Key result
Device-based automatic cardiac resynchronization therapy optimization improved left ventricular ejection fraction from 30% to 60% and NYHA class from III/IV to II in a previous non-responder.
Why the study?
Does device-based automatic CRT optimization improve clinical status in a non-responding patient with dilated cardiomyopathy?
Case Report (n=1)
No
Does device-based automatic CRT optimization improve clinical status in a non-responding patient with dilated cardiomyopathy?
Device-based automatic AV and VV delay CRT optimization using a hemodynamic sensor can significantly improve symptoms and ventricular function in a non-responding patient.
Hypothesis-generating for automatic CRT optimization in non-responders; prospective trials needed before clinical adoption.
INTRODUCTION: Results on the evolution of the clinical status of patients undergoing cardiac resynchronization therapy with a defibrillator after automatic optimization of their cardiac resynchronization therapy are scarce. We observed a rapid and important change in the clinical status of our non-responding patient following activation of a sensor capable of weekly atrioventricular and interventricular delays' optimization. CASE PRESENTATION: A 78-year-old Caucasian man presented with dilated cardiomyopathy, left bundle branch block, a left ventricular ejection fraction of 35 %, New York Heart Association class III/IV heart failure, and paroxysmal atrial fibrillation. Our patient was implanted with a cardiac resynchronization device with a defibrillator and the SonRtip atrial lead. Right ventricular and left ventricular leads were also implanted. Because of the recurrence of atrial fibrillation, the automatic optimization was set off at discharge. Consequently, the device did not optimize atrioventricular and interventricular delays (programming at discharge: 125 ms for the atrioventricular delay and 0 ms for the interventriculardelay). Our patient was treated with an anti-arrhythmic drug. Five months after implantation, his clinical status remained impaired (left ventricular ejection fraction = 30 %). The SonR signal amplitude had also decreased from 0.52 g to 0.29 g. Nevertheless, because our patient was no longer presenting with atrial fibrillation, the anti-arrhythmic treatment was stopped and the SonR optimization system was activated. After 2 months of automatic cardiac resynchronization therapy with defibrillator optimization, our patient's clinical status had significantly improved (left ventricular ejection fraction = 60 %, New York Heart Association class II) and the SonR signal amplitude had doubled shortly after the first weekly automatic optimization. CONCLUSION: In this non-responding patient, device-based automatic cardiac resynchronization therapy optimization was shown to significantly improve his clinical status.
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Volpicelli et al. (2015) conducted a case report in Dilated cardiomyopathy and heart failure (n=1). Device-based automatic cardiac resynchronization therapy optimization (SonR sensor) vs. Pre-optimization baseline was evaluated on Clinical status (LVEF and NYHA class). Device-based automatic cardiac resynchronization therapy optimization improved left ventricular ejection fraction from 30% to 60% and NYHA class from III/IV to II in a previous non-responder.
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