• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • Bepridil is a multichannel blocker suggesting that


    Bepridil is a multichannel blocker, suggesting that its pharmacological effects on cardiac myocytes are exerted by blocking Na [21], Ca [22], and K [23–25] channels. It has recently been reported that bepridil has a cardioprotective effect [26] by opening ATP-dependent K fda approved vegf inhibitor in mitochondria and suppressing ATP-dependent K channels in sarcomeres. In addition, it attenuates Ca overload by blocking the Na+-Ca2+ interchange mechanism [27–28] and increases Ca2+ susceptibility [29,30], thus maintaining cardiac hemodynamics. Furthermore, bepridil has been shown to have a reverse remodeling effect on atrial myocytes in a frequent pacing experimental model [31], and reportedly attenuates the premature contractions that trigger AF via suppression of the stretch-activated channels of cardiac myocytes [32]. Thus, it is probable that the anti-arrhythmic efficacy of bepridil and its pleiotropic actions such as myocardial protection, atrial pressure load reduction, reverse remodeling, and attenuation of premature contractions contribute to its efficacy in preventing postoperative AF, where the underlying cardiac disease is strongly correlated with AF development. In addition, aprindine requires several days to reach a stable and effective blood concentration. It is thus probable that the rapid pharmacological efficacy of bepridil influenced the results of the present study. The predictors of AF recurrence and chronicity after anti-arrhythmic treatment for maintaining sinus rhythm reportedly include the duration of AF [33], AF history [34], left atrial dimension [35], underlying cardiac disease [36], aging [37], and development of the mixed type [38]. In this prospective randomized study, these factors did not differ significantly between the bepridil and aprindine groups. There is thus a low probability that these factors significantly influenced our results.
    Conflict of interest
    Introduction Systemic thromboembolism, including ischemic stroke and transient ischemic attack, is a serious complication in patients with atrial fibrillation (AF). Several randomized prospective trials investigating nonvalvular atrial fibrillation (NVAF) have confirmed that warfarin administration significantly reduces the risk of stroke, thereby providing a basis for guidelines promoting the use of warfarin in patients with NVAF [1,2]. The congestive heart failure (CHF), hypertension, age, diabetes mellitus, and prior stroke (CHADS2) scoring system is easy for physicians to remember and apply. Additionally, it has been widely validated for risk stratification to predict stroke in patients with NVAF [3]. The CHADS2 score assigns 1 point each for CHF, hypertension, age ≥75 years, and diabetes mellitus, and 2 points each for prior stroke or transient ischemic attack. Current guidelines recommend anticoagulant therapy for patients with a CHADS2 score ≥2, because the risk of ischemic stroke outweighs the risk of bleeding with anticoagulant therapy [4–6]. Most thrombi associated with NVAF originate in the left atrial appendage (LAA) [7–9]. We previously reported that the serum d-dimer level is clinically useful for guiding the management of patients. In addition, the presence of CHF, a history of embolic events, and the serum d-dimer level are significant predictors of LAA thrombus [10]. Various studies consider CHF as involving the following factors: acute pulmonary edema [3], low ejection fraction (EF) [2,11], New York Heart Association (NYHA) functional classification ≥II [10], and a history of hospitalization for CHF [2,11]. However, the abovementioned clinical criteria are qualitative; therefore, the quantitative definition of CHF remains unclear. Brain natriuretic peptide (BNP) is widely used as a clinical index of the severity of CHF [12]. Therefore, the present study aimed to elucidate the relationship between LAA thrombus and the BNP level and to determine if the BNP level is a quantitative marker of CHF in patients with unanticoagulated NVAF.