AimsThe purpose of the present study was too explore the role of interatrial dyssynchrony in heart failure with preserved ejection fraction (HFPEF). Methods and resultsFor the case study we selected seven patients with severe HFPEF, with interatrial block on electrocardiogram (ECG), and a delayed and interrupted A wave on mitral Doppler. Echocardiographic left atrial (LA) volumes/functions, mitral E/A and E/e' ratios, mitral A wave duration/deceleration time, and interatrial mechanical delays (IAMDs) at tissue Doppler, were studied. We performed right heart catheterization, and an electrophysiological study (EPS) for the measurement of interatrial conduction delay (IACD) and left atrioventricular interval (LAVI). Mean IAMD was 106 ms. All the patients exhibited a restrictive mitral Doppler pattern, high E/A and E/e' ratios, and short A wave duration/deceleration time. Left atrial volume was increased, with severely depressed functions. Right heart catheterization showed severe post-capillary pulmonary hypertension. The EPS showed an IACD of 170 + 20 ms, with a short LAVI. Left atrial pacing through the coronary sinus reduced the IACD to 25 + 15 ms. In the pilot study, 29 patients with HFPEF were compared with 27 age-matched control patients. HFPEF patients had longer P waves, shorter A waves, and a longer IAMD than the controls. Prevalence of severe IAMD .60 ms was 59% in HFPEF and 0% in controls. In the HFPEF group, patients with an IAMD .60 ms had significantly shorter A waves and higher E/e' ratio. ConclusionSome HFPEF patients present with IACD, delayed LA systole, shortened LA emptying, decreased LA compliance, and increased filling pressures. Whether the condition of these patients could be improved by atrial resynchronization deserves further investigation.--

Aims Our group has recently shown that in some patients, heart failure with preserved ejection fraction (HFPEF) may be explained by ‘atrial dyssynchrony syndrome’ (ADS) due to interatrial conduction delay (IACD), a short left atrioventricular interval (LAVI), and increased left atrial (LA) stiffness. Our primary objective was to evaluate LA pacing therapy as a new treatment to restore left ventricular active filling in patients with no other known causes for HF than ADS. Methods and results Six patients with severe HFPEF with IACD (P wave duration >120 ms in lead II), short LAVI during electrophysiological studies (<70 ms), a restrictive filling pattern (E/e' >15), and no standard indication for a pacemaker were implanted with a lead screwed inside the coronary sinus for active LA pacing. After 3 months of active pacing, a 2 week randomized double‐blind crossover phase compared active vs. inactive LA pacing. After 3 months of pacing, the mean distance walked in 6 min (6MWD) was 21% greater (240 ± 25 m vs. 190 ± 15m, P < 0.05), mitral A wave duration was longer (104 ± 8 vs. 158 ± 25 ms, P = 0.002), and E/A and E/e' ratios were smaller (3.4 ± 1.3 vs. 1.8 ± 0.9, P = 0.009, and 22.6 ± 4.6 vs. 15.3 ± 4.3, P = 0.006, respectively). Inactivation of pacing for 1 week led to a significant reduction in the 6MWD, with an on/off response. Conclusion The beneficial effects of LA pacing observed in this pilot study will have to be confirmed by the randomized, controlled crossover ‘LEAD’ study.

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