration, which is in contrast to that of tricuspid stenosis.
- Mitral regurgitation: The murmur of mitral regurgitation is blowing, soft and best heard at the apex.
- Mitral stenosis: The murmur of mitral stenosis is mid-diastolic, rumbling, and best heard after the opening snap.
- Tricuspid regurgitation: The murmur of tricuspid regurgitation is blowing, holosystolic, and best heard over the fourth intercostal area at the left sternal border.
Tricuspid stenosis should also be differentiated from diseases causing a similar clinical presentation,such as:
Epidemiology and Demographics
TS is the least common valvular disease. TS is rarely an isolated disease, it is mostly associated with mitral and/or aortic valve abnormalities with/without concomitant tricuspid regurgitation.
Prevalence
A prospective study of the echocardiographic profile of tricuspid valve disease in 788 patients with rheumatic heart disease in India was done. 9% of the patients had tricuspid valve disease and half of these patients with tricuspid valve disease had tricuspid stenosis with/without tricuspid regurgitation.[10] The prevalence of TS is lower in developed countries compared to the developing countries due to the low prevalence of rheumatic heart disease.
Gender
Most patients with rheumatic tricuspid stenosis are young women with mitral and aortic valve disease.[1]
Risk Factors
One of the most recognized risk factors for TS is rheumatic fever.
Natural History, Complications, and Prognosis
Natural history
The natural course of tricuspid stenosis is not well defined. It is extremely rare for TS to occur in isolation, it is usually associated with existing mitral valve disease with/without concormitant tricuspid regurgitation.[11] The most common cause of TS is rheumatic heart disease and it is usually associated with coexisting mitral valve and/or aortic valve abnormality.[11] TS of rheumatic etiology usually occurs with tricuspid regurgitation. Tricuspid stenosis takes years to develop, with some exceptions such as congenital causes. Complications of tricuspid stenosis include heart failure, liver failure, and stroke.[12]
Complications of TS[11][12]
- Right atrial enlargement
- Atrial fibrillation
- Heart failure
- Infective endocarditis
- Cerebrovascular accident
- Liver failure
Prognosis
With medical intervention, severe tricuspid stenosis appears well tolerated over several years of follow-up.[11]
Diagnosis
History and Symptoms
Tricuspid stenosis is mostly associated with mitral valve abnormalities.[13] Common symptoms include dyspnea, peripheral edema, and fatigue.
Signs and Symptoms[13]
- Fatigue
- Dyspnea
- Abdominal discomfort (due to hepatomegaly secondary to systemic venous congestion)
- Pedal edema
- Jugular venous distension
- Heart murmur
Physical Examination
Tricuspid stenosis often co-exists with mitral stenosis, thus depending on the severity of mitral valve pathology, symptoms differ. The diagnosis of TS may also be missed when they coexist. Patients can lay flat without any symptoms in the absence of serious mitral valve pathology and thus, not present with any signs of dyspnea. Characteristic findings of TS include an opening snap and a diastolic rumbling murmur that is localized to the lower left sternal border at the fourth intercostal space and it increases with inspiration.
Echocardiogram
Transthoracic echocardiography (TTE) should be performed among patients with suspected TS to confirm the diagnosis, determine the etiology, and establish the baseline severity. TTE commonly reveals findings associated with other valvular diseases, such as tricuspid regurgitation and/or mitral stenosis. TS is mainly characterized by an elevated transvalvular gradient.[4] TTE helps in the determination of the anatomic and hemodynamic characteristics of the tricuspid valve. TTE allows the evaluation of the following:[4]
- Tricuspid valve thickening and calcification
- Chordal thickening and calcification
- Decreased mobility
- Immobility of the leaflets (suggestive of carcinoid syndrome)
- Tumors or metastatic lesions
- Valvular vegetations (suggestive of infective endocarditis)
- Right atrial ball valve thrombus
Doppler echocardiography is useful to assess the severity of TS through the evaluation of the transvalvular gradient. TS is mainly characterized by an elevated transvalvular gradient.[4] Using continuous wave doppler across the tricuspid valve, the peak gradient can be calculated using the modified Bernoulli equation. Pressure half time can be used but is not validated for TS. The assessment of the tricuspid valve area is limited by the common association of TS with tricuspid regurgitation. The coexistence of tricuspid regurgitation causes the underestimation of the tricuspid valvular area. A tricuspid valve area < 1.0 cm2 is associated with increased severity of the TS. The tricuspid valve area can be calculated using the continuity equation:[14]
Tricuspid valve area = ( annulus PW Vti * Cross sectional area of the annulus) / valve CW Vti
Findings Associated with Increased Severity
TTE findings that are associated with increased severity of tricuspid stenosis include:[4]
- Mean pressure gradient >5 mm Hg,
- Pressure half-time >190 milliseconds
- Tricuspid valve area < 1.0 cm2
- Enlargement of the right atrium
- Enlargement of the inferior vena cava
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary[15]
| Class I |
| "1. TTE is indicated in patients with TS to assess the anatomy of the valve complex, evaluate severity of stenosis, and characterize any associated regurgitation and/or left-sided valve disease. (Level of Evidence: C)" |
Electrocardiogram
The electrocardiogram of patients with TS can demonstrate a sinus rhythm with or without right atrial hypertrophy.[12] Patients with TS experience frequent arrhythmias, particularly atrial flutter and/or atrial fibrillation due to the enlargement of the right atrium. EKG findings suggestive of coexisting mitral disease can also be seen.
Chest X ray
The chest X-ray in a patient with tricuspid stenosis may show right atrial enlargement. The heart size can range from a normal-sized heart to cardiomegaly, with additional findings suggestive of coexisting valvular pathology such as mitral stenosis.
Cardiac MRI
While echocardiography remains the diagnostic imaging modality of choice, cardiac MRI is useful to evaluate tricuspid stenosis when the results of the echocardiography are insufficient.
ACC/AHA Guidelines- ACCF/ACR/AHA/NASCI/SCMR 2010 Expert Consensus Document on Cardiovascular Magnetic Resonance[16] (DO NOT EDIT)
| “ |
CMR may be used for assessing individuals with valvular heart disease in which evaluation of valvular stenosis, regurgitation, para- or perivalvular masses, perivalvular complications of infectious processes, or prosthetic valve disease are needed. CMR may be useful in identifying serial changes in LV volumes or mass in patients with valvular dysfunction. |
” |
Cardiac Catheterization
While echocardiography remains the diagnostic imaging modality of choice, cardiac catheterization is useful to evaluate tricuspid stenosis when the results of the non-invasive testing are insufficient, particularly among patients who are being evaluated for other conditions such as mitral stenosis and pulmonary hypertension.[2] In the older pre-surgery population, cardiac catheterization may be necessary in order to assess concomitant artery disease.
Cardiac Catheterization
Catheterization of the right heart is useful for the evaluation of:
- The gradient across the tricuspid valve
- Associated congenital defects
Catheterization of the left heart is useful for the assessment of hemodynamic changes related to the aortic and mitral valves in patients with rheumatic heart disease.
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary[15]
| Class IIb |
| "1. Invasive hemodynamic assessment of severity of TS may be considered in symptomatic patients when clinical and noninvasive data are discordant. (Level of Evidence: C)" |
Treatment
Medical Therapy
Medical therapy with diuretics and sodium restriction is the mainstay of treatment among patients with TS complicated by systemic and pulmonary congestion. Patients with TS should receive medical therapy for left heart failure, and/or pulmonary hypertension if case they are present.[15]
Surgery
Surgical tricuspid valve replacement in TS is recommended among patients undergoing surgical intervention for left valvular disease as well as among patients with severe symptomatic isolated TS.[15]
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary[15]
| Class I |
| "1.Tricuspid valve surgery is recommended for patients with severe TS at the time of operation for left-sided valve disease. (Level of Evidence: C)" |
References
- ↑ 1.0 1.1 Roguin A, Rinkevich D, Milo S, Markiewicz W, Reisner SA (1998). "Long-term follow-up of patients with severe rheumatic tricuspid stenosis". Am Heart J. 136 (1): 103–8. PMID 9665226.
- ↑ 2.0 2.1 2.2 Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA; et al. (2014). "2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". J Am Coll Cardiol. 63 (22): e57–185. doi:10.1016/j.jacc.2014.02.536. PMID 24603191.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Waller BF, Howard J, Fess S (1995). "Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part I." Clin Cardiol. 18 (2): 97–102. PMID 7720297.
- ↑ 4.0 4.1 4.2 4.3 4.4 Baumgartner H, Hung J, Bermejo J, Chambers JB, Evangelista A, Griffin BP; et al. (2009). "Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice". Eur J Echocardiogr. 10 (1): 1–25. doi:10.1093/ejechocard/jen303. PMID 19065003.
- ↑ Jellis CL, Navia JL, Flamm SD, Rodriguez LL (2016). "Severe Functional Tricuspid Stenosis Secondary to a Giant Saphenous Vein Bypass Graft Aneurysm". Circulation. 133 (21): 2099–102. doi:10.1161/CIRCULATIONAHA.115.014772. PMID 27217436 PMID: 27217436 Check
|pmid=value (help). - ↑ Taira K, Suzuki A, Fujino A, Watanabe T, Ogyu A, Ashikawa K (2006). "Tricuspid valve stenosis related to subvalvular adhesion of pacemaker lead: a case report". J Cardiol. 47 (6): 301–6. PMID 16800373.
- ↑ Changchien C, Lin MT, Wang CC, Liu HM, Wang CC, Chiu SN; et al. (2015). "Neonatal tricuspid stenosis caused by device closure of a large coronary fistula". EuroIntervention. 11 (7): e1. doi:10.4244/EIJV11I7A162. PMID 26603866 PMID: 26603866 Check
|pmid=value (help). - ↑ 8.0 8.1 Nili M, Liban E, Levy MJ (1982). "Tricuspid stenosis due to intravenous leiomyomatosis--a call for caution: case report and review of the literature". Tex Heart Inst J. 9 (2): 231–5. PMC 351617. PMID 15226964.
- ↑ 9.0 9.1 Kim KH, Park CH, Park HS, Kim YR, Choi EY (2014). "Amyloidosis-induced tricuspid stenosis mimicking rheumatic heart disease". Eur Heart J Cardiovasc Imaging. 15 (10): 1167. doi:10.1093/ehjci/jeu075. PMID 24797117.
- ↑ Goswami KC, Rao MB, Dev V, Shrivastava S (1999). "Juvenile TS and rheumatic tricuspid valve disease: an echocardiographic study". Int J Cardiol. 72 (1): 83–6. PMID 10636636.
- ↑ 11.0 11.1 11.2 11.3 Roguin A, Rinkevich D, Milo S, Markiewicz W, Reisner SA (1998). "Long-term follow-up of patients with severe rheumatic tricuspid stenosis". Am Heart J. 136 (1): 103–8. PMID 9665226 Check
|pmid=value (help). zero width space character in|pmid=at position 8 (help) - ↑ 12.0 12.1 12.2 Diaof M, Ba SA, Kane A, Sarr M, Diop IB, Diouf SM (2004). "[Tricuspid valve stenosis. A prospective study of 35 cases]". Dakar Med. 49 (2): 96–100. PMID 15786615.
- ↑ 13.0 13.1 Roguin A, Rinkevich D, Milo S, Markiewicz W, Reisner SA (1998). "Long-term follow-up of patients with severe rheumatic tricuspid stenosis". Am Heart J. 136 (1): 103–8. PMID 9665226 PMID: 9665226 Check
|pmid=value (help). - ↑ Fawzy ME, Mercer EN, Dunn B, al-Amri M, Andaya W (1989). "Doppler echocardiography in the evaluation of tricuspid stenosis". Eur Heart J. 10 (11): 985–90. PMID 2591399.
- ↑ 15.0 15.1 15.2 15.3 15.4 Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA; et al. (2014). "2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". Circulation. doi:10.1161/CIR.0000000000000029. PMID 24589852.
- ↑ American College of Cardiology Foundation Task Force on Expert Consensus Documents. Hundley WG, Bluemke DA, Finn JP, Flamm SD, Fogel MA; et al. (2010). "ACCF/ACR/AHA/NASCI/SCMR 2010 expert consensus document on cardiovascular magnetic resonance: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents". Circulation. 121 (22): 2462–508. doi:10.1161/CIR.0b013e3181d44a8f. PMC 3034132. PMID 20479157.