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| REVIEW ARTICLE |
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| Year : 2022 | Volume
: 4
| Issue : 2 | Page : 46-58 |
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Tricuspid regurgitation etiologies, current diagnostic methods, and management: A 2022 update and review of the literature
Retaj Al Haroun1, Raja Dashti2, Rajesh Rajan2, Mohammed Al Jarallah2, Khalid AI Mulla2, Joud Al Balool3, Zhanna Davidona Kobalava4, Suprateeka Talukder5, Endurance Osas Evbayekha6, Gary Tse7, Helen Huang8
1 Department of Medicine, Faculty of Medicine and Health Science, Royal College of Surgeons in Ireland, Dublin, Ireland
2 Department of Cardiology, Sabah Al Ahmad Cardiac Centre, Al Amiri Hospital, Kuwait City, Kuwait
3 Department of Medicine, Faculty of Medicine, Kuwait University, Jabryia, Kuwait
4 Department of Internal Medicine with the Subspecialty of Cardiology and Functional Diagnostics Named after V.S. Moiseev, Institute of Medicine, Peoples' Friendship University of Russia (RUDN University), Moscow, Russia
5 Department of Medicine, Norfolk and Norwich University Hospital, Colney Lane, Norwich, United Kingdom
6 Department of Internal Medicine, St. Luke's Hospital, St. Louis, MO, USA
7 Department of Medicine, Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom; Department of Cardiology, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, China; Department of Medicine, Kent and Medway Medical School, Canterbury, United Kingdom
8 Department of Medicine, Faculty of Medicine and Health Science, Royal College of Surgeons in Ireland, Dublin, Ireland; Heart Failure and Structural Heart Disease Unit, Cardiovascular Analytics Group, China-UK Collaboration, Hong Kong, China
| Date of Submission | 24-Oct-2022 |
| Date of Decision | 18-Dec-2022 |
| Date of Acceptance | 19-Dec-2022 |
| Date of Web Publication | 21-Feb-2023 |
Correspondence Address:
Ms. Helen Huang
Faculty of Medicine and Health Science, Royal College of Surgeons in Ireland, Dublin 2
Rajesh Rajan
Department of Cardiology, Sabah Al Ahmed Cardiac Centre, Kuwait City - 13001
Kuwait
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/ACCJ.ACCJ_20_22
Tricuspid regurgitation (TR) is a common finding. Any changes to the components of the tricuspid valve (TV), such as the tricuspid annulus, valve leaflets, papillary muscles, and chordae tendinae can lead to TR. This valvular disease has recently sparked interest after it was long forgotten. This paper examines the anatomy of the TV, etiology of TR, and critically appraises the diagnostic methods used to assess the TV and the current medical treatment options for TR. This paper aims to give a detailed review of TR in hopes that more research will be conducted to help better assess patients with tricuspid regurgitation.
Keywords: Tricuspid regurgitation, tricuspid regurgitation diagnosis, tricuspid regurgitation treatment, tricuspid valve
How to cite this article:
Al Haroun R, Dashti R, Rajan R, Al Jarallah M, AI Mulla K, Al Balool J, Kobalava ZD, Talukder S, Evbayekha EO, Tse G, Huang H. Tricuspid regurgitation etiologies, current diagnostic methods, and management: A 2022 update and review of the literature. Ann Clin Cardiol 2022;4:46-58 |
How to cite this URL:
Al Haroun R, Dashti R, Rajan R, Al Jarallah M, AI Mulla K, Al Balool J, Kobalava ZD, Talukder S, Evbayekha EO, Tse G, Huang H. Tricuspid regurgitation etiologies, current diagnostic methods, and management: A 2022 update and review of the literature. Ann Clin Cardiol [serial online] 2022 [cited 2023 Jun 4];4:46-58. Available from: http://www.onlineacc.org/text.asp?2022/4/2/46/370094 |
| Introduction | |  |
Tricuspid regurgitation (TR) is commonly under-researched and undertreated due to the common belief that TR is harmless and less common than other valvular diseases.[1],[2],[3] However, it has been well established in the literature that patients with severe TR have higher mortality rates than those without. TR occurrence has been linked to patients with a history of previous heart surgery and carries an increased risk in elderly individuals.[1],[2],[4] As a result, it is predicted that the incidence of TR is likely to increase in the upcoming decades due to the rise in rates of cardiovascular interventions and life expectancy.
TR is defined by a backflow of blood from the right ventricle (RV) to the right atrium (RA) and is often seen in normal individuals as trivial TR.[5] This can cause the RV to become displaced and causes the anterior and posterior septa to stretch out. TR in healthy patients is not concerning or alarming, as small amounts of blood are likely to leak with aging.[6] However, given the mortality associated with patients that have co-morbidities that increase the risk of TR and the paucity of TR in the literature, it remains a much-needed area of research and discussion for clinical practices.
| Tricuspid Valve Anatomy | | |
The tricuspid valve (TV) consists of three leaflets (anterior, septal, and posterior), an annulus, the chordae tendineae from the ventricular septum, and two papillary muscles: anterior and posterior [Figure 1].[2],[5] The tricuspid annulus (TA) is saddle-shaped and contains properties that can allow morphological changes in response to load, which makes it more likely to dilate[2] [Figure 1]. The shorter leaflet (septal) is attached to the TA above the interventricular septum, often communicating with the chordae tendinae [Figure 1]. The longest is the anterior leaflet and is often the most mobile out of the three, while the posterior leaflet (PL) has the shortest circumference. The size and anatomical shape of these leaflets often guide imaging of the TV. The anatomical landmark of the septal and PLs is located near the entrance of the RA and is crucial in its function.[7] Because the RA and RV have low-pressure differences, the large size of the TV contributes to lower diastolic output compared with the other cardiac valves. The papillary muscles are crucial in support of all three leaflets and arise from the interventricular septum. In TR, certain anatomical functionalities are compromised and lead to the dilation of multiple structures, including the RV and TA, which are irreversible processes.[2] Because the TA consists of fibrous tissue, it is sensitive to the preload and afterload and can become more circular in architecture during TR. Research is still underway to determine whether the degree of TR is related to the degree of stretch in the leaflets. The current consensus shows that larger annular areas and more circular configurations are associated with a greater degree of TR and can guide surgical repair options in clinical practice.[7] However, the emergence of three-dimensional (3D) echocardiographic can be promising in the context of better understanding the anatomical basis of leaflet morphology and further aid in the measurement of the tricuspid annular region, as current diagnostic modalities rely on linear measurements that may not be as accurate.[8] | Figure 1: Anatomy of the TV. TV: Tricuspid valve, LC: Left cusp, RC: Right cusp, NC: Noncoronary cusp, AL: Anterior leaflet, PL: Posterior leaflet, AV node: Atrioventricular node. Original work created with biorender.com by HH
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| Hemodynamics of Tricuspid Regurgitation | | |
The physiology of TR is highly dependent on the concepts of hemodynamics. RA and RV volumes are often important determinants in the severity of TR. The RA and vena cavae are highly compliant; therefore, only severe TR presents noticeable hemodynamic changes. The extent of TR severity depends on several factors such as RV preload and afterload, cardiac rhythm (atrial fibrillation [AF] in particular) and the functionality of the left side of the heart.[9] The pressures of the RA are typically increased when TR is severe. The “S” wave (systolic wave) is usually present alongside a noticeable Y descent. Upon ventricularization of the RA, the contours of the RA and RV are nearly the same; however, the RA contour pressure presents with a lower amplitude. This finding is very specific to severe TR; however, it is not that common in TR patients. The RV end-diastolic pressure is elevated, and when patients exercise, the cardiac output (CO) is decreased. This leads to the development of signs and symptoms of right-sided heart failure (HF).[10]
| Epidemiology | | |
The prevalence of TR is 1.6 million in the United States, but the incidence of TR in the United States is 0.9%.[11] No sex or racial discrepancies were distinguished in the incidence rate; however, several differences were recognised in the prevalence and severity of TR. The Framingham heart study confirmed that the prevalence rates of TR (excluding trace TR) are 14.8% in males and 18.4% in females, meaning that females are 4.3 times more likely to be affected by TR.[12] Depending on the underlying cause of TR, the age group it affects differs. In newborns, the most common cause of TR is Ebstein anomaly due to the congenital nature of the condition. Individuals over 15 years of age with TR usually suffer from rheumatic valvular disease. It has also been established that the severity of TR increases with age, particularly in patients over the age of 70. The progression of TR from mild-moderate to severe TR is also seen more often in females than in males.[5],[12],[13],[14]
| Etiology | | |
TR can be classified into primary (organic) TR, secondary (functional) TR, or isolated TR [Figure 2]. Primary TR is caused by conditions that affect the valve directly and can be sub-classified into acquired and congenital TR [Figure 2]. Primary TR can be subclassified into acquired and congenital TR.[15] Ebstein anomaly is the most common congenital cause of TR, characterised as a rare heart defect where the TVs are misplaced, and the leaflets are malformed. Due to the absence of identifiable chordae, the valves cannot work efficiently and cause a backflow of blood. The enlargement of the heart from the pressure will cause HF and may present with cyanosis.[16] On the other hand, acquired causes are intrinsic abnormalities of the valve and can be caused by several conditions: iatrogenic injury from the placement of leads and pacemakers, valvular disorders such as infective endocarditis and rheumatic disease, trauma, drug-induced damage (i.e., dopamine agonists), systemic conditions such as lupus erythematosus, or tumors (myxoma).[17] In the literature, iatrogenic injuries are the most common cause of primary TR. However, organic causes of TR are far less common than secondary (functional) TRs. | Figure 2: Causes of TR. TR: Tricuspid regurgitation. AV defects: Atrioventricular defects, RV: Right ventricle. Original work created with biorender.com by HH
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Secondary TR accounts for approximately 80%–90% of all TR cases.[1] Functional TR is triggered by conditions that cause the RV and the RA to dilate.[1] The mechanism by which TR occurs differs depending on the underlying cause. Conditions such as pulmonary hypertension (PTN) and left-sided heart disease result in TV leaflet tethering.[18] The increased afterload and dilation of the RV can contribute to the reduced function of heart, predisposing patients to HF. Myocardial infarctions (MIs) can cause ischemia and tissue death, which can also affect the function of the RV. The progression of TR is often due to co-existing valvular diseases [Table 1] and is linked to higher mortality rates when found in AS patients. Moreover, patients who had prior mitral valve replacement are at an increased risk of mortality in the presence of TR.[19] The causes for pulmonary stenosis and tricuspid stenosis are quite similar to the causes for TR; for this reason, it is possible that more than 1 valve is affected in certain conditions.[20],[21],[22],[23],[24] The progression of severe secondary TR can be caused by patients who are generally sicker and required previous defibrillators or permanent pacemaker implantations, as they are at a higher risk of hospitalisation for HF.[25] An interesting populations to consider are pregnant women and fetuses with TR, given that they are most vulnerable in events of cardiac dysfunction. An earlier study by Wiechec et al. (2015) estimated that up to 7% of all normal fetuses have TR. Systemic reviews have suggested that screening for TR (in the 1st trimester) in conjunction with other parameters can help predict congenital heart disease or aneuploidy. However, the screening of TR alone is not enough to predict any birth abnormalities.[26],[27] Dilation of the TV annulus occurs in pregnant women and can result in functional TR presenting with murmurs.[28] TR is often harmless in pregnancy and is mostly well tolerated unless other preexisting heart conditions are present (i.e., cardiomyopathy).[29] | Table 1: Tricuspid regurgitation in realtion to other valvular heart disorders
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Isolated TR, though recognized as secondary TR, is increasingly becoming its own sub-category due to the morphological nature of isolated TR. The true prevalence of isolated TR is unknown, but increasing in incidence amongst AF patients [Figure 2]. These patient groups present without pulmonary HTN or co-existing heart diseases and can be found in elderly patients with a high risk of AF. The progression of TR is highly influenced by the chronicity of AF, which can cause a markedly dilated RA and tricuspid annular dilation over longer periods of time. Studies have suggested that atrial remodeling in the context of AF is associated with severe functional TR, but there is a lack of conclusive data that would suggest its significance in the progression of TR.[18],[30] In pregnancy, the presence of isolated TR can raise the susceptibility index for diastolic-dysfunction.[9]
| Assessment of Tricuspid Regurgitation | | |
TR is classified according to morphological types and underlying mechanisms: primary, secondary and isolated. As outlined by the American Heart Association/American College of Cardiology (AHA/ACC) guidelines, transthoracic echocardiography (TTE) is recommended for the initial evaluation of TR after clinical symptoms raise suspicion.[31],[32] TTE is a noninvasive method used to evaluate the presence and severity of TR, determine the etiology, measure the sizes of the inferior vena cava and right-sided chambers and calculate pulmonary artery systolic pressure (PASP) using various qualitative and quantitative parameters.[32] There are different echocardiographic characteristics of primary, secondary, and isolated TR.[33] TTE can differentiate between primary TR and secondary TR and any accompanying left-sided valvular or myocardial disease, as well as provide estimates of PASP. When clinical and noninvasive methods become inadequate, invasive measurement of the cardiac index, right-sided diastolic pressures, pulmonary vascular resistance, pulmonary pressures and right ventriculography can be useful in determining severity.[32] Right ventriculography can be used to evaluate the severity of TR.[32] Transoesophageal echocardiography (TOE) may be required if TTE is poor quality, endocarditis, or pacemaker lead infection. Primary and secondary TR can be distinguished based on structural abnormalities of the valve.[34] For example, in primary TR, leaflet thickening and vegetations may be identified, whereas RV dimension and function and degree of annular dilatation should be measured if suspecting secondary TR.[34] The following sections summarise the evidence-based findings on each individual diagnostic parameter [Figure 3]. | Figure 3: Diagnostic algorithm for TR. RHF: Right heart failure, TTE: Trans-thoracic echocardiography, TOE: Trans-oesophageal echocardiography, PISA: Proximal isovelocity surface area, VC: Vena contracta, CO: Cardiac output, RV: Right ventricle, HTN: Hypertension, SVC: Superior vena cava, IVC: Inferior vena cava, CT: Computer tomography, TV: Tricupsid valve, RA: Right atrium, EDV: End-diastolic volume, TR: Tricuspid regurgitation. Original work created with biorender.com by HH
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Physical examination
TR is often clinically silent within the first stages, with signs and symptoms becoming more apparent as regurgitation becomes more aggressive and severe. Physical examination revealed distended jugular veins (giant c-V waves), noticeable y-descent and symptoms of right-sided HF, including peripheral edema, hepatomegaly, or ascites. If the underlying pathology of TR is pulmonary HTN, patients may suffer from the low CO, increased fatigue, intolerance to exercise and palpation. Upon cardiac auscultation, a holosystolic or pansystolic murmur is heard over the left lower sternal border. The murmur's intensity increases with inspiration and is termed Cavallo's sign.[1],[5] RV dimensions and function, presence of associated lesions, left ventricle function are also evaluated for symptoms of right heart failure (RHF), which can be used to evaluate the severity of TR.[34]
Echocardiography
There are two types of echocardiograms that are recommended to confirm TR: TTE and TOE. TTE assesses the heart using four different views, including the parasternal, subcostal, suprasternal and apical views. In a standard 2D TTE, it is crucial to visualise the TV from multiple windows because no single window captures all leaflets of the TV. The apical view is often the preferred window. The short axis at the aortic levels and the left parasternal windows can also be utilised to assess the TV. However, a 3D TTE has become interesting to visualise all TV leaflets from a single view.[2] The advantage of 3D echocardiography is superior in accurately measuring RV volumes and the valve area. While 2D echocardiography takes only cross-sectional views of the chambers, 3D transesophageal echocardiography (TEE) has been appraised for its ability to detect the various morphologies of TV leaflets and define the geometry of the TA.[35] However, the anatomy of the TV is tricky to visualize in itself and presents limitations to effective 3D imaging due to the location of TVs and its inability to determine characteristics of fibrosis or calcifications.[36]
Expected findings on Doppler echocardiography are dilation of the RA, RV and TA [Figure 4] the identification of diastolic overload is often seen as a paradoxical interventricular movement on TTE. The Bernoulli equation can be used to estimate the degree of pulmonary HTN. However, errors when using this equation might occur in severe TR, as the pressure in the RA is hard to measure.[5] The RV and pulmonary systolic pressure can be estimated using the peak flow velocity. TEE is important to assess TV function fully. TEE is helpful because it can show abnormalities typically missed in a standard TTE. The American Society of Echocardiography recommends that physicians use the mid-esophagal plane to capture all heart chambers when using TEE or the 40° transgastric view (anteflexed).[2] | Figure 4: Severe TR echocardiographic findings. PISA: Proximal isovelocity surface area, VC: Vena contracta, TR: Tricuspid regurgitation. AHA: American Heart Association, ACC: American College of Cardiology. Original work created with biorender.com by HH
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When assessing TR patients using echocardiograms, several parameters are used. First, the valve morphology is used to quantify TR. The TA annulus, color flow jet, vena contracta width and proximal isovelocity surface area method can all be utilized to assess TR better. If moderate or severe TR is found, a full assessment of the RV should be carried out. This includes dimensions, volume and function. PASP and inferior vena cava diameter values should also be part of the study. While tricuspid annular plane systolic excursion and systolic myocardial velocities can be used when assessing RV function, they are weak predictors of RV function. Hepatic vein flow is another parameter that can be used; however, it can be affected by AF. Peak E flow shares the same limitations as hepatic vein flow. Last, the continuous wave regurgitation jet profile is widely available, but it is considered a qualitative finding.[37] There are new classification systems that are being developed to evaluate morphological variants of TV and leaflets using TEE imaging.[38] For example, Hahn et al. describes a proposed algorithm by which TR is classified into types based on a numbering system of leaflets present on TEE evaluation. For example, Type I can be characterized as the classic three-leaflet visualization, while Type II contains two-leaflets and Type III contains four leaflets. The numbering of leaflets would start at the anterior septal commissure and potentially improve preprocedural surgical planning and visualization of the anatomy, but the algorithm is not universally adopted and requires a further critical appraisal from the literature.
Catheterization
Cardiac catheterization is commonly done to determine increased end-diastolic pressure in the right atrium and ventricle, which is often characteristic of TR.[5] Generally, right heart catheterization is an important tool in the Cardiologist's diagnostic tool bag. It is used to determine the direct haemodynamic data that can be used to calculate CO, and examine intra-cardiac shunts and valve dysfunction.[39],[40] Haemodynamic alteration is a common finding in severe TR. Patients with severe TR usually undergo invasive diagnostic procedures such as right heart catheterization. Cardiac catheterization also has a role in differentiating severe TR from constrictive pericarditis. The differentiation between severe TR and constrictive pericarditis as a cause for RHF has important clinical implications-as misdiagnosis can lead to a referral for inappropriate surgery.[41] There is limited sensitivity of TEE in detecting severe TR due to pacemaker or defibrillator leads.[42] Due to this limitation, absolute pressure measurements during cardiac catheterization are important in differentiating these two conditions.[43]
Right-heart catheterization can assess the transpulmonary-gradient measurement, a parameter associated with increased risk in mortality, and is calculated by the pulmonary wedge pressure. These factors are limitations in echocardiography. However, due to the invasive nature in measuring pulmonary artery pressures, the AHA/ACC guidelines in 2014 advised for the use of catheterization when noninvasive echocardiograms are inconclusive and lacks the consistency to determine the patient's etiology of TR.[44] The use of such invasive intracardiac pressure measurements is necessary for situations where noninvasive testing, such as echocardiographic data are nondiagnostic, or there is a discrepancy between the echocardiographic findings and clinical presentation.[39] It is often rare for patients with valvular heart diseases to require further evaluation with invasive pressure measurements or angiography due to well-rounded advancements in echocardiography. There remain mixed opinions on the use of cardiac catheterization in diagnosing the severity of all valve lesions, obstruction of the coronary artery, and prosthetic TV malfunctions.[44] The paucity of literature that investigates the benefits of catheterization in accurately diagnosing TR makes it unclear whether the modality should be used in practice.
Additional diagnostic modalities
Electrocardiography findings differ depending on the stage and the underlying cause. In mild TR, ST and T wave abnormalities in the right precordial leads (a sign of RV dysfunction) are seen. In the case of RV infarction, Q waves are seen in leads V3R to V5R. TR caused by pulmonary HTN presents as RV hypertrophy and tall R waves in V1 and V2. On some occasions, the right bundle block is present (complete or incomplete). In severe pulmonary HTN, right atrial hypertrophy and P pulmonale usually occur in leads II, III, aVF, and V1. In AF, right atrial hypertrophy occurs, which manifests as an increase in the amplitude and the presence of fibrillatory waves.[5]
Chest radiography can reveal right atrial and ventricular enlargement (cardiomegaly), superior vena cava and inferior vena cava enlargement, elevation of the diaphragm, ascites, pulmonary venous HTN, pulmonary arterial HTN and pleural effusions. However, chest radiography can yield un-specific outcomes and are not specific to detect TR.
Computed tomography (CT) imaging results are often similar to chest radiography[7] and not routinely utilized for TR evaluation. A cardiac CT can visualize the four-chambers of the heart and delinate the location of TV leaflets and the interventricular septum, though it is difficult in itself. CT imaging has been reported to be accurate in the analysis of RV function, with good reproducibility of magnetic resonance images and its useful application in complex heart disease patients with implanted devices. A CT image can help determine the severity of TR by measuring the geometry of the TA and tethering height, a predictor for recurrent TR.[45]
Cardiac magnetic resonance imaging (MRI) provides precise imaging of TV function. Distension of hepatic veins and dilation of the RV and RA when present can be diagnostic markers for TR on spin-echo MRI. Cardiac MRI of the RV is considered one of the best predictive markers for postoperative outcomes for patients who have undergone TV surgery for severe TR. Assessing the RV end diastolic volume can predict the mortality rates.[46]
Liver function tests can reveal elevation in right atrial pressure, which can cause hepatic dysfunction. Liver function can be used as a tool to assess the severity of TR. Increased levels of bilirubin in the blood can be present.[47]
| Staging Tricuspid Regurgitation | | |
TR staging can be performed over 4 stages (A, B, C and D). Stage A is for the at-risk category. Patients with valve prolapse, infective endocarditis, rheumatic changes, repeated biopsies after a transplant, blunt trauma, carcinoid depositions, and early annular dilation are all at risk for TR. At this stage, the valve hemodynamics are normal, and no symptoms are usually present. Stage B, progressive TR, can present with some alteration in the valve anatomy and hemodynamics. No symptoms are present at this stage. Patients in Stages C and D often have poor prognoses despite the age group in which they fall. If a patient presents with signs of right-sided HF, they are placed in Stage D regardless of whether they meet the criteria mentioned below or not[47] [Table 2] and [Table 3].
| Treatment Guidelines | | |
The approach to managing TR depends on the etiology, severity, and simultaneous presence of HF, PTN, and other co-morbidities such as left ventricular valvular disease that may be amenable to surgical interventions. Doppler echocardiography is the modality for diagnosis and severity assessment,[48] and cardiac catheterization may be employed in scenarios where echocardiography results are equivocal.[49],[50] The 1999 Framingham Heart Study recognized trace to mild TR as prevalent in over 75% of the normal population.[51] Hence, mild asymptomatic TR is considered normal, and “Stage A” is not classified within the staging of TR. The AHA/ACC guideline classification stages TR into B, C, and D based on valve hemodynamics and clinical presentation.[52]
The first line for mild, moderate, progressive functional TR, and severe TR is medical therapy targeting underlying conditions such as HF, PTN, AF, Pacemaker, Pregnancy, etc., Loop Diuretics are recommended for Stages C and D with clinical RHF secondary to severe TR [Figure 5]. For secondary causes of severe TR leading to RHF, the approach targets underlying pathologies; rhythm control in AF [Figure 5], treatment of pulmonary HTN, and standard therapy for HF with reduced ejection fraction are examples.[52] | Figure 5: Treatment guidelines based on types of TR. TR: Tricuspid regurgitation, ACE inhibitors: Angiotensin-converter enzyme inhibitors, RHF: Right heart failure, TV: Tricupsid valve. Original work created with biorender.com by HH
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Lifestyle modification, as recommended by the 36th Bethesda conference for individuals with primary TR and other normal RV, LV, right ventricular systolic pressure, and RA pressure <20 mmHg, may participate in all forms of exercise.[53] However, individuals with multiple valvular diseases of moderate severity are at risk and should not engage in any form of competitive sports. They may require individualized risk assessment and recommendations.[53]
The 2020 AHA/ACC categorises surgical interventions into Class 1, 2a, and 2b according to the strength of recommendation and level of evidence. A Class 1 recommendation indicates that TV surgery should be administered, and Class 2a represents clinical scenarios where TV surgery is reasonable to carry out. In contrast, 2b depicts situations where surgical intervention might be considered.[52]
The Guideline recommends TV surgery for individuals with asymptomatic or symptomatic severe TR and concomitant left-sided valvular disease undergoing surgery, i.e., class 1[54],[55] [Figure 5]. In persons with severe isolated secondary TR with RHF and poor response to medical therapy, patients with progressive TR with a history of RHF or >40 mm of tricuspid annular diameter on echocardiography, or individuals with past or current history of RHF with severe primary TR, and person's with past or recent history of RHF with severe isolated secondary TR who respond poorly to medical therapy, all these candidates fit into the class 2a category, i.e., it is reasonable to carry out TV and left-sided valve surgery simultaneously, or isolated TV surgery[56],[57],[58],[59] [Figure 5]. For individuals with asymptomatic severe TR and right ventricular dysfunction or patients who have had surgical interventions previously on a left-sided valve and now present with isolated severe TR and RHF, isolated TV intervention can be considered, i.e., class 2b[60],[61],[62] [Figure 5].
Pharmacological therapy
Pharmacological therapy remains the first line of treatment for TR. The treatment plan differs for each patient based on the severity of symptoms, the underlying cause, and other coexisting morbidities that increase the risk of heart failure and subsequent mortality [Figure 4]. The Mayo clinic study found that in 87 patients, almost three-quarters of patients with severe TR were treated with pharmacological agents and had a 1-year survival rate of 76%.[63],[64] Another retrospective study by Axtell et al., 2019 showed that 95% of all patients with severe isolated TR were managed medically, while the remaining 5% were treated surgically. The analysis did not confirm any significant differences in the survival rates between the two groups.[65],[66],[67]
Given that HF contributes to mortality in TR patients, pharmacological therapy is centred around reducing the volume contributing to the failing heart. Patients with left-sided HF are usually placed on Furosemide, a loop diuretic, to control volume overload and improve symptoms of pulmonary congestion. However, diuretics can fail to function optimally in TR patients. In such cases, it is difficult to increase the dosage of certain diuretics if patients have impaired renal function or have a history of cardiorenal. Other medical recommendations for patients with TR due to left-sided HF include low salt intake and elevating the head on the bed, as these measures can improve the effects of HTN and symptoms of dyspnea, respectively. If left systolic dysfunction causes HF, beta blockers are indicated, given the patient does not have any contraindications. Angiotensin-convertase-enzyme inhibitors (ACE) are also commonly used to treat HF and block the actions of angiotensin II, leading to a decrease in systemic blood pressure and reducing the pressure load of the heart. Angiotensin receptor blockers are second in line to ACE inhibitors if patients fail to tolerate the latter. Aldosterone antagonists are also the effective medication of choice, as studies have found the drug to reduce mortality in patients with advanced HF with reduced left ventricle ejection fraction (New York Heart Association Class III to IV) and HF post-MI.[66] Drugs that target angiotensin and aldosterone play a major role in the renin-angiotensin-aldosterone system in HF by blocking fluid retention and protecting renal function to treat pulmonary and hepatic congestion. However, other medications that can target pathways that cause HF include calcium channel blockers, endothelin receptor antagonists, and PDE5 inhibitors.[1] Based on co-morbidities, patients with a history of recurrent pulmonary embolism secondary to RV/RA dilation can be placed on anticoagulation medications, while anti-arrhythmic is indicated for patients with AF.[1]
Surgical indications
Contrary to popular belief, left-sided heart surgery does not correct severe TR. It was thought that mitral valve repair may improve TR and has been discussed in the literature as an efficacious procedure. This common misconception has been debunked, as 70% of all patients continue to present with TR after left-sided heart surgery.[1],[22] Research also shows that ring annuloplasty has better outcomes for TR patients than suture annuloplasty as it reduces the likelihood of TR recurrence[1],[23] recurrence. However, the type of ring used (flexible, rigid, 3D) remains controversial and spare in the literature. The 2020 AHA/ACC and the 2021 European Society of Cardiology (ESC) have similar guidelines if the surgery is not for isolated tricuspid [Table 4]. The 2021 ESC valvular strongly recommends TV surgery for patients with asymptomatic primary severe TR and RV dilation.[68] However, the AHA/ACC weakly recommends isolated TR surgery for the same population. These recommendations seem to conflict with patients who might need isolated TV surgery. | Table 4: Similarities and differences between American Heart Association/American College of Cardiology 2020 guidelines with the European Society of Cardiology 2021 Guidelines
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When comparing early and late outcomes of TV replacement with TV repair (TV replacement [TVr]), the general consensus indicates TVr to confer with better short-term and long-term outcomes in perioperative and event-free survival, while TV replacement was associated with higher in-hospital mortality.[69],[70],[71] Though these findings are applicable to primary and secondary TR, the most optimal surgical treatment for isolated TR is not fully understood. Despite isolated TR being associated with higher risks of mortality, stand-alone surgery is rarely performed and poses as a serious risk of TR recurrence even after valve repairs.[72] Percutaneous intervention has been a proposed treatment to reduce the risk of HF in surgical scenarios but there is no evidence-based studies that would ratify this effect in isolated TR. The optimal timing of TV surgery also remains questionable; however, it is known that TR can cause life-long damage to the RV if surgical intervention is delayed[1] [Table 4].
Transcatheter
The use of transcatheter interventions when treating patients with TR remains new and is currently under research. Transcatheter interventions can include annuloplasty and caval valve implantation. Research also shows that ring annuloplasty has better outcomes for TR patients than suture annuloplasty,[1],[2],[4] as it reduces the likelihood of TR recurrence. However, the type of ring used (flexible, rigid, 3D) remains controversial. The 2021 ESC guidelines include new recommendations for transcatheter techniques. It is a class 2B recommendation that symptomatic patients with severe secondary TR who are deemed not fit surgery by an expert might undergo transcatheter treatment.[68]
| Complications and Prognosis | | |
Several complications can occur due to TR, such as thrombus formation and embolization. In addition, patients with TR are more likely to be admitted to the hospital and will have longer hospital stays.[73] Cirrhosis and ascites are major complications that TR patients develop.[5] A recent study with 385 patients showed that 50% of all deaths in patients with severe TR were caused by HF.[74] Postoperative complications include heart block, arrhythmias, and thrombus formation on the new valve, which is why valve repair remains the superior surgical intervention.[1],[5] This may also shed light to why isolated TR has higher mortality, given the risk of embolus formation in AF. The risk of infection is also present as is any surgical intervention, with endocarditis being the most reported infectious complication in valve replacements.[75] Sarcopenia is also an objective prognostic marker in older surgical patients and has historically been linked to poor outcomes postoperatively. This remains true in isolated TV surgery, where sarcopenia was associated with major postoperative complications 30 days after the procedure and caused a reduction in skeletal muscle mass.[76] The severity of secondary TR can often dictate the risk of recurrence if patients had undergone a concomitant tricuspid annuloplasty during surgery.[77] In addition, pulmonary HTN and RV dysfunction were independent prognostic factors in patients who had undergone surgery.[78] However, there is a lack of data that mentions varying prognostic factors depending on the type of TR and the population who received surgical management for TR, such as children or pregnant women.
| Pacemaker and Transcatheter Associated Tricuspid Regurgitation | | |
Cardiac implantable electronic devices (CIEDs) have improved the quality and duration of life for many patients through the support of heart rate, prevention of sudden cardiac death and atrioventricular and interventricular synchrony.[79],[80] TR can be a complication of pacemaker and implantable cardioverter-defibrillator (ICD) implantation. At baseline, generally, ICD recipients have moderate or severe left ventricular systolic dysfunction and therefore are likely to be predisposed, independent of the impact of the device, to secondary TR and right-sided HF.[81] TV dysfunction during lead implantation or manipulation can occur in various ways: lead perforation, avulsion (during lead extraction), laceration and transection of chordae tendineae or papillary muscles. Incidence of TV damage during lead placement is unknown, case reports describing this consequence are limited due to lack of baseline TR assessment. Mechanical interference with TV leaflet mobility and impingement may occur after cardiac implantable electronic device (CIED) implantation.[3]
TR related to pacemaker can occur due to direct leaflet injury, for example, lead entanglement, leaflet perforation, or lead adherence secondary to fibrosis. Moderate or severe TR has been shown to occur at a significantly higher rate in patients with pacemakers which in turn has been associated with increased mortality and HF-related hospitalization compared to their risk-matched cohorts.[82],[83],[84] Occurrence of pacemaker related TR has been associated with AF and a history of open-heart surgery. It is recommended to have echocardiographic surveillance of pacemaker related TR in patients who underwent pacemaker implantation– especially in those who have had a history of open-heart surgery and AF.[85] When pacemaker/transcatheter device procedure related TR is evident from clinical, haemodynamic and echocardiographic assessment, timely corrective intervention is advised before the beginnings of annular and chamber dilatation and severe right ventricular dysfunction. Future prospects of CIEDs involves nontransvalvular or absence of endocardial leads, which may lead to a decrease in lead-related cardiac dysfunction.
| Prospects of Three-Dimensional Printing and Artificial Intelligence | | |
The combination of 3D TTE and printing, newer advancements are surrounding patient-specific 3D-printing of TVs for preprocedural assessments and percutaneous repair amongst TR patients.[86] Vukicevic et al. intricately explored the repair and structural interventions of mitral valve using catheters with 3D printing, given that percutaneous intervention can present with high procedural-related complications.[87] 3D models require transthoracic 3D datasets of TV obtained from extensive imaging studies and the integration of mathematical analytics, such as linear and volume measurements, which can be paired to create 3D printed models; a study by Muraru et al. first demonstrate this method to be feasible in clinical practice and highly accurate in producing leaflet morphology compared to current techniques.[88] 3D printing models are crucial in patients with complex history, such as previous mitral valve replacements, which often require invasive procedures that are in need of highly delicate procedures when considering the positioning of the TV for replacement.[89],[90]
In addition, the advent of artificial intelligence (AI) has also been explored in improving current state-of-art diagnostic tools for TR. The modalities explored with AI integration involve cardiac CT/MRI chamber measurements and echocardiography, which are paired with newer analytical softwares that offer image segmentation and view identification.[91] Acquiring images of valvular disorders can improve current physiological measurements of jet flow and visualize leaflets in specific. One such developed AI algorithm has been assessed by comparing the quality of images acquired by novice nurses, which obtained evaluable images of the TVs at 83.3%.[92] The application of AI was also extended to the phenotypic assessment of valves. In a case study of a patient with pulmonary HTN presenting as severe TR, an AI model was trained with an extreme gradient boosting algorithm. It was found to accurately predict the mean pulmonary artery pressure from echocardiography and better distinguished the severity of TR and the risk of mortality after transcatheter tricuspid valve intervention.[93] In other valvular studies, an unsupervised machine learning algorithm was created to distinguish the progression of mild and severe AS using echocardiography and clinical variables.[94] Advancements in 3D printing and AI are promising despite the applications to TR being limited to case studies and single-centre observations. The relative novelty of these concepts in valvular disorders requires extensive employment and risk-testing to distinguish its efficacy from traditional models.
| Clinical Implications and Future Recommendations | | |
We propose that further research be carried out to fill in the gaps in the literature when discussing TR. While multiple review articles and new studies are slowly being conducted, our knowledge about TR remains limited when compared to other valvular diseases. While TR at its early stages is considered benign, it can quickly become dangerous. The optimal timing of surgical intervention should be well established, as the fact that the AHA/ACC and the ESC suggest different approaches for some populations can be confusing for physicians. Previous work has also failed to distinguish the benefits of the different types of rings used in annuloplasty. While it is promising that the 2021 ESC mentioned transcatheter interventions, the recommendations require an expert physician to classify patients who should benefit from transcatheter techniques. Therefore, bias may occur, as this classification will be solely based on the physician's opinion. Last, increasing TR prevalence will inevitably be an issue that we can no longer ignore. This could translate into more patients being hospitalised, which could cause a huge burden on the healthcare system. We are confident that our paper will serve as a basis for future studies on TR.
| Conclusions | | |
TR is currently a disease of growing interest. It is linked to poor prognosis and irreversible damage to the heart chambers. While elderly individuals and females are more likely to develop TR, all age groups can develop TR. TR can be caused by organic or secondary causes. TR can exist alone or can coexist with other valvular diseases. Both pharmacological and surgical interventions are used to treat TR. This paper aims to help widen our knowledge about TR to help better treat patients with TR.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1], [Table 2], [Table 3], [Table 4]
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