• 2018-07
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  • br Conclusion Conduction disorders were localized


    Conclusion Conduction disorders were localized and inhomogeneous in patients with ischemic heart disease, in whom CRT efficacy was slightly low; therefore, detailed optimization using echocardiography, radioisotopes, Swan–Ganz catheterization, and other methods should be carefully performed as needed [83,84]. Here, methods for interventricular delay optimization were categorized into four groups. The first category emphasized wall motion and dyssynchrony and used ultrasonography. If dyssynchrony was judged to be high, VV delay optimization using ultrasonography was needed. The second focused heavily on conduction delays and disorders using electrocardiography. If the QRS duration was very wide or had a left bundle branch block pattern, VV delay optimization was needed. Signal-averaged electrocardiography was also useful, but the meaning of its results was uncertain [85]. The third category placed great weight on cardiac output. In patients with very low cardiac output, conduction disorders tended to be high and diffuse and not require optimization. Similarly, in the fourth category, heart disease in which a diffuse conduction disorder was implied did not require optimization. In any case, the need for VV delay optimization might be judged according to a specific disease or conduction disorder pattern; hence, the most effective and least costly settings should be identified.
    Conflict of interest
    Introduction Vasovagal syncope (VVS) is the most common cause of syncope. VVS is designated as one of the types of reflex syncope (neurally-mediated syncope) in both the Japanese and European guidelines regarding syncope [1,2]. The phenomenon of VVS consists of hypotension and bradycardia or asystole. Therefore, implantation of a permanent pacemaker is thought to be a reasonable treatment. In carotid sinus syncope, pacing therapy is regarded as one of the first-line treatments in patients with recurrent syncope and cardioinhibitory response during carotid sinus massage [1,2]. Although a glucose assay cardioinhibitory component has been observed in most patients with carotid sinus syncope [3], the vasodepressor factor seems to be the main cause of fainting in most VVS patients. The efficacy of pacing therapy for VVS has been controversial so far. The purpose of this review is to assess the historical background and the efficacy of cardiac pacing in patients with VVS.
    Clinical experience with pacemaker treatment for vasovagal syncope before the randomized clinical trial (RCT) era The data in the 1990s concerning the outcomes of permanent cardiac pacemaker use in patients with VVS were conflicting. The usual pacemaker therapy, even DDD pacing, could not prevent VVS during head-up tilt (HUT) testing owing to insufficient efficacy of the vasodepressor factor [4,5]. Sra et al. [4] found that cardiac pacing for VVS was less effective than drug therapy. Conventional pacing treatment (i.e., DDD pacing for patients with sinus rhythm or VVI pacing for patients with atrial fibrillation) did not prevent hypotension and syncope or presyncope during HUT testing in VVS patients with asystole or bradycardia [4]. The lack of efficacy of pacing in these patients suggested that even in patients with a cardioinhibitory response, hypotension is predominantly due to vasodepression, whereas vagally mediated bradycardia may play only a secondary part in the pathogenesis of VVS [4,6]. However, it was argued that permanent pacemaker therapy may be useful in preventing syncope in patients with so-called “malignant vasovagal cardioinhibitory response,” in which the onset of syncope is thought to be abrupt [6]. In addition, Sra et al. [4] showed that a potential benefit of pacing therapy was that cardiac pacing could diminish the magnitude of hypotension in some VVS patients. This suggested the idea that early intervention with cardiac pacing might prevent or at least alleviate hypotension and syncope. Petersen et al. [7] reported a possible role for permanent pacing in selected patients with cardioinhibitory malignant VVS in a retrospective, uncontrolled 1994 study. Cardiac pacemakers were implanted in 37 patients. Most of these were programmed to DDI mode with rate hysteresis. During the follow-up period of 50.2±23.9 months, symptomatic improvement occurred in 89% of the patients, with 62% remaining free of syncope and 27% being completely symptom free. In 1997, Benditt et al. [8] reported the results of pacemaker treatment with the rate-drop response (RDR) algorithm in 28 patients with tilt-positive VVS and induced bradycardia. During an average follow-up of 6 months, 78% of patients did not faint at all and an overall 67% reduction in syncope frequency was observed. In 1998, Sheldon et al. [9] also reported efficacy of pacemaker therapy. They implanted a dual-chamber pacemaker with automatic rate smoothing in 12 patients with frequent syncope (median: 3 episodes per month). After implantation, the frequency of syncope decreased by 93% and quality of life improved markedly.