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.

These results indicate that SAM-P8 presents a high degree of cardiovascular oxidative stress and a higher susceptibility to I/R injury, which confirms the senescence of the cardiovascular system in these animals. However, they remain sensitive to cardioprotection afforded by in vitro PostC.

We wondered if Zucker obese (ZO) rats would be a good experimental model to evaluate cardiovascular complications of metabolic syndrome (MS). ZO rats were compared with both their littermate controls, Zucker lean (ZL) rats and to Wistar rats (reference strain). We designed this work:(i) to measure certain physical and biochemical characteristics of MS; (ii) to evaluate coronary and cardiac function in isolated conditions and after ischemia; and (iii) to study plasma and heart tissue oxidative stress markers. In vivo, ZO rats had higher levels of plasma glucose, cholesterol and triglycerides than their ZL littermates, but there was no difference between the groups for systolic arterial blood pressure and heart rate. In vitro, coronary endothelial function was notably impaired in ZO and ZL rats. After global ischemia, the worse ventricular recovery in ZO and ZL rats was associated with arrhythmias during reperfusion. We detected similar levels of plasma ascorbyle free radical, oxygen radical absorbance capacity and vitamin C concentrations in the three groups. Dihydroethidium staining showed higher superoxide production in the coronary vessels of ZO rats than in ZL and Wistar rats. Our results show that ZO might only correspond to early‐stage cardiovascular complications associated with MS.

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