• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • br Discussion Variant angina was described by


    Discussion Variant KC7F2 was described by Prinzmetal et al. in 1959 [1]. It can involve serious arrhythmias such as ventricular tachycardia, ventricular fibrillation, and atrioventricular block, and patients are particularly susceptible to sudden cardiac death in such cases [2,3]. Coronary spastic angina without any significant coronary artery constriction responds well to drug therapy with calcium blockers and has a favorable prognosis [4]. However, in a long-term observational study, angina recurred despite the use of oral calcium blockers, with a 3.2% incidence of sudden cardiac death and a 6.5% incidence of acute myocardial infarction over a period of 89 months [5]. Although significant coronary stenosis is a risk factor for acute myocardial infarction, it does not affect the development of fatal arrhythmias [6]. Smoking is the only clear risk factor for coronary artery spasms [7]. Therefore, an important clinical issue is the treatment of coronary spastic angina that recurs despite proactive drug therapy with calcium blockers, long-acting nitrates, and nicorandil, as well as smoking cessation and management of obesity, hypertension, impaired glucose tolerance, and abnormal lipids as recommended in the current guidelines [8]. This is of major interest, particularly in Japanese patients who experience coronary artery spasms more frequently [9]. Implantable cardioverter defibrillators (ICDs) were reportedly effective in patients who developed ventricular fibrillation despite maximal drug therapy [10]. However, the Japanese guidelines for coronary spastic angina state that ICDs should only be considered in refractory cases, and there is still no consensus on this matter [8]. Furthermore, no treatment guidelines have been specified for PEA or complete atrioventricular block in the absence of ventricular tachycardia or ventricular fibrillation [8]. In previous reports, drug therapy in patients with resuscitated PEA resulted in favorable progress [11] and a DDD pacemaker was implanted in a patient with complete atrioventricular block and non-sustained ventricular tachycardia [12]. In the present case, cardiopulmonary arrest was caused by PEA and bradycardia, not ventricular fibrillation or ventricular tachycardia. Therefore, the present patient\'s condition was not amenable to electrical defibrillation, and pacemaker therapy was selected instead. The pacemaker settings for pacemaker therapy also required some ingenuity. The maximum ventricular output was set at 7.5V because settings of longer duration could potentially result in an increase in the pacing threshold [13]. However, a rate drop response (RDR) setting was selected to ensure efficient pacing only when needed because ventricular pacing during normal conditions shortens battery life. In this case, the pacemaker was set to ensure pacing at a high heart rate (70ppm) when the heart rate fell to ≤40bpm or there was a sudden decrease in the heart rate of more than 15bpm. The pacemaker used in this case was selected because we felt that it could provide pacing therapy suitable for this patient\'s condition. Commercially available ICD devices are not capable of RDR settings, and back-up pacing is the only available setting for brady pacing. Pacing can therefore be done only at the lowest set heart rate even during attacks. The selection of settings that anticipate pacing at a higher heart rate during attacks leads to more frequent pacing when the heart rate is lower during normal conditions, and may result in pacing discomfort and battery depletion. However, pacing stimulation in ischemic regions runs the risk of provoking serious arrhythmias such as ventricular fibrillation [13], and concomitant ICD is therefore more desirable in that regard. Chest compression and epinephrine are effective for PEA, whereas electrical defibrillation is not. Medium voltage therapy (MVT) has recently been attempted, where electrical stimulation by a cardiac device during ventricular fibrillation or PEA induces skeletal muscle contractions and maintains coronary blood flow in the same manner as chest compression [14,15]. Although this technique has not yet been put to practical use, it would appear to be well suited to cases such as the present one.