Archives

  • 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
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • However she had an attack on Day The ECG monitor

    2019-06-12

    However, she had an attack on Day 7. The ECG monitor was normal until 4:25 AM (Fig. 1a). ST segment elevation was evident, and the patient experienced chest pain at 4:30 AM (Fig. 1b). ST segment elevations were seen in leads II, III, and aVF on the 12-lead ECG. As sublingual nitroglycerin was ineffective, intravenous isosorbide nitrate was started. Bradycardia with a heart rate of 37bpm because of complete atrioventricular block occurred at 4:40 AM (Fig. 1c), and atropine sulfate was therefore administered. At 4:55 AM, the patient lost consciousness and went into cardiopulmonary arrest because of PEA. Chest compression was started, and epinephrine was administered (Fig. 1d). The patient\'s heart started beating again at 5:00 AM, with the ECG showing ST segment elevation (Fig. 1e). The patient regained consciousness and the ST segment elevation disappeared at 5:25 AM, followed by persistent ST segment depression (Fig. 1f). The cause of cardiopulmonary arrest was determined to be bradycardia and PEA associated with variant angina. Ventricular fibrillation or ventricular tachycardia was not detected. The patient was started on continuous intravenous infusions of isosorbide nitrate, and treatment with oral nicorandil was resumed. Drug therapy was enhanced with the addition of oral benidipine, as well as diltiazem (30mg twice a day) and pitavastatin (2mg once a day). The patient was also administered magnesium oxide orally (330mg thrice a day) for regular bowel movements, and the magnesium was expected to help control coronary artery spasms. The patient\'s decreased blood pressure precluded any further dose increases. Coronary arteriography was performed after optimization of drug therapy. Low-dose order Flavopiridol hydrochloride loading was performed while the patient continued her oral medication. A pacing lead was inserted into the right ventricle in case of bradycardia, and back-up pacing was performed at 50ppm (paces per minute) in VVI mode. Intracoronary infusion of 10μg acetylcholine into the left coronary artery resulted in obstruction of the anterior descending branch (segment 7), and 90% constriction in the diagonal branch (segment 9) and circumflex branch (segment 13) (Fig. 2a). ECG showed ST segment elevation in the precordial lead, resulting in chest symptoms. Pacing in VVI mode was activated because of bradycardia induced by complete atrioventricular block. The pacing threshold was measured before the coronary artery spasms had subsided. The pacing threshold was ≤1V, and the pacing was continuously captured at 3V in VVI 90 with a stable hemodynamic condition of 110/60mmHg, until the coronary artery spasms subsided. Arteriography performed after the attack had subsided showed that the constriction had resolved (Fig. 2b). Subsequent intracoronary infusion of 10μg acetylcholine into the right coronary artery resulted in 99% constriction in segment 3 (Fig. 2c). ECG showed ST segment elevation and complete AV block, resulting in chest symptoms. The pacing threshold was similarly kept within 1V, and the pacing was continuously captured at 3V in VVI 90 with a stable hemodynamic condition. Under these conditions, concomitant pacing therapy did not result in hemodynamic disruption, at least in the short term. The induction of coronary artery spasms did not lead to ventricular fibrillation or ventricular tachycardia until the spontaneous reduction of coronary spasms. Intracoronary infusion of nitroglycerin revealed no significant coronary stenosis (Fig. 2d). The state of the right coronary artery walls was assessed by optical coherence tomography (OCT) following coronary artery dilatation with nitroglycerin. An ImageWire® (Lightlab Imaging Inc., Westford, MA, USA) was inserted, segment 2 was occluded with a balloon, and red blood cells were washed out by infusion of Ringer\'s solution at 0.5mL/s. In the areas of segment 2 that appeared to be nearly normal on angiography, OCT showed that the normal three-layered structure of the vessel wall was intact (Fig. 2e). Meanwhile, pronounced intimal and medial thickening was observed in segment 3, where the coronary artery spasms had been induced (Fig. 2f). The cause of variant angina with ST segment elevation at rest thus appeared to be coronary spastic angina involving multiple vessel spasms.