• 2018-07
  • 2019-04
  • pka kinase Atrial fibrillation AF is the most common type of


    Atrial fibrillation (AF) is the most common type of arrhythmia in developed countries. Its prevalence almost doubles with each decade of life [1], with a lifetime prevalence of 25% [2]. AF is also an important risk factor for mortality [3]. Along with stroke, heart failure (HF), which is a significant complication of AF, was identified as an independent predictor of mortality in patients with AF [4]. Our previous data suggested that HF remains an important target for the treatment of AF to improve patient prognosis [5]. To prevent hospital admission or death from HF, identifying the population with a high-risk for such HF events is mandatory. Therefore, we developed the H2ARDD scoring system to measure the risk for HF events in patients with AF by assigning points as follows: organic heart disease, 2 points; anemia (hemoglobin level<11g/dL), 1 point; renal dysfunction (estimated glomerular filtration rate [GFR]<60mL/minm2), 1 point; diabetes mellitus (DM), 1 point; and diuretic use, 1 point [6]. Although it is a simple scoring system, it was a strong predictor of the risk of HF events (hospital admission or death from HF) in our AF patient population; the incidence rates of HF events in patients scoring 0 and 6 points were 0.2% and 40.8% per patient-year, respectively; C-statistic, 0.840 [6]. However, although the clinical implications of the H2ARDD score were statistically suggested, its pathophysiological basis has not been fully evaluated. Cardiopulmonary exercise testing (CPX) is the criterion standard for assessing exercise capacity, with much evidence for the benefits of its use in the clinical setting, especially for patients with systolic HF [7–14]. That evidence has also been extended to patients with HF who have preserved left ventricular ejection fraction [15–17]. The most important measurements obtained from CPX include peak oxygen uptake (peak O2) [7,8,15,16], pka kinase (gas exchange) threshold (AT) [9–11], increase rate in ventilation per unit increase in carbon dioxide production (E–CO2 slope) [12,13,17], and the ratio of the increase in O2 to the increase in work rate (ΔO2/ΔWR) [14], all of which reflect heart disease severity and the ability of cardiac patients to perform activities of daily living. In the present study, we evaluated whether H2ARDD score is related to these 4 classic CPX parameters in patients with AF to clarify its pathophysiological implications.
    Materials and methods
    Conflict of interest
    Introduction Intravenous amiodarone has been established as the first-line drug for cardiopulmonary resuscitation (CPR) in patients with fatal ventricular arrhythmias [1]. However, in Japan, intravenous (i.v.) nifekalant hydrochloride was in common use from 1999 until i.v. amiodarone was approved in June 2007. Nifekalant interferes with the delayed rectifier K+ channels, particularly the rapid component of the IKr current, as well as the inward rectifier IK1 current and the transient outward Ito channel [2,3]. In contrast, amiodarone has multiple effects, including blockade of the beta-adrenergic receptors, the fast inward Na+ current, the L-type Ca2+ current, and the fast and slow components of the delayed rectifier K+ current (IKr and IKs) [4]. According to the 2005 CPR guidelines of the American Heart Association (AHA) [1], 300mg of i.v. amiodarone should be used for the initial dose. The following recommendations have been issued in Japan as a first guideline [5]: (1) 125mg/10min i.v. for the initial dose, (2) 50mg/h drip i.v. (d.i.v.) for 6h, and (3) 25mg/h d.i.v. for maintenance. We have used nifekalant for CPR and for the first time reported the favorable defibrillation effect of nifekalant in the treatment of refractory ventricular tachycardia and fibrillation (VT/VF) [6–8]. We also compared the usefulness of amiodarone with Nuclear matrix of nifekalant and reported that the defibrillation efficacy was equivalent between these drugs [9]. In contrast, Yoshioka et al. [10] reported the dynamic variance of the ventricular late potentials induced by the Na+ channel-blocking action of intravenous amiodarone and suggested the possibility of a negative chronotropic action of amiodarone when delivered i.v. for CPR.