Tricuspid regurgitation overview: Difference between revisions
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{{Tricuspid regurgitation}} | {{Tricuspid regurgitation}} | ||
{{CMG}}; {{AE}} {{Rim}} {{FB}} | {{CMG}}; {{AE}} {{Rim}}, {{FB}} | ||
== | ==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 | 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 due to dilation | 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. 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. | 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. TR might not be recognized clinically until fairly late in its natural history. Patients with significant TR may remain [[asymptomatic]], despite impaired [[Right ventricle|right ventricular]] function. Approximately 30% to 50% of patients with severe MR have significant secondary TR. Significant degrees of TR has been noted with the onset of [[atrial fibrillation]], especially in older patients above 75 years of age. Moderate and severe TR are associated with increased [[morbidity]] and [[mortality]]. The higher the severity of TR, the worse the [[prognosis]]. | ||
==Diagnosis== | ==Diagnosis== | ||
===Stages=== | ===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: | 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: | ||
* At risk of TR | * At the risk of TR | ||
* Progressive TR | * Progressive TR | ||
* Asymptomatic severe TR | *[[Asymptomatic]] severe TR | ||
* Symptomatic severe TR | *[[Symptomatic]] severe TR | ||
===History and Symptoms=== | ===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. | 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=== | ===Physical Examination=== | ||
On examination, the [[jugular venous pressure]] is usually elevated, and ' | 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=== | ===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. | [[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. [[Echocardiography]] is also useful for the assessment of [[Right ventricle|right ventricular]] function and diameter. | ||
===Chest X ray=== | ===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]]. | 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]]. | ||
===Electrocardiogram=== | ===Electrocardiogram=== | ||
A [[electrocardiogram]] ([[The electrocardiogram|ECG]]) might have no significant abnormalities. Findings suggestive of [[right atrial enlargement]] and [[right atrial hypertrophy|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 Test=== | ||
[[Cardiac stress testing]] might be useful in the evaluation of asymptomatic patients with evidence of severe tricuspid regurgitation. | [[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. | ||
===Cardiac MRI=== | ===Cardiac MRI=== | ||
[[Cardiac magnetic resonance]] ([[CMR]]) may be beneficial | [[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. | ||
===Cardiac | |||
[[Cardiac catheterization]] is useful to evaluate tricuspid regurgitation when the results of the non-invasive testing are insufficient. | ===Cardiac Catheterization=== | ||
[[Cardiac catheterization]] is useful to evaluate [[tricuspid regurgitation]] when the results of the [[Non-invasive (medical)|non-invasive]] testing are insufficient. [[Cardiac catheterization]] can be performed when there is discrepancy between the clinical findings and the results of [[Non-invasive (medical)|non-invasive]] testing, in order to rule out [[cardiac]] etiologies of [[pulmonary hypertension]] as the cause of the patient's symptoms. [[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== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
The main therapy is treatment of underlying cause. | 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. | ||
===Surgery=== | ===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 [[Symptom|symptoms]]. It should be considered in mild/moderate secondary TR with significant dilation of the [[tricuspid]] annulus. [[Tricuspid valve]] surgery can also be beneficial for patients with severe primary TR that is unresponsive to medical therapy. | |||
==References== | ==References== | ||
Latest revision as of 15:10, 30 April 2020
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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. 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. TR might not be recognized clinically until fairly late in its natural history. Patients with significant TR may remain asymptomatic, despite impaired right ventricular function. Approximately 30% to 50% of patients with severe MR have significant secondary TR. Significant degrees of TR has been noted with the onset of atrial fibrillation, especially in older patients above 75 years of age. Moderate and severe TR are associated with increased morbidity and mortality. The higher the severity of TR, the worse the prognosis.
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:
- 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. Echocardiography is also useful for the assessment of right ventricular function and diameter.
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.
Electrocardiogram
A 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.
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.
Cardiac Catheterization
Cardiac catheterization is useful to evaluate tricuspid regurgitation when the results of the non-invasive testing are insufficient. 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 of pulmonary hypertension as the cause of the patient's symptoms. 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.
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. It should be considered in mild/moderate secondary TR with significant dilation of the tricuspid annulus. Tricuspid valve surgery can also be beneficial for patients with severe primary TR that is unresponsive to medical therapy.