Abstract
The onset of atrial fibrillation is associated with the development of significant tricuspid regurgitation in the setting of progressive right atrial and tricuspid annular dilatation. This case demonstrates the positive impact on tricuspid regurgitation of cardioversion and rhythm control of atrial fibrillation.
Key Words: atrial fibrillation, cardioversion, rhythm control, tricuspid regurgitation
Graphical Abstract
History of Presentation
The patient was a 75-year-old man with multiple comorbidities, including a history of paroxysmal atrial fibrillation (AF) and tricuspid regurgitation (TR), who presented to an outside hospital because of a 1-week experience of progressive exertional dyspnea, fatigue, and lower extremity edema. He was admitted for his heart failure symptoms and was transferred to our hospital (Columbia University Irving Medical Center, New York, New York, USA) following a diagnosis of severe TR for consideration for tricuspid valve intervention. His AF history included electrical cardioversion 11 months before admission, and he received anticoagulant therapy with apixaban.
Take-Home Messages
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This case highlights that aggressive rhythm control in patients with AF and TR can lead to significant improvement in TR severity and emphasizes the importance of early rhythm management.
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A multidisciplinary approach, involving cardiologists and electrophysiologists, may be beneficial for optimal management.
Past Medical History
The patient’s other past cardiovascular medical history included hypertension, hyperlipidemia, coronary artery disease with previous percutaneous intervention to the left circumflex and left anterior descending coronary arteries, non–insulin-dependent diabetes mellitus, and chronic kidney disease (baseline creatinine, 1.9 mg/dL).
Differential Diagnosis
There were multiple possible causes of TR progression in this patient. Studies suggested that elevated pulmonary artery systolic pressure, right and left atrial enlargement, age, and a history of AF, as well as left-sided heart disease (myocardial or valvular), could be important risk factors.1
Investigations
The patient underwent a transthoracic echocardiogram, which showed normal left ventricular size and function (ejection fraction, 55%), moderate right ventricular enlargement with mildly reduced function, biatrial enlargement, and mild mitral regurgitation and massive TR by the extended grading scheme (Figures 1A to 1E, Table 1, Videos 1A to 1C). An electrocardiogram showed AF with a controlled ventricular rate and a nonspecific T-wave abnormality. A chest radiograph showed pulmonary vascular congestion. Results of laboratory studies included the following: N-terminal pro–B-type natriuretic peptide, 9,728, pg/mL; high-sensitivity troponin, 21 ng/L; hemoglobin, 8.4 g/dL; creatinine, 3.0 mg/dL; and glomerular filtration rate, 16 mL/min.
Figure 1.
Baseline Cardiac Studies
(A) The electrocardiogram shows atrial fibrillation with a nonspecific T-wave abnormality. (B to E) Echocardiographic findings consistent with massive tricuspid regurgitation. (B) A biplane color Doppler image showing the widths of the tricuspid regurgitation vena contracta: right ventricular (RV) inflow view, 1.6 cm; and apical 4-chamber (4Ch) view, 0.79 cm. (C) The color Doppler image with a baseline shift required to calculate the effective regurgitant orifice area (EROA) by the proximal isovelocity surface area (PISA) method. (D) Holosystolic hepatic vein flow reversal shown by pulsed wave Doppler imaging from the subcostal view. (E) The 3-dimensional (3D) vena contracta area (VCA) of 1.1 cm2 consistent with massive tricuspid regurgitation. bpm = beats/min.
Table 1.
Right Atrial and Right Ventricular Assessment
| Baseline | Follow-Up | |
|---|---|---|
| TV annular dimensions | ||
| Anteroposterior | 4.1 cm | 3.9 cm |
| Septolateral | 4.0 cm | 3.7 cm |
| RV size | ||
| 4-chamber base | 4.6 cm | 3.8 cm |
| 4-chamber middle | 4.3 cm | 2.9 cm |
| RA volume | ||
| 4-chamber MOD | 39 mL/m2 | 27 mL/m2 |
| RV function | ||
| RV S′ | 8 cm/s | 12 cm/s |
| TAPSE | 1.3 cm | 2.2 cm |
| FAC | 32% | 41% |
| RVFWS | −23.5% | −22% |
| 3D RVEF | 38% | 50% |
3D RVEF = 3-dimensional right ventricular ejection fraction; FAC = fractional area change; MOD = method of discs; RA = right atrial; RV = right ventricular; RVFWS = right ventricular free wall strain; S′ = tissue Doppler systolic velocity; TAPSE = tricuspid annular plane systolic excursion; TV = tricuspid valve.
Management
The patient underwent intensive inpatient intravenous diuresis guided by the heart failure team. Initial right-sided heart catheterization after 7 kg of weight loss showed a right atrial pressure 18 of mm Hg, a mean pulmonary artery pressure of 32 mm Hg, and a pulmonary capillary wedge pressure of 25 mm Hg. After an additional 6 days of diuresis and a further 8 kg of weight loss, repeat right-sided heart catheterization showed a right atrial pressure of 9 mm Hg, a mean pulmonary artery pressure of 24 mm Hg, and a pulmonary capillary wedge pressure of 16 mm Hg. A transesophageal echocardiogram confirmed severe atrial secondary TR and no evidence of an intracardiac thrombus (Videos 2A to 2D). The tricuspid valve leaflet configuration was type IIIb, with 1 anterior leaflet, 1 septal leaflet, and 2 posterior leaflets. The patient was initially treated with intravenous heparin, with rate control with metoprolol. The patient underwent electrical cardioversion with conversion from AF to sinus rhythm. His medical regimen was adjusted with escalation of his diuretics (Table 2). Metoprolol and amiodarone were continued, and the patient was discharged in sinus rhythm. A repeat transthoracic echocardiogram during a 4-month clinic follow-up showed mild to moderate TR, and an electrocardiogram showed sinus rhythm (Figures 2A to 2D, Videos 3A and 3B).
Table 2.
Medical Management
| Admission | Discharge |
|---|---|
| Apixaban, 5 mg twice daily | Warfarin 2.5, mg daily |
| Metoprolol succinate, 100 mg twice daily | Metoprolol succinate, 25 mg daily |
| Amiodarone, 200 mg daily | Amiodarone, 200 mg daily |
| Furosemide, 60 mg twice daily | Torsemide, 60 mg daily |
| Empagliflozin, 25 mg daily | Spironolactone, 12.5 mg daily |
Figure 2.
Follow-Up Cardiac Studies
(A) The electrocardiogram at follow-up shows sinus bradycardia with first-degree atrioventricular block and nonspecific T-wave abnormality. (B) The transthoracic echocardiographic findings are consistent with mild tricuspid regurgitation. (C) A normal hepatic vein flow pattern is noted. (D) The 3-dimensional vena contracta area is 0.11 cm2. bpm = beats/min.
Discussion
AF has been shown to lead to enlargement of both atria and atrioventricular annuli, increased mitral regurgitation and TR, and subsequent ventricular enlargement.2 Valvular heart disease, including TR, can cause atrial stretch, which is proarrhythmic and decreases the efficacy of preventive AF treatments.3 In addition, AF may lead to reduced cardiac output from irregular contractions or tachycardia, impaired diastolic filling, and loss of atrial systole. AF is a known risk factor for progression of TR and the development of severe atrial secondary TR, which is associated with excess mortality and morbidity.4
As demonstrated in this case, electrical cardioversion with restoration of sinus rhythm in addition to medical management for TR had a meaningful impact on the severity of TR, cardiac remodeling of the right side of the heart, and resolution of HF symptoms. Similar findings have been shown in patients who underwent direct current cardioversion, surgical AF ablation, and catheter AF ablation.5,6 Current guidelines support this treatment strategy in our patient with a Class IIa recommendation for rhythm control in patients with AF with the following: 1) symptoms; 2) a recent diagnosis (<1 year); and 3) AF with heart failure.7 This case demonstrates how multiple treatment strategies (antiarrhythmic agents and electrical cardioversion) and persistent attempts to restore sinus rhythm may be required to treat paroxysmal AF with a rhythm control strategy. Comanagement with the electrophysiology team may be needed, and catheter ablation will be considered in this patient with recently diagnosed AF if this arrhythmia recurs. Timing of repeat cardiac imaging to reassess TR severity after restoration of sinus rhythm should be deferred for a period to allow positive cardiac remodeling to occur. In the study by Soulat-Dufour et al,6 where patients were evaluated at 6 months and 12 months following either spontaneous or active restoration of sinus rhythm, reductions in right-sided heart size and regurgitation were seen at 6 months for both strategies. However, continued reduction in both right-sided heart remodeling and regurgitant severity occurred between 6 and 12 months for the active restoration of sinus rhythm group. In our case, we saw remodeling at 4 months of follow-up, a finding suggesting that chamber remodeling following conversion to sinus rhythm is likely a continuous process, and if follow-up at 3 to 6 months suggests reverse remodeling and improvement of TR, continued medical and rhythm management would be justified.
Follow-Up
Over an 8-month period, there was sustained improvement in right atrial and right ventricular size, with a decrease of TR to mild in severity (Table 1, Videos 3A and 3B). Transcatheter or surgical intervention for the patient’s TR has not been required.
Conclusions
In patients with AF and TR, we advocate for the restoration of sinus rhythm early in the disease course of AF, when reverse remodeling of the right side of the heart and improvement in TR are still possible.
Funding Support and Author Disclosures
Dr Hahn has received speaker fees from Abbott Structural, Baylis Medical, Edwards Lifesciences, Medtronic, and Philips Healthcare; has received institutional consulting contracts for which she receives no direct compensation with Abbott Structural, Edwards Lifesciences, Medtronic, and Novartis; and has served as Chief Scientific Officer for the Echocardiography Core Laboratory at the Cardiovascular Research Foundation for multiple industry-sponsored tricuspid valve trials for which she receives no direct industry compensation. Dr Lebehn has reported that he has no relationships relevant to the contents of this paper to disclose.
Footnotes
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.
Appendix
For supplemental videos, please see the online version of this paper.
Appendix
Initial Transthoracic Echocardiogram With Massive Tricuspid Regurgitation
Initial transthoracic echocardiogram with color Doppler imaging of the tricuspid valve showing massive tricuspid regurgitation from the (A and B) parasternal window and (C) apical 4-chamber window.
Transesophageal Echocardiogram
(A and B) Transesophageal echocardiographic imaging of the tricuspid valve confirmed the presence of massive tricuspid regurgitation with an elliptical orifice. Multileaflet morphology was seen in both the (B) transgastric short-axis view and (C) 3-dimensional rendered image. (D) No left atrial appendage thrombus was seen.
Follow-Up Transthoracic Echocardiogram With Mild Tricuspid Regurgitation
Follow-up transthoracic echocardiogram with biplane color Doppler imaging of the tricuspid valve showing mild tricuspid regurgitation from the (A) parasternal window and (B) apical window.
References
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Associated Data
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Supplementary Materials
Initial Transthoracic Echocardiogram With Massive Tricuspid Regurgitation
Initial transthoracic echocardiogram with color Doppler imaging of the tricuspid valve showing massive tricuspid regurgitation from the (A and B) parasternal window and (C) apical 4-chamber window.
Transesophageal Echocardiogram
(A and B) Transesophageal echocardiographic imaging of the tricuspid valve confirmed the presence of massive tricuspid regurgitation with an elliptical orifice. Multileaflet morphology was seen in both the (B) transgastric short-axis view and (C) 3-dimensional rendered image. (D) No left atrial appendage thrombus was seen.
Follow-Up Transthoracic Echocardiogram With Mild Tricuspid Regurgitation
Follow-up transthoracic echocardiogram with biplane color Doppler imaging of the tricuspid valve showing mild tricuspid regurgitation from the (A) parasternal window and (B) apical window.