Original article FDG PET as a predictor of response to resynchronisation therapy in patients with ischaemic cardiomyopathy C. M. C. van Campen 1 , Frans C. Visser 1 , Arno P. van der Weerdt 1 , Paul Knaapen 1 , Emile F. I. Comans 2 , Adriaan A. Lammertsma 2 , Carel C. de Cock 1 , Cees A. Visser 1 1 Department of Cardiology, VU University Medical Centre, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands 2 Deparment of Nuclear Medicine and PET Research, VU University Medical Centre, Amsterdam, The Netherlands Received: 20 February 2006 / Accepted: 25 June 2006 / Published online: 26 September 2006 © Springer-Verlag 2006 Abstract. Purpose: Although resynchronisation therapy (CRT) is a promising addition to heart failure therapy, a substantial number of patients do not respond to CRT. As FDG PET has routinely been used for prediction of improvement after revascularisation in ischaemic cardio- myopathy, it was hypothesised that there is also a relationship between the extent of viable tissue and improvement as a result of CRT. Methods: Thirty-nine patients with ischaemic cardiomy- opathy (ejection fraction 27±9%) and a wide QRS complex underwent temporary pacing to determine the optimal pacing combination, i.e. that with the highest increase in cardiac index (CI) compared with baseline (measured by Doppler echocardiography). All patients also underwent FDG PET imaging. In 19 patients, CI measurements were repeated 10–12 weeks after permanent biventricular pacemaker implantation. Results: Echocardiography (13-segment model) showed a mean of 9.8±1.6 dyssynergic segments, with preserved FDG uptake in 4.1±2.4 segments. CI improvement at the optimal pacing site was 20±9%. There was a linear relationship between the extent of viable tissue and CI improvement during pacing (p <0.001). Using a cut-off value of more than three viable segments (ROC analysis), FDG PET had a sensitivity of 72% and a specificity of 71% for detection of the presence of haemodynamic improvement (i.e. a CI improvement >15%). The relation between CI improvement and viable tissue was similar at follow-up. Conclusion: A correlation was found between the extent of viable tissue and the haemodynamic response to CRT in patients with ischaemic cardiomyopathy, suggesting that FDG PET imaging may be useful to discriminate between responders and non-responders to CRT. Keywords: Viability – Ischaemic cardiomyopathy – FDG-PET – Resynchronisation therapy – Heart failure Eur J Nucl Med Mol Imaging (2007) 34:309–315 DOI 10.1007/s00259-006-0235-y Introduction Heart failure is an increasing problem, owing to the growing number of patients in combination with the associated high morbidity and mortality. Despite improve- ments in pharmacological therapy, prognosis remains poor, especially in patients with a wide QRS complex [1]. Resynchronisation therapy is an additional therapy which has been shown to improve exercise tolerance, quality of life, functional class and left ventricular (LV) function. Moreover, it decreases the need for hospitalisation and possibly improves survival [2–5]. However, a substantial number of patients (18–50%) do not respond to this [2, 4, 6–11]. Several techniques for discriminating between responding and non-responding patients have been pro- posed, but none of these are reliable enough for use in routine clinical practice [8, 12, 13]. Earlier studies have shown that the presence of viable tissue as documented by 18 F-fluorodeoxyglucose (FDG) positron emission tomography (PET) predicts functional improvement in patients with ischaemic cardiomyopathy undergoing revascularisation [14, 15]. Therefore, the purpose of the present study was to assess whether there is a relation between the extent of viability and the degree of functional improvement in ischaemic cardiomyopathy patients who are candidates for resynchronisation therapy. Materials and methods Thirty-nine consecutive heart failure patients with ischaemic cardio- myopathy and a wide QRS complex, who were selected for C. M. C. Campen ()) Department of Cardiology, VU University Medical Centre, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands e-mail: fc.visser@vumc.nl Tel.: +31-20-4440123, Fax: +31-20-4442446 European Journal of Nuclear Medicine and Molecular Imaging Vol. 34, No. 3, March 2007