Tricuspid regurgitation overview
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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]
Overview
Tricuspid regurgitation (TR) refers to the failure of the heart's tricuspid valve to close properly during systole. As a result, with each heart beat, a portion of the blood is pumped out from the right side of the heart backwards in the opposite direction into the right atrium rather than forwards into the right ventricle.
Classification
TR can be classified into primary and secondary. Primary (or organic) TR results from an organic lesion of the tricuspid valve itself, whereas secondary (or functional) TR is caused by left heart failure or pulmonary hypertension without an intrinsic abnormality of the tricuspid valve.
Pathophysiology
TR refers to the failure of the tricuspid valve to close properly during systole. As a result, with each heart beat some blood passes from the right ventricle to the right atrium, the opposite of the normal direction. 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.[1] Secondary TR results from hemodynamic and structural changes in the right ventricle and tricuspid valve apparatus secondary to left heart failure 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.[2]
Causes
Most cases of tricuspid regurgitation are due to dilation of the right ventricle, although congenital causes exist. Such dilation leads to derangement of the normal anatomy and mechanics of the tricuspid valve and the muscles governing its proper function. The result is incompetence of the tricuspid valve. Common causes of right ventricular dilation include left heart failure, pulmonary hypertension, and right ventricular infarction. One notable exception to right ventricular dilation as a cause of tricuspid insufficiency occurs in right-sided endocarditis (i.e. infection affecting the right side of the heart). In that case, there is direct damage to the tricuspid valve as as a result of infection.
Differential Diagnosis
The blowing holosystolic murmur of tricuspid regurgitation must be distinguished from mitral regurgitation and a ventricular septal defect.
Epidemiology and Demographics
The prevalence of TR of a severity ≥ mild is approximately 15% in men and 18% in women.[3] Secondary TR is more common than primary TR.[4]
Natural History, Complications and Prognosis
TR is a common finding. TR is mostly a trace or mild regurgitation and has no symptoms when pulmonary hypertension and heart failure are absent.[5] Opposite to trace and mild MR, moderate and severe TR are associated with increased morbidity and mortality. The higher the severity of TR is, the worse the prognosis is.[5]
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 the following: at risk of TR, progressive TR, asymptomatic severe TR, and symptomatic severe TR.[6]
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 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 best heard low on the left sternal border. It tends to increase with inspiration. However, the murmur may be inaudible reflecting the relatively low pressures in the right side of the heart. A third heart sound may also be present.
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.[7]
Electrocardiogram
The electrocardiogram (ECG) in tricuspid regurgitation (TR) 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 consequence of TR itself. In case of TR secondary to left heart disease, the ECG might demonstrate changes related to the underlying condition.
Echocardiography
Transthoracic echocardiography (TTE) should be performed in a patient with suspected tricuspid regurgitation to confirm the diagnosis, determine the etiology, and establish the baseline severity. Echocardiography is useful for the assessment of the function of the right ventricle prior to surgery.
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][8]
Cardiac MRI
Cardiac magnetic resonance (CMR) may be beneficial to evaluate 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.[9] In addition, cardiac catheterization might be performed when there is lack of consistency between the clinical findings and the results of the 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 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.[6] Medical therapy with diuretics is the mainstay of treatment. Unfortunately, this can lead to volume depletion and decreased cardiac output. Indeed, one must often accept a certain degree of symptomatic tricuspid regurgitation in order to prevent a decrease in cardiac output. Treatment with medicines to reduce cardiac afterload may also be of benefit but a similar risk of depressed cardiac output applies.
Surgery
The main therapy is treatment of underlying cause. In most cases, surgery is not indicated since the root problem lies with a dilated or damaged right ventricle. When surgical treatment is done it is usually done as part of another procedure, most commonly mitral valve repair for mitral regurgitation.
References
- ↑ Rogers JH, Bolling SF (2009). "The tricuspid valve: current perspective and evolving management of tricuspid regurgitation". Circulation. 119 (20): 2718–25. doi:10.1161/CIRCULATIONAHA.108.842773. PMID 19470900.
- ↑ Taramasso M, Vanermen H, Maisano F, Guidotti A, La Canna G, Alfieri O (2012). "The growing clinical importance of secondary tricuspid regurgitation". J Am Coll Cardiol. 59 (8): 703–10. doi:10.1016/j.jacc.2011.09.069. PMID 22340261.
- ↑ Singh JP, Evans JC, Levy D, Larson MG, Freed LA, Fuller DL; et al. (1999). "Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation (the Framingham Heart Study)". Am J Cardiol. 83 (6): 897–902. PMID 10190406.
- ↑ Cohen SR, Sell JE, McIntosh CL, Clark RE (1987). "Tricuspid regurgitation in patients with acquired, chronic, pure mitral regurgitation. I. Prevalence, diagnosis, and comparison of preoperative clinical and hemodynamic features in patients with and without tricuspid regurgitation". J Thorac Cardiovasc Surg. 94 (4): 481–7. PMID 3657250.
- ↑ 5.0 5.1 Nath J, Foster E, Heidenreich PA (2004). "Impact of tricuspid regurgitation on long-term survival". J Am Coll Cardiol. 43 (3): 405–9. doi:10.1016/j.jacc.2003.09.036. PMID 15013122.
- ↑ 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: 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.
- ↑ 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) - ↑ 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.