Assessment of right ventricular oxidative metabolism by PET in patients with idiopathic dilated cardiomyopathy undergoing cardiac resynchronisation therapy

Purpose: Right ventricular (RV) performance is known to have prognostic value in patients with congestive heart failure (CHF). Cardiac resynchronisation therapy (CRT) has been found to enhance left ventricular (LV) energetics and metabolic reserve in patients with heart failure. The interplay between the LV and RV may play an important role in CRT response. The purpose of the study was to investigate RV oxidative metabolism, metabolic reserve and the effects of CRT in patients with CHF and left bundle brach block. In addition, the role of the RV in the response to CRT was evaluated. Methods: Ten patients with idiopathic dilated cardiomyopathy who had undergone implantation of a biventricular pacemaker 8 5 months earlier were studied under two conditions: CRT ON and after CRT had been switched OFF for 24 h. Oxidative metabolism was measured using [C-11]acetate positron emission tomography (K-mono). The measurements were performed at rest and during dobutamine-induced stress (5 mug/kg, per minute). LV performance and interventricular mechanical delay (interventricular asynchrony) were measured using echocardiography. Results: CRT had no effect on RV K-mono at rest (ON: 0.052 +/- 0.014, OFF: 0.047 +/- 0.018. NS). Dobutamine-induced stress increased RV K-mono significantly under both conditions but oxidative metabolism was more enhanced when CRT was ON (0.076 +/- 0.026 vs 0.065 +/- 0.027, p=0.003). CRT shortened interventricular delay significantly (45 +/- 33 vs 19 +/- 35 ms, p=0.05). In five patients the response to CRT was striking (32% increase in mean LV stroke volume, range 18-36%). while in the other five patients no response was observed (mean changge +2%, range -6% to +4%). RV K-mono and LV stroke volume response to CRT correlated inversely (r=-0.66 p=0.034). None of the other measured parameters, including all LV parameters and electromechanical parameters, were associated with the response to CRT. In responders. RV K-mono with CRT OFF was significantly lower than in non-responders (0.036 +/- 0.01 vs 0.058 +/- 0.02, p=0.047). Conclusion: CRT appears to enhance RV oxidative metabolism and metabolic reserve during, stress. Patients responding to CRT appear to have lower RV oxidative metabolism at rest, suggesting that the RV plays a significant role in the response to CRT.