Quick Fire Session
SCMR 22nd Annual Scientific Sessions
Christopher Saunderson
Clinical Research Fellow
University of Leeds
John Gierula, PhD
NIHR Post Doctoral Research Fellow
University of Leeds
Maria Paton, MSc
Clinical Academic Doctoral Research Fellow
University of Leeds
Louise Brown, BSc, MB
CMR Research Fellow
University of Leeds
Pei Chew
CMR Research Fellow/Cardiology SpR
University of Leeds
Arka Das
Clinical Research Fellow
Multidisciplinary Cardiovascular Research Centre & Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom
Eylem Levelt, PhD
Cardiologist
University of Leeds
Erica Dall'Armellina, PhD
BHF Intermediate Clinical Research Fellow
University of Leeds
Klaus Witte, MD
Consultant Cardiology and Honorary Lecturer
University of Leeds
.jpg "John Greenwood, PhD photo")
John Greenwood, PhD
Professor of Cardiology
University of Leeds
Sven Plein, MD, PhD
BHF Professor of Cardiovascular Imaging; Consultant Cardiologist
University of Leeds
Peter Swoboda, PhD
NIHR Clinical Lecturer
University of Leeds
Background:
Deterioration in left ventricular ejection fraction (LVEF) has been observed in up to one third of patients with pacemakers. Heart failure (HF) is a major long-term complication of permanent pacing. The determinants of pacing-induced cardiomyopathy are incompletely understood. We hypothesised that forced right ventricular (RV) pacing in patients with left ventricular (LV) ischaemic scar leads to acute haemodynamic changes that may predispose patients to HF in the longer term.
Methods:
16 asymptomatic patients with an MRI conditional pacemaker without atrioventricular (AV) block and ≤10% RV pacing underwent cardiovascular magnetic resonance to compare the effect of intrinsic AV conduction (AOO) vs RV pacing (DOO) (Table 1). Patients were scanned in both AOO and DOO modes (random order) with the base rate set at 10bpm above intrinsic rate. The scan protocol included a short axis ventricular volume stack and late gadolinium imaging (LGE). LV strain analysis was performed using commercially available feature tracking software (CVI42, Circle Cardiovascular Imaging). Mechanical dyssynchrony index (MDI) was calculated using the standard deviation of the time to peak strain of all AHA segments. LGE images were visually reviewed for the presence or absence of ischaemic scar.
Results:
Patients were divided into 2 groups based on presence or absence of scar (Table 1). There were no significant differences in heart rate, percentage of atrial or ventricular pacing and LVEF between groups. The group with scar were significantly older with longer QRS durations in both AOO (116ms vs. 89ms; p=0.02) and DOO (166ms vs. 138ms; p=0.02) modes. There were significant reductions in LVEF from AOO to DOO pacing in both groups (No scar: 53.3±4.7% to 50.8±4.4%; p<0.01 and Scar: 46.5±6.2% to 40.3±6.9%; p<0.01) (Figure 1). The absolute change between AOO and DOO modes was greater in the group with scar (-6.3±1.7% vs -2.5±1.5%; p<0.01). There was a non-significant trend to increased MDI from AOO to DOO modes (No scar: 108.2±29.7ms to 130.8±36.8ms; p=0.12 and Scar: 115.3±10.8ms to 127.3±36.2ms; p=0.36).
Conclusion:
Forced RV pacing leads to acute LV haemodynamic changes compared with intrinsic AV conduction in patients with and without ischaemic scar. These changes are more pronounced in patients with ischaemic scar. There was a trend to worsening mechanical dyssynchrony with forced RV pacing suggesting this may contribute to the observed haemodynamic changes. Further work is needed to evaluate if chronic RV pacing in patients with ischaemic LV scar leads to an increased long term risk of HF.