<Originals>Experimental Evaluation on ST-segment Elevation and Depression Mechanism by Electrocardiogram of Angina Pectoris : In Relation to Contralateral Coronary Artery Lesions of Ischemic Myocardium

  • ISHIKAWA Kinji
    First Department of Internal Medicine, Kinki University School of Medicine
  • KANAMASA Ken
    First Department of Internal Medicine, Kinki University School of Medicine
  • OSATO Shuichiro
    First Department of Internal Medicine, Kinki University School of Medicine
  • OGAI Toshihiro
    First Department of Internal Medicine, Kinki University School of Medicine
  • ODA Akio
    First Department of Internal Medicine, Kinki University School of Medicine
  • KADOWAKI Hiroyuki
    First Department of Internal Medicine, Kinki University School of Medicine
  • OGAWA Iwao
    First Department of Internal Medicine, Kinki University School of Medicine
  • SHIMIZU Minoru
    First Department of Internal Medicine, Kinki University School of Medicine
  • OTSUKI Toshiko
    First Department of Internal Medicine, Kinki University School of Medicine
  • SAKAGUCHI Yoshihide
    First Department of Internal Medicine, Kinki University School of Medicine
  • YAMASHITA Keizo
    First Department of Internal Medicine, Kinki University School of Medicine
  • KATORI Ryo
    First Department of Internal Medicine, Kinki University School of Medicine

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Other Title
  • <原著>心筋虚血に伴う心電図ST上昇型, 下降型出現機序に関する実験的考察 : 対側病変との関連

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It is not known why an inverse ECG pattern occurs in the patients with angina pectoriselevation and/or depression of ST-segment. Since elevated ST-segment is frequently observed in patients with single vessel disease and infrequently found in patients with multivessel disease and vice versa, effect of contralateral coronary artery lesions of ischemic myocardium might reflect on this cardiac electrical events. We made two experimental models of reflecting ST-segment elevation and depression in the same lead, and studied the mechanism of this different cardiac electrical pattern. In 21 dogs, left anterior descending coronary artery (LAD) and left circumflex (LCX) were cannulated and epicardial ECG on the myocardium supplied by LAD were recorded (Experiment 1). Gradual reduction of LAD flow into approximately one fourth (from 18.4±1.8 to 5.3±1 .4ml/min) caused ST-segment elevation in 109 and ST-segment depression in 2 leads accompanied by a compensatory increase in LCX flow from 24.1±1.4 to 26.3±1.4ml/min. N critical stenosis was made on LCX to prevent compensatory increase in LCX flow in response to LAD stenosis. Gradual occlusion of LAD flow from 15.5±1.5 to 6.2±1.2ml/min (a reduction smaller than the previous one) caused ST-segment shifts including ST-segment depression in 11 out of 111 leads. LAD flow reduction accompanied by a reduction of LCX flow brougth remote ischemia on LCX area. Under this condition, no collateral supply from LCX to LAD will take place. Accordingly, blood flow will shift from endocardium to epicardium causing endocardial ischemia characterized by ST-segment depression. In the second experiment, a plastic board was sutured on the left ventricular free wall to eliminate collateral supply from LCX to LAD in 10 dogs (Experiment 2). Gradual reduction of LAD flow from 17.1±2.3 to 11.9±2.1ml/min caused ST-segment depression in 27,elevation in 29 and no change in 2 epicardial leads. The results indicated that if collateral supply is strictly limited, ST-segment depression will appear. If ischemic myocardium is surrounded by normal myocardium, epicardial as well as endocardial myocardium with ischemia will get collateral supply. However, if the flow reduction is much excess to the collateral supply, epicardial as well as endocardial myocardium became ischemic causing transmural ischemia and ST-segment elevation. While, if there is a severe stenosis on the other side of LAD, so severe to be unable to send collateral supply to LAD, a relatively small reduction in LAD flow causes ST-segment depression because blood flow shift from endocardium to epicardium will take place.

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