Skip to main content
Journal of Cardiology Cases logoLink to Journal of Cardiology Cases
. 2020 Nov 26;23(5):227–230. doi: 10.1016/j.jccase.2020.11.012

Remarkable oxygen consumption improvement after auricular flutter ablation in a patient with constrictive pericarditis and severe mitral stenosis

Sebastián Giacoman a,, Ana Delia Ruiz a, Finn Akerström b, Pablo Toledo a, Francisco Burillo a, José Miguel Lozano a
PMCID: PMC8103318  PMID: 33995703

Abstract

Atrial function is a key factor in cardiac output and oxygen consumption (VO2). Substantial improvements in VO2 have been reported after restoring sinus rhythm (SR) in patients with atrial fibrillation. However, there are no published data on how atrial function affects VO2 in patients with both constrictive pericarditis (CP) and severe mitral stenosis (MS). A 53-year-old caucasian patient consulted for exacerbated heart failure (EHF). His medical record lists ischemic heart disease, severe MS, and CP after thoracic radiotherapy. The electrocardiogram showed atrial flutter (AFL) with controlled ventricular rate. Normal left ventricular ejection fraction was observed. Ergospirometry showed an impaired maximum VO2 (VO2 max) of 6 ml/kg/min. On the electrophysiological study typical AFL was diagnosed and ablated achieving a great exercise capacity improvement, correlated with an increase of VO2 max to 16 ml/kg/min a week after ablation, and disappearance of EHF symptoms. This case illustrates how restoration of SR resulted in a clinical substantial improvement. Radiofrequency catheter ablation is warranted as the most effective option in this context.

<Learning objective: Atrial function impairment has a marked impact on cardiac dynamics in patients with both severe constrictive pericarditis and mitral stenosis. In this setting, sinus rhythm restoration should be pursued.>

Keywords: Constrictive pericarditis, Severe mitral stenosis, Atrial flutter, Oxygen consumption

Introduction

Constrictive pericarditis (CP) and mitral stenosis (MS) secondary to radiotherapy are rare [1,2]. There are no published data on the potential impact on functional class and oxygen consumption (VO2) of losing sinus rhythm (SR) in this scenario. We report a case with both CP and severe MS secondary to radiotherapy, who had significantly improved New York Heart Association functional class and VO2 after restoration of SR.

Case report

This case involved a 53-year-old patient with a medical record of mediastinal Hodgkin lymphoma treated with radiotherapy. Subsequently he was diagnosed with ischemic heart disease (IHD) [left main coronary artery (LMCA) and left anterior descending artery (LAD) junction and chronic coronary artery disease stenosis], radiotherapy related MS and CP, among other sequelae (Fig. 1A,B,C,D). He was rejected for LMCA-LAD and mitral valve surgery, also for pericardiectomy. Percutaneous coronary intervention (PCI) was performed for LMCA and LAD junction. Normal ejection fraction but diastolic dysfunction (left atrial volume index 36 ml/m2, E 2.5 m/s, A 0,95 m/s, and E/A 2.6) were described.

Fig. 1.

Fig. 1

Echocardiography and chest X-ray. (A) Mitral valve planimetry in parasternal short axis: 0.82 cm2, compatible with severe mitral stenosis. (B) 4C apical projection: biauricular enlargement but normal dimensioned ventricles. Thickening and hyperechogenicity are observed in the pericardial space, especially in the atrioventricular groove, with ventricular contour distortion (blue arrow). Severe calcification of the mitral ring and body veils respecting their edge, compatible with radiotherapy damaging (yellow arrow). (C) Parasternal long-axis M mode of the left ventricle: protodiastolic rebound of the septum or “notch” (red arrow), a specific sign for pericardial constriction. (D) Chest X-ray showing perihilar linear densities and volume loss related to radiotherapy-induced paramediastinal pulmonary fibrosis, and moderate right pleural effusion.

He described worsening of dyspnea, paroxysmal nocturnal dyspnea, and ankle edema, with N-terminal prohormone of brain natriuretic peptide (NT-proBNP) of 4700 pg/ml, in the context of atrial flutter (AFL). Median heart rate (HR) was 55 rpm at rest in AFL on the beta-blocker tolerated dose, but no other anthyarrthmic. Ergospirometry was performed finding VO2 max of 6 ml / kg / min, and peak HR rounded 110 rpm during exercise. Worsening of diastolic function was observed (E 3,1 m/s). No new coronary lesions were found on PCI.

By high-density mapping supported by Abbott EnSite Precision navigation system and AdvisorTM HD Grid catheter (HD Grid, Abbott, Abbott Park, Illinois), we defined a large scar area in the right atrium voltage map (Fig. 2A). Typical AFL was confirmed (Fig. 2B, 2C) and cavotricuspid isthmus radiofrequency catheter ablation (RFCA) restored SR (Fig. 2D). A week later the patient reported clear clinical improvement, that has been sustained. VO2 max increased up to 16 ml/kg/min in the control ergospirometry, as well as the oxygen pulse (Fig. 3 A,B,C). Ventricular filling pressure slightly improved (E 2.5 m/s) and NT-proBNP was normalized (325 pg/ml).

Fig. 2.

Fig. 2

High-density maps and endocavitary electrograms (EGM) registry. (A) The voltage map shows large areas of low voltage compatible with scars, predominantly in the right atrial anterolateral region (gray area). (B) Activation map depicts a sequence compatible with typical counterclockwise flutter. (C) Surface electrocardiogram and EGM registry of the duodecapolar catheter around the tricuspid ring progressed to the proximal coronary sinus. Post-pacing interval from the cavotricuspid isthmus equal to the tachycardia cycle length, confirming typical atrial flutter. (D) Sinus rhythm after cavotricuspid isthmus radiofrequency catheter ablation line.

Fig. 3.

Fig. 3

Ergospirometry. (A) Oxygen consumption (VO2) (litres per minute) before (light blue line, blue arrow), compared to after ablation more than two- fold increase (dark blue line, red arrow), respectively. (B) Respiratory exchange ratio reflecting similar effort performance before (light blue line, green arrow), and after ablation (dark blue line, black arrow). (C) Histograms of heart rate (light and dark purple lines) and oxygen pulse (millilitres per beat) (light and dark blue lines) before and after ablation, respectively. The lower heart rate and increased left ventricle systolic volume led to a significant improvement in VO2.

Discussion

The role of atrial function in normal cardiac physiology is crucial and complex. In addition to contributing as a reservoir of pulmonary venous return during ventricular systole, its synchronized activation is essential during ventricular filling in protodiastole and especially in telediastole [3].

This case provides evidence for how anomalous atrial performance directly affects cardiac output and dynamics, resulting in the worsening of heart failure (HF) and VO2. It demonstrates the improvements related to SR restoration. There are publications related to this matter in atrial fibrillation (AF) patients [4], as well as reductions in VO2 in patients with severe MS in SR and AF [5]. The current case accounts the coexistence of two infrequent post-radiotherapy sequelae, and AFL.

In the presence of MS, late ventricular filling is compromised because of a smaller contribution of atrial contraction, being proportionately smaller the more severe the MS [6,7]. The same occurs in CP, where early equalization of pressures between atrium and ventricle makes late diastole filling insufficient. This patient's early filling was also impaired because of a deterioration in compliance due to ageing [8], CP, and IHD.

AFL in this clinical scenario significantly disturbed the already damaged cardiac dynamics. Dyssynchrony and the increased HR during exercise shortens diastole, worsening ventricular early filling. It also affects late filling, crucial in CP, severe MS, and diastolic dysfunction in the setting of IHD and ageing [9], leading to HF.

Achieving SR in this particular patient should become the standard approach, opting for RFCA when possible as it has been demonstrated to be the most effective and lasting strategy for AFL [10].

Declaration of Competing Interest

None.

References

  • 1.Malanca M, Cimadevilla C, Brochet E, Lung B, Vahanian A, Messika-Zeitoun D. Radiotherapy-induced mitral stenosis: a three-dimensional perspective. J Am Soc Echocardiogr. 2010;23(108):e1–e2. doi: 10.1016/j.echo.2009.08.006. [DOI] [PubMed] [Google Scholar]
  • 2.Muggia FM, Cassileth PA. Constrictive pericarditis following radiation therapy. Am J Med. 1968;44:116–123. doi: 10.1016/0002-9343(68)90242-8. [DOI] [PubMed] [Google Scholar]
  • 3.Fang F, Lee AP-W, Yu C-M. Left atrial function in heart failure with impaired and preserved ejection fraction. Curr Opin Cardiol. 2014;29:430–436. doi: 10.1097/HCO.0000000000000091. [DOI] [PubMed] [Google Scholar]
  • 4.Wozakowska-Kaplon B, Opolski G. Effects of sinus rhythm restoration in patients with persistent atrial fibrillation: a clinical, echocardiographic and hormonal study. Int J Cardiol. 2004;96:171–176. doi: 10.1016/j.ijcard.2003.05.033. [DOI] [PubMed] [Google Scholar]
  • 5.Cohen-Solal A, Aupetit JF, Dahan M, Baleynaud S, Slama M, Gourgon R. Peak oxygen uptake during exercise in mitral stenosis with sinus rhythm or atrial fibrillation: lack of correlation with valve area. A study in 70 patients. Eur Heart J. 1994;15:37–44. doi: 10.1093/oxfordjournals.eurheartj.a060377. [DOI] [PubMed] [Google Scholar]
  • 6.Meisner JS, Keren G, Pajaro OE, Mani A, Strom JA, Frater RW, Laniado S, Yellin EL. Atrial contribution to ventricular filling in mitral stenosis. Circulation. 1991;84:1469–1480. doi: 10.1161/01.cir.84.4.1469. [DOI] [PubMed] [Google Scholar]
  • 7.Parris TM, Mintz GS, Ross J, Panidis IP. Importance of atrial contraction to left ventricular filling in mitral stenosis. Am J Cardiol. 1988;61:1135–1136. doi: 10.1016/0002-9149(88)90147-6. [DOI] [PubMed] [Google Scholar]
  • 8.Strait JB, Lakatta EG. Aging-associated cardiovascular changes and their relationship to heart failure. Heart Fail Clin. 2012;8:143–164. doi: 10.1016/j.hfc.2011.08.011. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Goldstein JA. Cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy. Curr Probl Cardiol. 2004;29:503–567. doi: 10.1016/j.cpcardiol.2004.03.002. [DOI] [PubMed] [Google Scholar]
  • 10.Brugada J, Katritsis DG, Arbelo E, Arribas F, Bax JJ, Blomström-Lundqvist C, Calkins H, Corrado D, Deftereos SG, Diller GP, Gomez-Doblas JJ, Gorenek B, Grace A, Ho SY, Kaski JC. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. Eur Heart J. 2020;41:655–720. doi: 10.1093/eurheartj/ehz467. [DOI] [PubMed] [Google Scholar]

Articles from Journal of Cardiology Cases are provided here courtesy of Japanese College of Cardiology

RESOURCES