CORONARY SPASM INDUCED WITH PARASYMAPTHETIC ACTIVATION IN THE PATIENTS WITH ISCHEMIC HEART DISEASE

2000 Fiscal Year Final Research Report Summary

• Project/Area Number: 11671530
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Anesthesiology/Resuscitation studies
• Research Institution: KURUME UNIVERSITY
• Principal Investigator: WATANABE Seiji KURUME UNIVERSITY, ANESTHESIOLOGY, ASSISTANT PROFESSOR, 医学部, 講師 (10201196)
• Co-Investigator(Kenkyū-buntansha): KANO Tatsuhiko KURUME UNIVERSITY, ANESTHESIOLOGY, PROFESSOR, 医学部, 教授 (50040605) ; KANEKO Shinya KURUME UNIVERSITY, ANESTHESIOLOGY, ASSISTANT, 医学部, 助手 (00224600)
• Project Period (FY): 1999 – 2000
• Keywords: CORONARY SPASM / MYOCARDIAL ISCHEMIA / PARASYMAPATHEIC NERVE / CHOLINESTERASE INHIBITOR / コリンエステラーゼ阻害薬

Research Abstract

To investigate the effects of edrophonium (Edr), which could produce the parasympathetic activation, on electrocardiogram (ECG) and hemodynamics, we studied 32 patients receiving elective coronary artery surgery. The patients were randomly divided into two groups ; control (C) group with only saline injection (n=14) and Edr (E) group with Edr followed by the saline injection (n=18). A bolus dose of Edr (0.25 mg・kg^<-1>) was injected through a central venous catheter during harvesting of the left internal thoracic artery . Edr induced mild sinus bradycardia in all patients. The RR interval prolonged after Edr (p<0.01 vs. C group) and the peak prolongation appeared at 2-4 min (p<0.01 vs. baseline). The maximum reduction of heart rate (HR) after Edr was amplified proportionally with increasing baseline HR (r=-0.74, p<0.001). The relationship between the baseline HR and the maximum reduction of HR was apparently different between the two groups (p<0.01). The PQ duration on ECG was elongate d in 1 to 3 min after Edr (p<0.01 ) while QRS duration did not. The PQ duration quickly restored to the baseline value at 4 min after Edr, while the RR prolongation persisted for 20 min. There was no newly developed deviation of ST segments on the both leads ll and V_5 for 20 min-observation. Although mixed venous hemoglobin oxygen saturation (SvO_2) decreased for 15 min after Edr (p=0.01 vs. C group), none of the systemic and pulmonary arterial pressures, and central venous pressure changed during this period. A bolus injection of Edr showed a frequency -dependent, temporal depression on HR with little deterioration of hemodynamics except SvO_2. Edr could be expected to induce clinically tol erable sinus bradycardia without any severe A-V conduction block in patients with ischemic heart disease. We found no evidence of newly myocardial ischemia, which could be produced by the parasympathetic activation. Only the parasympathetic activation rarely produces the coronary spasm even in the patients with ischemic heart disease.