Longitudinal Follow-Up of a Right Atrial Appendage Aneurysm by Cardiac Magnetic Resonance Imaging

Abstract

A 13-year-old boy was referred to cardiology for evaluation of intermittent exertional breathlessness. Previous respiratory investigations had revealed normal lung function and no evidence of asthma on exercise spirometry. There was no past medical history of note. Cardiorespiratory examination was unremarkable except for a soft ejection systolic murmur at the lower left sternal border. ECG showed sinus rhythm and normal P-wave morphology and QRS axis, with a T-wave inversion in leads III and aVF. Chest radiograph demonstrated normal cardiothoracic ratio, but the heart was noted to be globular in shape (Figure 1).Transthoracic echocardiography revealed the presence of a large, thin-walled aneurysmal structure in continuity with the free wall of the right atrium, discrete from the caval veins ( Figure 2). There was mild tricuspid regurgitation, with a Doppler velocity of 2.1 m/s. Both ventricles were of normal size and function. To further characterize this cardiac abnormality, the patient was referred for cardiac magnetic resonance (CMR) imaging. Cine imaging using a balanced steady-state free precession sequence showed a noncontractile, smooth-walled, right atrial appendage aneurysm (RAAA) extending anterior to the body of the right atrium ( Figure 3A and 3B and Movie I of the online-only Data Supplement). The aneurysm had a broad-based pyramidal shape and was partially separated from the main atrial chamber by a membrane (total indexed right atrial volume 118 mL/m 2 at end-ventricular systole). There was mild distortion of the right ventricular (RV) inlet, but no significant compression. No intracavity thrombus was identified. The pulmonary arteries were unobstructed and of normal caliber. There was a small pericardial effusion.The patient subsequently underwent exercise tolerance testing, managing 12 minutes and 15 seconds on the standard Bruce protocol and achieving a workload of 13.8 metabolic equivalents. The test was stopped because of dyspnea, with no ST-segment changes detected. A 1-week cardiac rhythm monitor revealed no evidence of arrhythmia. On review in the outpatient clinic, the patient had symptomatically improved. He was therefore commenced on aspirin for thromboembolic prophylaxis and managed conservatively with annual imaging surveillance. During the next 2 years the patient was asymptomatic, with no significant change in the size of the RAAA on transthoracic echocardiography. However, repeat CMR imaging performed 3 years after the initial scan revealed a marked increase in the size of the aneurysm that was disproportionate to somatic growth (total indexed right atrial volume increased to 151 mL/m 2 ) ( Figure 3C and 3D). In addition, there was evidence of clear compression of the RV inlet by the RAAA (Movie II of the online-only Data Supplement), with flattening of the tricuspid annulus during ventricular diastole. Although the patient remained well, in view of the increase in relative size of the RAAA and associated RV inlet diastolic displacement, the patient was referred for surgical res...

Right Atrial Appendage Aneurysm: A Systematic Review

“…3,6,9,10 Periodic monitoring of RAAA in asymptomatic patients with cardiac MRI or CT for evidence of enlarging RAAA has been shown to be a useful tool in selecting patients for early surgical intervention. 14,17 Patients with evidence of enlarging RAAA should be considered for surgical excision as they are relatively at higher risk for atrial tachyarrhythmia and thromboembolic events. 3) of RAAA to decreases the risk of arrhythmias and thromboembolic complications.…”

A Case of Right Atrial Appendage Aneurysm in a 62‐Year‐Old Man

“…Right atrial appendage aneurysm is an extremely rare condition: a search on PubMed using combined keywords of “right atrial appendage” and “aneurysm” for title or abstract only yielded 13 case reports, until April 2013. RAAA is generally considered to be congenital, whereas the etiology remains largely unknown . Although the case we present is combined with CAD, myocardial ischemia is not considered as the cause of RAAA, because the RCA stenosis lies distal to the aneurysm.…”

Almanac 2012: Congenital heart disease. The national society journals present selected research that has driven recent advances in clinical cardiology

“…This lends itself to imaging, and congenital heart images brighten up the pages of many major cardiac journals. Therefore it seems appropriate to end this Almanac with reference to some of the more stunning images that reflect the key areas in congenital heart disease that were discussed above, including intervention, [85][86][87][88][89][90][91] foetal and neonatal, [92][93][94][95] heart failure and mechanical support, 9 adolescent and adult congenital heart disease, 97,98 advanced imaging with MRI and CT 99,100 and unusual morphology. [101][102][103][104][105][106][107] All of which are well worth a look to brighten up a night catching up on the cardiac journals.…”