Magnetic Determination of the Relationship between the S‐T Segment Shift and the Injury Current Produced by Coronary Artery Occlusion

Both the S-T segment shift and the injury current were measured using the direct-current magnetocardiogram (d-c MCG) in seven dogs undergoing coronary artery occlusion. The purpose of the measurements was to clarify the origin of the S-T shift in acute ischemia and infarction. Previous measurements, consisting of d-c electrograms recorded from the exposed epicardial surface in situ, are partially inconsistent; also, they are not necessarily representative of the surface electrocardiogram (ECG), which sums broadly over the myocardium. The d-c MCG allows steady myocardial currents in the intact torso to be measured externally; because the d-c MCG sums broadly over these currents, conclusions drawn from it are applicable to the ECG. Coronary artery occlusion was produced by inflating a tube which, about 1 week earlier, had been surgically installed around the artery and exteriorized. During occlusions carried out in the MIT magnetically shielded room, a sensitive magnetometer recorded the d-c MCG at various locations around the torso. Within 20 seconds after occlusion, equal and opposite S-T segment and base-line (d-c) shifts appeared on the d-c MCG; these shifts were maintained for at least 15 minutes, after which they slowly decreased. Therefore, during the acute ischemia produced by these occlusions, the S-T shift is a secondary result of a primary injury current that is interrupted during the S-T interval.

[1]  D. Cohen,et al.  Magnetocardiograms and their variation over the chest in normal subjects. , 1972, The American journal of cardiology.

[2]  J. C. Norman,et al.  Magnetocardiography of Direct Currents: S-T Segment and Baseline Shifts during Experimental Myocardial Infarction , 1971, Science.

[3]  M. Prinzmetal,et al.  ANGINA PECTORIS. VII. THE NATURE OF S-T DEPRESSION IN ACUTE MYOCARDIAL ISCHEMIA. , 1964, The American journal of cardiology.

[4]  D. Cohen,et al.  Ferromagnetic Contamination in the Lungs and Other Organs of the Human Body , 1973, Science.

[5]  A. Barger,et al.  Temporary coronary occlusion in conscious dogs: collateral flow and electrocardiogram. , 1967, The American journal of physiology.

[6]  A. Katcher,et al.  Effects of Experimental Regional Ischemia and Levarterenol on the RS‐T Segment and Baseline of Ventricular Surface Electrocardiograms Obtained by Direct‐Coupled Amplification , 1960, Circulation research.

[7]  L. Rakita,et al.  Studies on the mechanism of ventricular activity. XII. Early changes in the RS-T segment and QRS complex following acute coronary artery occlusion: experimental study and clinical applications. , 1954, American heart journal.

[8]  P. Libby,et al.  Precordial S-T segment elevation mapping: an atraumatic method for assessing alterations in the extent of myocardial ischemic injury. The effects of pharmacologic and hemodynamic interventions. , 1972, The American journal of cardiology.

[9]  J. Zimmerman,et al.  Design and Operation of Stable rf‐Biased Superconducting Point‐Contact Quantum Devices, and a Note on the Properties of Perfectly Clean Metal Contacts , 1970 .

[10]  M. Prinzmetal,et al.  Myocardial ischemia. Nature of ischemic electrocardiographic patterns in the mammalian ventricles as determined by intracellular electrographic and metabolic changes. , 1961, The American journal of cardiology.

[11]  A. Katcher,et al.  Correlation of Intramyocardial Electrocardiograms with Polarographic Oxygen and Contractility in the Nonischemic and Regionally Ischemic Left Ventricle , 1961, Circulation research.

[12]  D. Cohen,et al.  Measurements and a Simplified Interpretation of Magnetocardiograms from Humans , 1969, Circulation.

[13]  A. M. Scher,et al.  Mechanism of S‐T Segment Alteration During Acute Myocardial Injury , 1960, Circulation research.

[14]  M. Prinzmetal,et al.  Correlation between intracellular and surface electrograms in acute myocardial ischemia. , 1968, Journal of electrocardiology.

[15]  A. Ekmekci,et al.  Angina pectoris: III. Demonstration of a chemical origin of ST deviation in classic angina pectoris, its variant form, early myocardial infarction, and some noncardiac conditions∗ , 1959 .

[16]  B. Lown,et al.  Exercise during acute myocardial infarction: an experimental study. , 1973, Cardiovascular research.

[17]  V. ALZAMORA-CASTRO,et al.  The electrical manifestations observed in damaged or injured cardiac muscle; an experimental study. , 1957, American heart journal.