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Left ventricular wall thickness and epicardial ST segment mapping during acute ischemia and reperfusion
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LEFT VENTRICULAR WALL THICKNESS AND METABOLISM FOLLOWING REPERFUSION OF ACUTELY ISCHEMIC MYOCARDIUM. J. J. Kane, C. F. Peng, K. D. Straub, J. K. Bissett, J. E. Doherty and M. L. Murphy, University of Arkansas and VA Hospital, Little Rock, Arkansas Reperfuslon after 2 hrs of acute myocardial ischemia is associated with striking abnormalities of left ventricular wall (LVW) thickness and mitochondrlal (M) function. This study evaluates LVW thickness and M function after a shorter period of ischemla. The left anterior descending coronary artery was occluded in 8 mature pigs 30 mln followed by 2 hrs reperfusion. LVW thickness, measured with a 5 mHz ultrasound transducer, is shown below. M calcium uptake was measured by 45Ca++; M A T P w a s determined by luclferase assay. Results using glutamate substrate are shown. Mitochondrial Function ATP(nmoles) QO2(nAO/mg/min) 45Ca++(nmoles/mg) Normal LV 278 + 26297 + 66 199 + 64 Reperfused LV 265 ~ 28 133 ~ 58 119 ~ 65 Lg-W Thlckness(mm+_SD) Control 30 - Occlusion 120 - Reperfusion Systole II.0 ~ 1.5 2.5 ~ I.I 9.2 ~ 3.3 Diastole 4.8 + 1.0 3.4 + 0.7 8.8 + 3.0 Tissue Ca ++ was assayed and--was 4 times Treater in r,,perfused vs. normal LV. Results demonstrate thickening of reperfused LVW with relatively intact M function. Thus, M damage is not tile primary cause of abnormal LVW thickness which occurs with reperfuslon. Increased tissue Ca++ suggests a cell membrane defect. LEFT VENTRICULAR WALL THICKNESS AND EPICARDIAL ST SEGMENT MAPPING DURING ACUTE ISCHEMIA AND REPERFUSION. J. J. Kane, K. D. Straub, M. L. Murphy, C. F. Peng, and J. K. Bissett, Dept. of Med. VA Hosp-Univ of Ark. Med. Center, Little Rock, Arkansas Reperfuslon of acutely ischemic myocardium markedly alters left ventricular wall (LVW) motion and thickness. This study correlates LVW thickness with another index of ischemia, epicardial ST mapping. Nine mature pigs had occlusion of the left anterior descending coronary artery for 2 hrs followed by i hr reperfusion and i hr arterial reocclusion. LVW thickness (mm• determined by placing a 5 mHz ultrasound transducer directly over normal or involved LVW, and sum of epicardial ST elevation (ZST, mV• is shown: LVW Systole LVW Diastole ZST 12:1• 5.7• 0 Control 15 3.7• 4.0• 30.0• Min Occlusion 120 3.6• 3.4• 14.5• 15 10.3• 10.2• 5.1• Min Reperfusion 60 9.9• 9.5• 1.4• 15 7.1• 7.6• 8.3• Min Reocclusion 60 6.0• 6.7• 5.1• With occlusion, there was marked thinning of ischemic LVW and increase in EST. Upon reperfusion, LVW became thick and non-contractile while EST returned to near control. With reocclusion, LVW again became thin and E ~ rose, but less than initial ischemia. Thus, LVW thickness accurately predicted alterations in the epicardial ST segment.
LEFT VENTRICULAR WALL THICKNESS AND METABOLISM FOLLOWING REPERFUSION OF ACUTELY ISCHEMIC MYOCARDIUM. J. J. Kane, C. F. Peng, K. D. Straub, J. K. Bissett, J. E. Doherty and M. L. Murphy, University of Arkansas and VA Hospital, Little Rock, Arkansas Reperfuslon after 2 hrs of acute myocardial ischemia is associated with striking abnormalities of left ventricular wall (LVW) thickness and mitochondrlal (M) function. This study evaluates LVW thickness and M function after a shorter period of ischemla. The left anterior descending coronary artery was occluded in 8 mature pigs 30 mln followed by 2 hrs reperfusion. LVW thickness, measured with a 5 mHz ultrasound transducer, is shown below. M calcium uptake was measured by 45Ca++; M A T P w a s determined by luclferase assay. Results using glutamate substrate are shown. Mitochondrial Function ATP(nmoles) QO2(nAO/mg/min) 45Ca++(nmoles/mg) Normal LV 278 + 26297 + 66 199 + 64 Reperfused LV 265 ~ 28 133 ~ 58 119 ~ 65 Lg-W Thlckness(mm+_SD) Control 30 - Occlusion 120 - Reperfusion Systole II.0 ~ 1.5 2.5 ~ I.I 9.2 ~ 3.3 Diastole 4.8 + 1.0 3.4 + 0.7 8.8 + 3.0 Tissue Ca ++ was assayed and--was 4 times Treater in r,,perfused vs. normal LV. Results demonstrate thickening of reperfused LVW with relatively intact M function. Thus, M damage is not tile primary cause of abnormal LVW thickness which occurs with reperfuslon. Increased tissue Ca++ suggests a cell membrane defect. LEFT VENTRICULAR WALL THICKNESS AND EPICARDIAL ST SEGMENT MAPPING DURING ACUTE ISCHEMIA AND REPERFUSION. J. J. Kane, K. D. Straub, M. L. Murphy, C. F. Peng, and J. K. Bissett, Dept. of Med. VA Hosp-Univ of Ark. Med. Center, Little Rock, Arkansas Reperfuslon of acutely ischemic myocardium markedly alters left ventricular wall (LVW) motion and thickness. This study correlates LVW thickness with another index of ischemia, epicardial ST mapping. Nine mature pigs had occlusion of the left anterior descending coronary artery for 2 hrs followed by i hr reperfusion and i hr arterial reocclusion. LVW thickness (mm• determined by placing a 5 mHz ultrasound transducer directly over normal or involved LVW, and sum of epicardial ST elevation (ZST, mV• is shown: LVW Systole LVW Diastole ZST 12:1• 5.7• 0 Control 15 3.7• 4.0• 30.0• Min Occlusion 120 3.6• 3.4• 14.5• 15 10.3• 10.2• 5.1• Min Reperfusion 60 9.9• 9.5• 1.4• 15 7.1• 7.6• 8.3• Min Reocclusion 60 6.0• 6.7• 5.1• With occlusion, there was marked thinning of ischemic LVW and increase in EST. Upon reperfusion, LVW became thick and non-contractile while EST returned to near control. With reocclusion, LVW again became thin and E ~ rose, but less than initial ischemia. Thus, LVW thickness accurately predicted alterations in the epicardial ST segment.