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Effect of atrioventricular asynchrony on platelet activation
  1. Psagot, DN Mizrach Binyamin
  2. Israel 90–624

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Sir,—I read with great interest the article on the effect of atrioventricular asynchrony on platelet activation by Lau,et al.1 The authors conclude that “loss of atrioventricular synchrony related to single chamber ventricular pacing is a major cause of increased platelet activation.”

However, the tables and text indicate that in both modes of DDD pacing, platelet activation is increased by approximately 160–200% compared with the control group. Twelve of their patients had a permanent pacemaker implanted because of sick sinus syndrome—most probably a defect in impulse generation with or without accompanying tachyarrhythmias. In those patients, an attempt at AAI pacing could have proven effective, perhaps with concentrations of both platelet factor and β thomboglobulin in the normal (control) range. This could have clinical and practical implications regarding the choice of pacemaker when significant bradyarrhythmias are the primary reason for pacemaker implantation.

As the only single chamber mode of pacing was in the ventricle, there is the possibility that single chamber atrial pacing would be as beneficial (from a haemostatic aspect) and as effective (from a haemodynamic aspect) as DDD(R). It is a pity to have missed an opportunity to establish whether it is asynchrony that causes increased platelet activation (as the authors claim) or whether single chamber pacing (be it atrial or ventricular) is the culprit.

Moreover, the increase in platelet activation could be attributed to pacing in the ventricle and, maybe, if patients were paced in the atrium only, concentrations of platelet activity would be in the control range. Such clarification could have a significant impact both on policy making and economics considering the difference in price for single (AAI, VVI) versus dual chamber pacemakers.


This letter was shown to the authors, who reply as follows:

We thank Dr Mazouz for his interest. We agree that in patients with sick sinus syndrome, AAI pacing is as effective and beneficial as DDD pacing. In fact, a long term follow up, randomised, prospective trial1-1 demonstrated that AAI pacing in patients with sick sinus syndrome is associated with significantly lower cardiovascular mortality (p = 0.022) and fewer thromboembolic events (p = 0.028) than VVI pacing. We found that all patients with pacemakers have evidence of increased systemic platelet activation,1-2 which is likely to relate to contact of platelets with an artificial surface. More importantly, with the patients acting as their own controls, VVIR pacing was associated with a significantly higher degree of platelet activation than DDD or DDDR modes.

AAI mode was not tested in our study for the following reasons. First, our study population included some patients with complete heart block and some with sick sinus syndrome, thus AAI mode could not be used in all of them. Second, all patients had a dual chamber pacemaker, so even when they are paced in AAI mode the effects of an additional ventricular lead on platelet activation could not be assessed. Finally, if we only compare platelet activation during VVI versus AAI mode, we could not establish whether it was the atrioventricular asynchrony or ventricular pacing itself that causes increased platelet activation.

Our results demonstrated that there was no relation between platelet activation and the frequency of ventricular pacing, suggesting that ventricular pacing itself did not increase platelet activation. Future studies comparing platelet activation in AAI versus VVI mode in patients with sick sinus syndrome may provide further insight into the mechanism of reduced thromboembolism associated with AAI pacing.


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