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Noninvasive determination of infarct size 5 hours after coronary occlusion in the conscious dog
ABSTRACTS
linear regression in the age range 40 to 68 years was evident (HR = 184 - 0.79 [age 40 years] ), below which occurred 128 positive HR responses (98yG). HR x SBP provided a wider dispersion of data than HR alone. A level was found (35 mm Hg/min) which would include 95% of those with positive responses, but <75c/, of those with negative responses reached even 30 mm Hg/min, so aiming for such a product would be pointless. In summary, the merit of HR x SBP for predicting onset of ischemia in the individual patient does not appear to hold for general application as a stress endpoint in exercise testing, but 35 mm Hg/min may be used as an effective end-point for the occasional subject who achieves this level. However, there is an age regression of exercise HR that includes 98’;, of those with positive responses, the attainment of which is therefore a strongly negative result if no evidence of ischemia is manifested. Noninvasive Determination of Infarct Size 5 Hours After Coronary Occlusion in the Conscious Dog WILLIAM E. SHELL, MD*; BURTON E. SOBEL, MD, FACC; JAMES W. COVELL, MD; JOHN F. LAVELLE, MS, La Jolla, California
This study was designed to predict infarct size (IS) within 5 hours in the conscious dog subjected to coronary occlusion and to measure changes in IS following isoproterenol administration. We have previously shown that IS is reflected by the pattern of serial serum creatine phosphokinase (CPK) changes during the 24 hours following occlusion. In the present study, serum CPK changes were measured in 21 conscious dogs subjected to coronary occlusion. Results were fit to a log normal function by least squares approximation. When the function was fit with values obtained during only the first 5 hours following occlusion, the derived curve predicted IS accurately (IS,,). Correlation coefficients between fit curves and actual serial 24 hour values in animals with occlusion alone were 0.94 2 0.03 (mean % SE), no. = 10. Differences between IS,, calculated from CPK changes during only the first 300 minutes and infarct size (range: 0.4 = 60 g) based on myocardial CPK analysis were small, 0.3 ? 2.4 g (mean t SE). In 11 additional dogs isoproterenol, 0.015 mg/kg subcutaneously, was administered at least 10 hours after coronary occlusion, In all, subsequent serum CPK values deviated from those predicted by the log normal function. Hence, IS calculated from 24 hour serum CPK changes exceeded IS,, by an average of 219’: (P
The cardiovascular effect of changes in fetal arterial oxygen tension (PO,) was studied in 7 closed-chest
292
fetal lambs maintained in normal physiologic condition connected to an extracorporeal circuit functioning as an “artificial placenta.” While fetal rectal temperature was maintained at 3’7 to 39C, umbilical arterial (UA) pH 7.30 to 7.40, UA pCOZ 35 to 45 mm Hg and placental flow (extracorporeal) 110 to 130 ml/kg per min, fetal circulation was investigated by dye-dilution technique at UA p0, of 20 to 30 mm Hg (fetal normoxia) and 35 to 45 mm Hg (fetal hyperoxia). Dye was injected successively into superior vena cava (SVC), inferior vena cava, right ventricle (RV) and left ventricle (LV) while being sampled from the ascending and descending aorta (DA). During fetal normoxia, effective cardiac output was 305 2 28 ml/kg per min, LV output 153 & 25 ml/kg per min, pulmonary circulation time 5.8 % 0.8 seconds and a large right to left (R-L) ductal shunt was present in each instance. SVC flow was directed to the right ventricle and through the ductus arteriosus into the descending aorta. During fetal hyperoxia LV output increased markedly to 269 * 26 ml/kg per min, approximating the effective cardiac output, pulmonary circulation time decreased to 2.1 -C 0.3 seconds, whereas R-L ductal flow disappeared in 5 and markedly decreased in 2 instances. From this study it appears that, in fetal lambs, hyperoxia beyond an UA p0, of 35 mm Hg leads to closure of ductus arteriosus and marked decrease in pulmonary vascular resistance while allowing a sizable shunt through the foramen ovale.
A Method of Quantifying the Need for Surgical Therapy in Clinical Myocardial Infarction Shock JOHN H. SIEGEL, MD*; EDWARD J. FARRELL, ES; ISAAC MD; DAVID BREGMAN, MD, NewYork, NewYork
LEWIN,
Determining the need for mechanical support or acute revascularization, or both, before irreversible myocardial damage occurs presents a major problem in the treatment of myocardial infarction (MI) shock. By describing the magnitude and the shape of the central indicator-dilution curve using a mathematic model which quantifies the dye curve by 4 independent indexes, flow, and the delay, dispersion (non-mixing) and mixing mean transit times, more than 1,000 indicator curves from 197 patients with septic, nonseptic, and myocardial infarction shock, and from preoperative control patients without shock were analyzed. Mixing time (t,,,) reflects changes in the durational aspects of myocardial contractility. Dispersive time (t,,) ordinarily reflects transit across pulmonary small vessels, but some patients with MI have a large cardiac nonmixing volume which appears related to the size of the infarct and its penumbra of isehemic myocardium. The persistence of a t,,, >7.5 seconds and presence of a cardiac nonmixing volume with a t,, of >7.5 are signs of medically refractory MI shock requiring circulatory support. Of 28 patients with MI shock none survived in whom both t,, and t,,, values were not decreased below 7.5 seconds by medical or mechanical support therapy. Intraaortic double balloon counterpulsation was used in 9 MI patients. The 3 patients resuscitated from acute MI shock all had reductions in t,, and t,,,. The 6 nonsurviving patients did not. With these indexes it appears possible to quantify the effectiveness
The
American
Journal
of
CARDIOLOGY
linear regression in the age range 40 to 68 years was evident (HR = 184 - 0.79 [age 40 years] ), below which occurred 128 positive HR responses (98yG). HR x SBP provided a wider dispersion of data than HR alone. A level was found (35 mm Hg/min) which would include 95% of those with positive responses, but <75c/, of those with negative responses reached even 30 mm Hg/min, so aiming for such a product would be pointless. In summary, the merit of HR x SBP for predicting onset of ischemia in the individual patient does not appear to hold for general application as a stress endpoint in exercise testing, but 35 mm Hg/min may be used as an effective end-point for the occasional subject who achieves this level. However, there is an age regression of exercise HR that includes 98’;, of those with positive responses, the attainment of which is therefore a strongly negative result if no evidence of ischemia is manifested. Noninvasive Determination of Infarct Size 5 Hours After Coronary Occlusion in the Conscious Dog WILLIAM E. SHELL, MD*; BURTON E. SOBEL, MD, FACC; JAMES W. COVELL, MD; JOHN F. LAVELLE, MS, La Jolla, California
This study was designed to predict infarct size (IS) within 5 hours in the conscious dog subjected to coronary occlusion and to measure changes in IS following isoproterenol administration. We have previously shown that IS is reflected by the pattern of serial serum creatine phosphokinase (CPK) changes during the 24 hours following occlusion. In the present study, serum CPK changes were measured in 21 conscious dogs subjected to coronary occlusion. Results were fit to a log normal function by least squares approximation. When the function was fit with values obtained during only the first 5 hours following occlusion, the derived curve predicted IS accurately (IS,,). Correlation coefficients between fit curves and actual serial 24 hour values in animals with occlusion alone were 0.94 2 0.03 (mean % SE), no. = 10. Differences between IS,, calculated from CPK changes during only the first 300 minutes and infarct size (range: 0.4 = 60 g) based on myocardial CPK analysis were small, 0.3 ? 2.4 g (mean t SE). In 11 additional dogs isoproterenol, 0.015 mg/kg subcutaneously, was administered at least 10 hours after coronary occlusion, In all, subsequent serum CPK values deviated from those predicted by the log normal function. Hence, IS calculated from 24 hour serum CPK changes exceeded IS,, by an average of 219’: (P
The cardiovascular effect of changes in fetal arterial oxygen tension (PO,) was studied in 7 closed-chest
292
fetal lambs maintained in normal physiologic condition connected to an extracorporeal circuit functioning as an “artificial placenta.” While fetal rectal temperature was maintained at 3’7 to 39C, umbilical arterial (UA) pH 7.30 to 7.40, UA pCOZ 35 to 45 mm Hg and placental flow (extracorporeal) 110 to 130 ml/kg per min, fetal circulation was investigated by dye-dilution technique at UA p0, of 20 to 30 mm Hg (fetal normoxia) and 35 to 45 mm Hg (fetal hyperoxia). Dye was injected successively into superior vena cava (SVC), inferior vena cava, right ventricle (RV) and left ventricle (LV) while being sampled from the ascending and descending aorta (DA). During fetal normoxia, effective cardiac output was 305 2 28 ml/kg per min, LV output 153 & 25 ml/kg per min, pulmonary circulation time 5.8 % 0.8 seconds and a large right to left (R-L) ductal shunt was present in each instance. SVC flow was directed to the right ventricle and through the ductus arteriosus into the descending aorta. During fetal hyperoxia LV output increased markedly to 269 * 26 ml/kg per min, approximating the effective cardiac output, pulmonary circulation time decreased to 2.1 -C 0.3 seconds, whereas R-L ductal flow disappeared in 5 and markedly decreased in 2 instances. From this study it appears that, in fetal lambs, hyperoxia beyond an UA p0, of 35 mm Hg leads to closure of ductus arteriosus and marked decrease in pulmonary vascular resistance while allowing a sizable shunt through the foramen ovale.
A Method of Quantifying the Need for Surgical Therapy in Clinical Myocardial Infarction Shock JOHN H. SIEGEL, MD*; EDWARD J. FARRELL, ES; ISAAC MD; DAVID BREGMAN, MD, NewYork, NewYork
LEWIN,
Determining the need for mechanical support or acute revascularization, or both, before irreversible myocardial damage occurs presents a major problem in the treatment of myocardial infarction (MI) shock. By describing the magnitude and the shape of the central indicator-dilution curve using a mathematic model which quantifies the dye curve by 4 independent indexes, flow, and the delay, dispersion (non-mixing) and mixing mean transit times, more than 1,000 indicator curves from 197 patients with septic, nonseptic, and myocardial infarction shock, and from preoperative control patients without shock were analyzed. Mixing time (t,,,) reflects changes in the durational aspects of myocardial contractility. Dispersive time (t,,) ordinarily reflects transit across pulmonary small vessels, but some patients with MI have a large cardiac nonmixing volume which appears related to the size of the infarct and its penumbra of isehemic myocardium. The persistence of a t,,, >7.5 seconds and presence of a cardiac nonmixing volume with a t,, of >7.5 are signs of medically refractory MI shock requiring circulatory support. Of 28 patients with MI shock none survived in whom both t,, and t,,, values were not decreased below 7.5 seconds by medical or mechanical support therapy. Intraaortic double balloon counterpulsation was used in 9 MI patients. The 3 patients resuscitated from acute MI shock all had reductions in t,, and t,,,. The 6 nonsurviving patients did not. With these indexes it appears possible to quantify the effectiveness
The
American
Journal
of
CARDIOLOGY