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Morphologic Types of Tricuspid Regurgitation Characteristics and Prognostic Implications

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Morphologic Types of Tricuspid Regurgitation Characteristics and Prognostic Implications JACC: CARDIOVASCULAR IMAGING VOL. 12, NO. 3, 2019 ª 2019 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION PUBLISHED BY ELSEVIER STATE-OF-THE-ART PAPER Morphologic Types of Tricuspid Regurgitation Characteristics and Prognostic Implications a,b a c d Edgard A. Prihadi, MD, Victoria Delgado, MD, PHD, Martin B. Leon, MD, PHD, Maurice Enriquez-Sarano, MD, PHD, e a Yan Topilsky, MD, PHD, Jeroen J. Bax, MD, PHD ABSTRACT Tricuspid regurgitation (TR) is classified according to different morphologic types based on the underlying mechanisms: primary, secondary, and isolated TR. Primary TR is caused by an anatomical abnormality of the tricuspid valve apparatus. Secondary TR is caused by dilation of the tricuspid valve annulus, related to right ventricular (RV), or right atrial remodeling and increased RV pressures (often secondary to left-sided heart disease). Isolated TR can exist in patients without increased RV pressures and is frequently associated with atrial fibrillation. Two-dimensional echocardiography plays a pivotal role in the assessment of the etiology and severity of TR. Views from 3-dimensional techniques have significantly increased the understanding of the pathophysiology of each morphologic type of TR (leaflet damage, annular dilation, and distinct patterns of right-heart remodeling). The following review will describe the etiology, anatomical and functional characteristics, and outcomes of each morphologic type of TR, and furthermore addresses challenging pitfalls in the referral for tricuspid valve intervention. (J Am Coll Cardiol Img 2019;12:491–9) © 2019 by the American College of Cardiology Foundation. uring the last 2 decades, insights into the morphologic types of TR can be distinguished, D natural history and pathophysiology of depending on the presence of a primary abnormality tricuspid regurgitation (TR) have shifted of the TV apparatus (primary TR), dilation of the TV the treatment of TR from a conservative approach, annulus, leaflet tethering, and right ventricular (RV) to an approach of intervention and potential remodeling (due to left-sided heart disease and prevention. Advances in echocardiographic tech- pulmonary hypertension) (secondary TR) or atrial niques and the development of 3-dimensional (3D) fibrillation (AF) and right atrial (RA) remodeling imaging modalities have further allowed more accu- (isolated TR) (Central Illustration). Along with growing rate assessment of tricuspid valve (TV) morphology, insights into the deleterious outcomes of untreated mechanisms of TR, severity of TR, and more detailed TR and high mortality risk associated with surgical evaluation of the extent of right-heart remodeling, all intervention, novel transcatheter devices have been potentially contributing to TR progression. Different developed. This review will describe the different From the aDepartment of Cardiology, Leiden University Medical Center, Leiden, the Netherlands; bDepartment of Cardiology, ZNA Middelheim Hospital, Antwerpen, Belgium; cDepartment of Cardiology, Columbia University Medical Center, New York, New York; dCardiovascular Diseases Division, Mayo Clinic, Rochester, Minnesota; and the eDepartment of Cardiology, Tel Aviv Medical Center, Sackler Faculty of Medicine, Tel Aviv, Israel. The Department of Cardiology of the Leiden University Medical Center has received research grants from Boston Scientific, Medtronic, Biotronik, Edwards Lifesciences, and GE Healthcare. Dr. Delgado has received personal fees from Abbott Vascular. Dr. Enriquez-Sarano has received grants from Edwards LLC. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Manuscript received June 18, 2018; revised manuscript received September 17, 2018, accepted September 20, 2018. ISSN 1936-878X/$36.00 https://doi.org/10.1016/j.jcmg.2018.09.027 492 Prihadi et al. JACC: CARDIOVASCULAR IMAGING, VOL. 12, NO. 3, 2019 TR Phenotype and Prognosis MARCH 2019:491– 9 ABBREVIATIONS types of TR and their anatomical and reduced left ventricular (LV) ejection fraction pre- AND ACRONYMS functional characteristics and outcomes. senting with acute (19) or chronic (20–22) heart failure Furthermore, pitfalls in the preprocedural (HF), significant TR is commonly observed which can AF = atrial fibrillation risk stratification will be addressed. progress further despite optimal medical therapy and CI = confidence interval cardiac resynchronization therapy (Figure 1) (23). EROA TYPES OF TR: PRIMARY, SECONDARY, = effective regurgitant Pulmonary hypertension, arising from other causes orifice area AND ISOLATED than left-sided heart disease, includes primary pul- HF = heart failure monary hypertension, pulmonary embolism, and HR = hazard ratio TR is a relatively common valvular heart chronic pulmonary disease. These etiologies can LV disease which is classified based on the = left ventricular cause TR due to increased RV afterload, RV dilation, underlying mechanism as primary or sec- RV = right ventricular anddysfunction.Furthermore,intheabsenceof ondary. The estimated frequency of primary TR = tricuspid regurgitation pulmonary hypertension, diseases directly affecting TR is 8% to 10%, less frequent than second- TV = tricuspid valve the RV function such as ischemia in inferior myocar- ary TR which accounts for the most frequent dial infarction (24,25) or arrhythmogenic mechanism of TR. RV dysplasia/cardiomyopathy (26) can lead to TR Primary TR is caused by an abnormality of any of through apical displacement of the papillary muscles the components of the TV apparatus (tricuspid leaf- and increased tethering of the TV leaflets. lets, chordae, papillary muscles, or annulus), due to Finally, other than primary or secondary TR, congenital or acquired causes. The most common isolated TR is a morphologic type of TR which is congenital abnormality of the TV is Ebstein’sdisease increasingly recognized as a separate entity. In the characterized by an apical displacement of the leaflets absence of concomitant pulmonary hypertension or which arise directly from the wall of the RV without co-existing left-sided heart disease, isolated TR is identifiable chordae (1). Acquired causes of primary mainly present in elderly patients with a high prev- TR include tumors (such as carcinoid disease and alence of AF causing RA dilation, TV annulus dilation, myxoma), iatrogenic injury (such as RV endomyo- and TV leaflets malcoaptation (Figure 1) (27–29). cardial biopsy, transvenous pacing, or defibrillator leads), drug-induced leaflet damage (such as HOW TO ASSESS THE ANATOMICAL AND anorectic drugs, dopamine agonists, and ergot FUNCTIONAL CHARACTERISTICS OF alkaloids) (2), systemic diseases (such as lupus VARIOUS TYPES OF TR erythematosus and sarcoidosis), radiation, rheumatic disease, endocarditis, and trauma (3).Amongac- Table 1 summarizes the different echocardiographic quired causes of TR, transvenous pacemaker or defi- characteristics of primary,secondary,andisolated brillator lead-induced TR is one of the most frequent TR. In primary TR, echocardiographic assessment of etiologies. With aging of the global population and individual leaflet pathology by 2-dimensional (2D) an increasing number of patients with pacemaker echocardiography is particularly challenging because devices, the prevalence of lead-induced TR may of anatomic variability in size and number of leaflets increase considerably. Among patients without TR and only 2 TV leaflets can be visualized simulta- before pacemaker implantation, up to 38% may neously on routine echocardiographic views. 3D develop significant TR over the following 1 to echocardiographic imaging permits more accurate 1.5 years after lead insertion (Figure 1) (4). individual leaflet identification by providing the “en SecondaryTRisfrequentlycausedbyRVdilation face” visualization of the TV, further improving and dysfunction, leading to leaflet tethering, assessment of leaflet morphology and mobility and tricuspid annulus dilation, and malcoaptation (5).The involvement of the subvalvular apparatus (30,31). most frequent causes of secondary TR include co- Whereas myxomatous valve disease is characterized existing left-sided valvular and myocardial disease by the presence of redundant tissue with excess associated with increased left atrial pressures, pul- leaflet mobility (32), thickened leaflets with a monary hypertension, and increased RV afterload. restrictive motion can be caused by carcinoid syn- Thirty percent to 50% of patients with severe mitral drome (33) or less frequently rheumatic involvement. regurgitation (6) and more than 25% of patients with Lead-induced TR can be caused by impingement severe aortic stenosis (7) show significant (moderate of the tricuspid leaflet by the lead itself, leaflet and severe) TR. Furthermore, after surgical or trans- perforation, laceration or avulsion, and transection catheter treatment of mitral regurgitation (8–13) or of papillary muscles or chordae tendineae (34,35). aortic stenosis (14–18), progression or late onset of TR In TR after pacemaker/defibrillator-lead implanta- can frequently occur. Similarly, in patients with tion, diagnosing the cause of TR remains challenging JACC: CARDIOVASCULAR IMAGING, VOL. 12, NO. 3, 2019 Prihadi et al. 493 MARCH 2019:491– 9 TR Phenotype and Prognosis CENTRAL ILLUSTRATION Schematic Drawing of the Different Morphologic Types of Tricuspid Regurgitation Prihadi, E.A. et al. J Am Coll Cardiol Img. 2019;12(3):491–9. Primary tricuspid regurgitation (A), where there is primary damage of the tricuspid valve apparatus (prolapse of the posterior
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