• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • A recent meta analysis has shown that an


    A recent meta-analysis has shown that an enlarged LA increases the risk of AF recurrence after a single CPVI, regardless of the follow-up duration [5]. This finding can be applied to paroxysmal and persistent AF [6,7]. In clinical practice, measurement of LAD can provide a window into the status of the structural remodeling of LA and may influence the ablation strategy. However, the pathophysiological mechanisms connecting a dilated LA to postablation AF recurrence are not fully understood. One plausible mechanism involves atrial interstitial fibrosis, as it could slow the intra-atrial conduction inhomogeneously, leading to reentry in LA [14]. By demonstrating that LAD was correlated positively with the interstitial fibrosis deposits in the LA, the results of the present study support this hypothesis. A second plausible mechanism involves C-reactive protein (CRP) [15], as a study revealed that CRP level was an independent risk factor of AF recurrences after ablation and was also associated with LA enlargement. In the present study, we observed immunohistochemical evidence that supports the results of the CRP clinical study on the basis that the infiltration of immune bethanechol chloride into LA represented a local inflammatory response. However, it should be noticed that the present results cannot be extrapolated directly to patients with AF without structural heart diseases; therefore, future investigations are required.
    Conflict of interest
    Introduction Implantable cardiac defibrillator devices, such as implantable cardiac cardioverter-defibrillators (ICDs) and cardiac resynchronization therapy with ICD (CRT-D), comprise the therapy of choice for prevention of sudden cardiac death, and are used widely for both primary and secondary prophylaxis [1–3]. ICDs were first approved by the Japanese government more than 20 years ago; they are widely used, and are considered the most effective therapy for lethal ventricular tachyarrhythmia, both in Japan and globally. The Japan Cardiac Device Treatment Registry (JCDTR), run by the Japanese Heart Rhythm Society (JHRS), founded in 2006, records the current clinical situation of cardiac implantable defibrillator devices [4,5]. Mortality rates from coronary artery disease (CAD) are between 10% and 12.5% lower in Japanese patients than in Eastern and Northern European cohorts, and are approximately 20% lower than in Western Europeans and North Americans [6]. The estimated incidence of acute myocardial infarction in Japan was reported as 30−60 per 100,000 males and 10−20 per 100,000 females, between 1990 and 2000 [7]. Mortality rates are expected to rise in Japan owing to changes in diet and lifestyle [8]. In fact, the incidence CAD was relatively stable until 2000 [9], though recent research suggests that rates have been increasing since then [10]. The rate of CAD in Japanese patients implanted with ICDs is lower than in Western countries; the percentage of devices implanted for primary prevention is also markedly lower [4,11,12]. The prognosis of Japanese patients with CAD was hypothesized to improve following application of MADIT-II criteria [1,13–15]; however, some investigators have suggested that application of MADIT-II criteria to Japanese patients may be inappropriate [13]. Nonetheless, patients with CAD and implanted devices for primary prevention in Japan had more frequent appropriate therapy and worse prognosis than expected [16]. One possible factor in these unexpected results may be the implantation of cardiac implantable devices in patients with relatively severe prognoses, or late-stage congestive heart failure [16].
    Material and methods
    Discussion In patients with a history of myocardial infarction and VT, an ICD can prevent sudden cardiac death and reduce total mortality [19]. A known history of myocardial infarction can help to establish the substrate for fatal ventricular tachyarrhythmias, either acutely or during short-term or long-term follow-up [20]. Regarding the risk of sudden cardiac death after acute myocardial infarction, typical survival curves demonstrate an initial sharp decline that plateaus between six and 12 months. In the VALIANT (Valsartan in Acute Myocardial Infarction) study, for example, the risk of sudden death was highest in the first month after myocardial infarction (1.4% per month) and subsequently declined over two years to 0.14% per month [21]. Nevertheless, several randomized clinical trials have failed to show a survival benefit for ICDs when implanted early after myocardial infarction in high-risk patients [22]. Although ICD therapy has been associated with a reduction in the rate of death due to arrhythmias, this was offset by an increase in the rate of death from non-arrhythmic causes [22]. The etiology of the acute myocardial infarction – sudden cardiac death paradox is unclear, but may be related to the changing nature of the substrate over a period of several months after acute myocardial infarction [22]. Further investigation is needed to explain the actual causes of death in the early post-myocardial infarction period, and to find which interventions can be applied to reduce the increased rate of sudden death [20].