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    • Arita et al reported that the

    2019-04-28

    Arita et al. reported that the mechanism of ST-segment elevation in inferior leads is right coronary artery hypoperfusion due to vasodilation by Bezold–Jarisch-like reflexes that are induced by stimulation of the Senexin B in the intra-atrial septum during transseptal puncture and extension [3]. Some authors have proposed that manipulation of the ganglion plexuses by transseptal puncture causes autonomic innervation imbalances that lead to coronary vasospasm and ST-segment elevation [5–8,10]. Seven of the 16 patients (43.8%) reviewed here had concomitant bradyarrhythmias such as sinus bradycardia, sinus arrest, and complete atrioventricular block. Although neither bradyarrhythmia nor hypotension was observed during the ST-segment elevation in our patient, a neutrally mediated pathway activated by the mechanical effects of transseptal puncture on the interatrial vagal network may be one of the causes of coronary vasospasm and these ECG findings. Because our patient had dyslipidemia and a history of smoking, he may have had an injured coronary endothelium and coronary vasospasm. Unfortunately, we could not confirm the suspected coronary vasospasm in our patient. When ST-segment elevation and VF occurred, we could not perform coronary angiography without ISDN. Acetylcholine could not be administered because he did not consent to the test at a later date.
    Conclusion
    Conflict of Interest
    Introduction Although its estimated incidence is only approximately 0.1%, it is a fatal complication that results in significant morbidity and mortality [1–4]. Some clinical studies have indicated the importance of luminal esophageal temperature (LET) monitoring using deflectable or single- or multi-thermocouple temperature probes to prevent fistula formation [5–7]. However, several potential limitations can impair accurate LET measurement, especially since optimal contact is required between the probe and esophageal wall. We performed barium esophagography after the transnasal insertion of a multi-thermocouple temperature probe (SensiTherm, St. Jude Medical, Inc., St. Paul, MN, USA) and noted that the temperature probe maintained full contact with the esophageal wall although sufficient space was observed on the pre-registered three-dimensional computed tomography image (Fig. 1).
    Conflicts of interest
    Case presentation A 75-year-old woman with syncope was hospitalized at our institute. The surface 12-lead electrocardiogram (ECG) at admission indicated a regular short RP rhythm at a rate of 95 beats per minute (bpm) with a narrow QRS complex (Fig. 1A). Echocardiography and enhanced multidetector computed tomography revealed a heart with a normal structure and without significant coronary artery disease. She developed dizziness and nausea while hospitalized. A 12-lead ECG at the time of her symptoms documented a prolongation of the RR interval up to 4s (Fig. 1B). What is the mechanism of the short-RP narrow QRS rhythm and the prolongation of the RR interval?
    Discussion A short RP rhythm without tachycardia (heart rate <100bpm) is generally recognized as a junctional rhythm with retrograde nodal atrial conduction. In the present case, the ECG during the patient\'s symptoms (Fig. 1A) indicated an accelerated junctional ectopic rhythm followed by a P wave. However, there was no QRS complex preceding the first P wave at the beginning of the RR prolongation (Fig. 1B). This absence of a QRS complex before the P wave suggests that the atrium is not passively activated by the ectopic beats originating from the atrio-ventricular (AV) node. An AV reciprocating rhythm with a concealed accessory pathway can be excluded. Thus, the mechanism of the short RP rhythm is likely either a sinus rhythm or an ectopic atrial arrhythmia with a long first-degree AV block. The positive P wave morphology in the inferior leads during the short RP rhythm also indicates that the atrium was not activated from the AV node. A positive P wave in lead V1 suggests that the origin of the ectopic rhythm is from the left atrium, with a sensitivity of 93% and a specificity of 88% [1]. In the present case, the morphology of the P wave at admission may have originated not from the sinus node but from the left atrium.