Cardiac sarcoidosis: the Christchurch experience
Article first published online: 23 JAN 2014
© 2013 The Authors; Internal Medicine Journal © 2013 Royal Australasian College of Physicians
Internal Medicine Journal
Volume 44, Issue 1, pages 70–76, January 2014
How to Cite
Adamson, P., Melton, I., O'Donnell, J., MacDonald, S. and Crozier, I. (2014), Cardiac sarcoidosis: the Christchurch experience. Internal Medicine Journal, 44: 70–76. doi: 10.1111/imj.12314
Conflict of interest: None.
- Issue published online: 23 JAN 2014
- Article first published online: 23 JAN 2014
- Accepted manuscript online: 25 OCT 2013 06:06AM EST
- Manuscript Accepted: 16 OCT 2013
- Manuscript Received: 28 AUG 2013
- cardiac magnetic resonance imaging;
Background and aims
To present an overview of the diagnosis, treatment and outcomes of patients with cardiac sarcoidosis managed in Christchurch Hospital, New Zealand.
A retrospective review of patients with cardiac sarcoidosis at Christchurch Hospital from January 2005 to December 2012.
Eighteen patients were identified with cardiac sarcoidosis. All the 12 patients that underwent cardiac magnetic resonance imaging (CMR) had abnormal scans. Angiotensin-converting enzyme (ACE) levels were elevated in 4 of 16 patients and troponin (cTn) was elevated in 5 of 15 patients. Endomyocardial biopsies were diagnostic in two of six patients. The principal causes for presentation related to symptomatic high-grade atrioventricular conduction block and congestive heart failure with six patients in each of these groups. In addition, three patients presented with ventricular tachycardia and the remaining three patients presented with atrial fibrillation, recurrent presyncope without proven heart block and an asymptomatic persistent elevation of cardiac troponin. Seven patients had pre-existing, extra-cardiac sarcoidosis and a concomitant diagnosis was made in a further eight cases. Three patients had isolated cardiac involvement at presentation. Sixteen patients received immunosuppressive therapy. Twelve patients had cardiac devices implanted; five pacemakers, five defibrillators and two resynchronising pacemaker defibrillators. During follow up for 0.1–30.8 years, median 4.8 years, two patients died.
In our patients CMR demonstrated high diagnostic sensitivity, while biomarkers (ACE and cTn) were frequently within the normal reference range. Cardiac sarcoidodis caused major arrhythmias or heart failure in the majority of patients. Most patients were treated with immunosuppression and cardiac device therapy. Long-term mortality was lower than previously reported.