Tricuspid regurgitation overview: Difference between revisions
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==Definition== | ==Definition== | ||
Tricuspid regurgitation (TR) occurs due to the failure of the heart's [[tricuspid valve]] to close properly during [[systole]]. As a result, with each right ventricular contraction, there is retrograde blood flow from the [[right ventricle]] into the [[right atrium]]. | [[Tricuspid regurgitation]] (TR) occurs due to the failure of the heart's [[tricuspid valve]] to close properly during [[systole]]. As a result, with each right ventricular contraction, there is retrograde blood flow from the [[right ventricle]] into the [[right atrium]]. | ||
==Classification== | ==Classification== | ||
TR can be classified as primary or secondary. | TR can be classified as primary or secondary. Primary (or organic) TR results from an organic lesion of the [[tricuspid valve]] itself, whereas secondary (or functional) TR is caused by left-sided heart disease and/or [[pulmonary hypertension]] without an intrinsic abnormality of the [[tricuspid valve]]. | ||
==Pathophysiology== | ==Pathophysiology== | ||
The pathophysiology of TR depends on whether TR is primary or secondary. Primary TR results from an organic abnormality in one or more parts of the [[tricuspid valve]], such as the leaflets, [[chordae tendineae]], or [[papillary muscle]]s. | The [[pathophysiology]] of TR depends on whether TR is primary or secondary. Primary TR results from an organic abnormality in one or more parts of the [[tricuspid valve]], such as the leaflets, [[chordae tendineae]], or [[papillary muscle]]s. Secondary [[tricuspid regurgitation]] accounts for more than 80% of TR encountered in clinical practice. Secondary TR results from [[hemodynamic]] and structural changes in the [[right ventricle]] and [[tricuspid valve]] apparatus secondary to left-sided heart disease (especially in the setting of [[mitral valve]] pathology) and/or [[pulmonary hypertension]]. Tricuspid annular dilation is the most important factor in the [[pathophysiology]] of secondary TR. In addition, tethering of the leaflets and inadequate leaflet coaptation also contribute to secondary TR. | ||
==Causes== | ==Causes== | ||
Most cases of tricuspid regurgitation are secondary (functional), primarily due to tricuspid annulus (TA) dilation and right ventricular enlargement and dysfunction. | Most cases of [[tricuspid regurgitation]] are secondary (functional), primarily due to [[tricuspid]] annulus (TA) dilation and [[Right ventricle|right ventricular]] enlargement and dysfunction. Such dilation leads to a derangement of the normal anatomy and mechanics of the [[tricuspid valve]] and the muscles governing its proper function, resulting in [[tricuspid valve]] incompetence. Common causes of right ventricular dilation include left-sided heart pathology, [[pulmonary hypertension]], and right ventricular [[infarction]] | ||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
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==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
Moderate or severe TR affects approximately 1·6 million individuals in the USA.<ref name="pmidPMID: 27048553">{{cite journal| author=Rodés-Cabau J, Taramasso M, O'Gara PT| title=Diagnosis and treatment of tricuspid valve disease: current and future perspectives. | journal=Lancet | year= 2016 | volume= 388 | issue= 10058 | pages= 2431-2442 | pmid=PMID: 27048553 | doi=10.1016/S0140-6736(16)00740-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27048553 }} </ref> Secondary TR is more common than primary TR, accounting for more than 80% of clinically encountered TR. | Moderate or severe TR affects approximately 1·6 million individuals in the USA.<ref name="pmidPMID: 27048553">{{cite journal| author=Rodés-Cabau J, Taramasso M, O'Gara PT| title=Diagnosis and treatment of tricuspid valve disease: current and future perspectives. | journal=Lancet | year= 2016 | volume= 388 | issue= 10058 | pages= 2431-2442 | pmid=PMID: 27048553 | doi=10.1016/S0140-6736(16)00740-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27048553 }} </ref> Secondary TR is more common than primary TR, accounting for more than 80% of clinically encountered TR. | ||
==Natural History, Complications and Prognosis== | ==Natural History, Complications and Prognosis== | ||
TR is a common finding. Trace or mild degrees of tricuspid regurgitation of no clinical consequence can be seen in patients with normal tricuspid valve leaflets and annular dimensions.<ref name="pmidPMID: 27048553" /> TR might not be recognized clinically until fairly late in its natural history.<ref name="pmidPMID: 27048553" /> Patients with significant TR may remain asymptomatic, despite impaired right ventricular function.<ref name="pmidPMID: 26022823" /> Approximately 30% to 50% of patients with severe MR have significant secondary TR.<ref name="pmidPMID: 26022823" /><ref name="pmidPMID: 12228791">{{cite journal| author=Koelling TM, Aaronson KD, Cody RJ, Bach DS, Armstrong WF| title=Prognostic significance of mitral regurgitation and tricuspid regurgitation in patients with left ventricular systolic dysfunction. | journal=Am Heart J | year= 2002 | volume= 144 | issue= 3 | pages= 524-9 | pmid=PMID: 12228791 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12228791 }} </ref> Significant degrees of TR has been noted with the onset of atrial fibrillation, especially in older patients above 75years of age.<ref name="pmidPMID: 27048553" /> Moderate and severe TR are associated with increased morbidity and mortality. The higher the severity of TR, the worse the prognosis.<ref name="pmidPMID: 26022823" /> | TR is a common finding. Trace or mild degrees of tricuspid regurgitation of no clinical consequence can be seen in patients with normal tricuspid valve leaflets and annular dimensions.<ref name="pmidPMID: 27048553" /> TR might not be recognized clinically until fairly late in its natural history.<ref name="pmidPMID: 27048553" /> Patients with significant TR may remain asymptomatic, despite impaired right ventricular function.<ref name="pmidPMID: 26022823">{{cite journal| author=Dreyfus GD, Martin RP, Chan KM, Dulguerov F, Alexandrescu C| title=Functional tricuspid regurgitation: a need to revise our understanding. | journal=J Am Coll Cardiol | year= 2015 | volume= 65 | issue= 21 | pages= 2331-6 | pmid=PMID: 26022823 | doi=10.1016/j.jacc.2015.04.011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26022823 }} </ref> Approximately 30% to 50% of patients with severe MR have significant secondary TR.<ref name="pmidPMID: 26022823" /><ref name="pmidPMID: 12228791">{{cite journal| author=Koelling TM, Aaronson KD, Cody RJ, Bach DS, Armstrong WF| title=Prognostic significance of mitral regurgitation and tricuspid regurgitation in patients with left ventricular systolic dysfunction. | journal=Am Heart J | year= 2002 | volume= 144 | issue= 3 | pages= 524-9 | pmid=PMID: 12228791 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12228791 }} </ref> Significant degrees of TR has been noted with the onset of atrial fibrillation, especially in older patients above 75years of age.<ref name="pmidPMID: 27048553" /> Moderate and severe TR are associated with increased morbidity and mortality. The higher the severity of TR, the worse the prognosis.<ref name="pmidPMID: 26022823" /> | ||
==Diagnosis== | ==Diagnosis== | ||
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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]
Definition
Tricuspid regurgitation (TR) occurs due to the failure of the heart's tricuspid valve to close properly during systole. As a result, with each right ventricular contraction, there is retrograde blood flow from the right ventricle into the right atrium.
Classification
TR can be classified as primary or secondary. Primary (or organic) TR results from an organic lesion of the tricuspid valve itself, whereas secondary (or functional) TR is caused by left-sided heart disease and/or pulmonary hypertension without an intrinsic abnormality of the tricuspid valve.
Pathophysiology
The pathophysiology of TR depends on whether TR is primary or secondary. Primary TR results from an organic abnormality in one or more parts of the tricuspid valve, such as the leaflets, chordae tendineae, or papillary muscles. Secondary tricuspid regurgitation accounts for more than 80% of TR encountered in clinical practice. Secondary TR results from hemodynamic and structural changes in the right ventricle and tricuspid valve apparatus secondary to left-sided heart disease (especially in the setting of mitral valve pathology) and/or pulmonary hypertension. Tricuspid annular dilation is the most important factor in the pathophysiology of secondary TR. In addition, tethering of the leaflets and inadequate leaflet coaptation also contribute to secondary TR.
Causes
Most cases of tricuspid regurgitation are secondary (functional), primarily due to tricuspid annulus (TA) dilation and right ventricular enlargement and dysfunction. Such dilation leads to a derangement of the normal anatomy and mechanics of the tricuspid valve and the muscles governing its proper function, resulting in tricuspid valve incompetence. Common causes of right ventricular dilation include left-sided heart pathology, pulmonary hypertension, and right ventricular infarction
Differential Diagnosis
The blowing holosystolic murmur of tricuspid regurgitation must be distinguished from mitral regurgitation and a ventricular septal defect.
Epidemiology and Demographics
Moderate or severe TR affects approximately 1·6 million individuals in the USA.[1] Secondary TR is more common than primary TR, accounting for more than 80% of clinically encountered TR.
Natural History, Complications and Prognosis
TR is a common finding. Trace or mild degrees of tricuspid regurgitation of no clinical consequence can be seen in patients with normal tricuspid valve leaflets and annular dimensions.[1] TR might not be recognized clinically until fairly late in its natural history.[1] Patients with significant TR may remain asymptomatic, despite impaired right ventricular function.[2] Approximately 30% to 50% of patients with severe MR have significant secondary TR.[2][3] Significant degrees of TR has been noted with the onset of atrial fibrillation, especially in older patients above 75years of age.[1] Moderate and severe TR are associated with increased morbidity and mortality. The higher the severity of TR, the worse the prognosis.[2]
Diagnosis
Stages
The stage of TR can be estimated based on specific criteria for the valve anatomy, valve hemodynamics, associated cardiac findings, and symptoms. The stages of TR are:[4]
- At the risk of TR
- Progressive TR
- Asymptomatic severe TR
- Symptomatic severe TR
History and Symptoms
The history of a patient with suspected or confirmed TR should include information about the possible etiologies of primary and secondary TR. TR occurs most commonly secondary to pulmonary hypertension and left heart failure; therefore, detailed information about these conditions should be obtained. The majority of TR cases are asymptomatic. Symptoms of TR include clinical manifestations related to right heart failure such as peripheral edema and abdominal distention. If left heart failure or pulmonary hypertension is the underlying etiology of TR, the patient might have symptoms related to these diseases.
Physical Examination
On examination, the jugular venous pressure is usually elevated, and 'cv' waves can be seen. The liver may be enlarged and is often pulsatile (the latter finding being virtually diagnostic of tricuspid insufficiency). Peripheral edema is often found. In severe cases, there may be ascites and even cirrhosis (so-called cardiac cirrhosis). Tricuspid insufficiency may lead to the presence of a pansystolic heart murmur. Such a murmur is usually of low frequency and is best heard at the left sternal border. It tends to increase with inspiration. However, the murmur may be inaudible, reflecting the relatively low pressures on the right side of the heart. A third heart sound may also be present.
Echocardiography
Transthoracic echocardiography (TTE) is the technique of choice for the evaluation of TR and it should be performed in a patient with suspected tricuspid regurgitation to confirm the diagnosis, determine the etiology, and establish the baseline severity.[5] Echocardiography is also useful for the assessment of right ventricular function and diameter.[5]
Chest X ray
A chest X-ray is a useful test during the initial evaluation as well as during follow-up among adolescent and young adult patients with tricuspid regurgitation.[4]
Electrocardiogram
An electrocardiogram (ECG) might have no significant abnormalities. Findings suggestive of right atrial enlargement and hypertrophy might be present secondary to either pulmonary hypertension or to the hemodynamic consequences of TR itself. In the case of TR secondary to left heart disease, the ECG might demonstrate changes related to the underlying condition.
Cardiac Stress Test
Cardiac stress testing might be useful in the evaluation of asymptomatic patients with evidence of severe tricuspid regurgitation. Cardiac stress testing might identify limitations in exercise, which can guide the consideration of surgery as a treatment modality.[6][7]
Cardiac MRI
Cardiac magnetic resonance (CMR) may be beneficial for the evaluation of the structure and function of the right atrium and right ventricle, as well as the severity of the tricuspid regurgitation when echocardiography findings are inconclusive, particularly before tricuspid valve surgery.[6]
Cardiac Catherization
Cardiac catheterization is useful to evaluate tricuspid regurgitation when the results of the non-invasive testing are insufficient.[8] Cardiac catheterization can be performed when there is discrepancy between the clinical findings and the results of non-invasive testing, in order to rule out cardiac etiologies or pulmonary hypertension as the cause of the patient's symptoms.[6] Right ventriculography and hemodynamic assessment by cardiac catheterization are used to assess the function of the right ventricle and estimate the severity of the valvular regurgitation.
Treatment
Medical Therapy
The main therapy is treatment of the underlying cause. The aim of medical therapy among patients with TR is to treat right heart failure, left heart failure, and/or pulmonary hypertension in case they are present. Medical therapy with diuretics helps improve volume overload.[6]
Surgery
In most cases, surgery is not indicated. However, tricuspid valve repair at the time of left-sided valve surgery is now recommended in cases of severe TR irrespective of symptoms.[9] It should be considered in mild/moderate secondary TR with significant dilation of the tricuspid annulus.[9] Tricuspid valve surgery can also be beneficial for patients with severe primary TR that is unresponsive to medical therapy.[6]
References
- ↑ 1.0 1.1 1.2 1.3 Rodés-Cabau J, Taramasso M, O'Gara PT (2016). "Diagnosis and treatment of tricuspid valve disease: current and future perspectives". Lancet. 388 (10058): 2431–2442. doi:10.1016/S0140-6736(16)00740-6. PMID 27048553 PMID: 27048553 Check
|pmid=value (help). - ↑ 2.0 2.1 2.2 Dreyfus GD, Martin RP, Chan KM, Dulguerov F, Alexandrescu C (2015). "Functional tricuspid regurgitation: a need to revise our understanding". J Am Coll Cardiol. 65 (21): 2331–6. doi:10.1016/j.jacc.2015.04.011. PMID 26022823 PMID: 26022823 Check
|pmid=value (help). - ↑ Koelling TM, Aaronson KD, Cody RJ, Bach DS, Armstrong WF (2002). "Prognostic significance of mitral regurgitation and tricuspid regurgitation in patients with left ventricular systolic dysfunction". Am Heart J. 144 (3): 524–9. PMID 12228791 PMID: 12228791 Check
|pmid=value (help). - ↑ 4.0 4.1 Bonow RO, Carabello BA, Chatterjee K; et al. (2008). "2008 Focused update incorporated into the ACC/AHA 2006 guidelines 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 (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons". Circulation. 118 (15): e523–661. doi:10.1161/CIRCULATIONAHA.108.190748. PMID 18820172. Unknown parameter
|month=ignored (help) - ↑ 5.0 5.1 Tornos Mas P, Rodríguez-Palomares JF, Antunes MJ (2015). "Secondary tricuspid valve regurgitation: a forgotten entity". Heart. 101 (22): 1840–8. doi:10.1136/heartjnl-2014-307252. PMC 4680164. PMID pmid26503944 Check
|pmid=value (help). - ↑ 6.0 6.1 6.2 6.3 6.4 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: 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 pmid24603191 Check
|pmid=value (help). - ↑ Kühn A, De Pasquale Meyer G, Müller J, Petzuch K, Fratz S, Röhlig C; et al. (2013). "Tricuspid valve surgery improves cardiac output and exercise performance in patients with Ebstein's anomaly". Int J Cardiol. 166 (2): 494–8. doi:10.1016/j.ijcard.2011.11.033. PMID 22204848.
- ↑ Nishimura RA, Carabello BA (2012). "Hemodynamics in the cardiac catheterization laboratory of the 21st century". Circulation. 125 (17): 2138–50. doi:10.1161/CIRCULATIONAHA.111.060319. PMID 22547754.
- ↑ 9.0 9.1 Pozzoli A, Elisabetta L, Vicentini L, Alfieri O, De Bonis M (2016). "Surgical indication for functional tricuspid regurgitation at initial operation: judging from long term outcomes". Gen Thorac Cardiovasc Surg. 64 (9): 509–16. doi:10.1007/s11748-016-0677-5. PMID pmid27329290 Check
|pmid=value (help).