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Detection of coronary artery disease and myocardial ischemia by electrocardiography and myocardial perfusion scanning with thallium 201
ABSTRACTS
ACCURATE DETECTION OF ELEVAT‘ED LEFT VENTRICULAR FILLING PRESSURE IN ACUTE MYOCARDIAL INFARCTION BY ECHOCARDIOGRAPHY: COMPARISON OF NON-INVASIVE TECHNIQUES WITH CARDIAC CATHETERIZATION. Juan Angel, MD, Ezra A. Amsterdam, MD, FACC, Dean T. Mason, MD, FACC, Lynn Weinnert, BS, and Anthony N. DeUniversity of California, Davis, CA. Maria, MD, FACC. Since left ventricular filling pressure (LVFP) is of quantitative, prognostic and therapeutic significance in acute myocardial infarction (AMI), the reliable identification of increased LVFP by atraumatic means would be of considerable clinical value. Thus this study compared the ability of chest x-ray (CXR), physical examination (PE), ECG, serum creatine phosphokinase (CPK), and echocardiography (U), to detect increased LVFP in 25 AM1 patients (pts) as determined by pulmonary artery wedge pressure. Of 51 determinations of LVFP by cardiac catheterization, 26 were elevated (E) (>16 mm Hg, mean 24) while 25 were normal (N) (mean 9 mm Hg). CXR and PE were scored from 1 to 5 for progressive signs of heart failure. Only minor differences existed between E and N by CXR (2.8 vs 1.7, pc.02) and PE (2.2 vs 1.8, pc.05). The number of Q waves (mean 3) and peak CPK (mean 1221) were similar in both the E and N groups. Although U stroke index and fiber shortening velocity were similar (mean 42 vs 0.98 circumference/sec), U end-diastolic dimension (EdD) was larger (6.43 vs 5.18 cm, pc.001) and ejection fraction smaller (39 vs 55%, pc.001) in E than N. Moreover, of 24 determinations with EdD >6 cm, 22 (88%) had elevated LVFP, whereas LVFP was elevated in only 5/27 (18%) instances From these comparative observations, it with EdD (6 cm. is concluded that echocardiography is superior to other non-invasive modalities in detection of elevated LVFP in AIiI. Importantly, an echographic end-diastolic dimension of 6 cm or more indicates that left ventricular end-diastolic pressure is + in nearly all such AM1 pts.
INCREASE IN POST-ISCHEMIC (EPERFUSION) CORONARY VASCULAR RESISTANCE DUE TO CARDIAC CONTRACTURE Carl S. Apstein, MD; Marc Mueller, BS; William B. Hood, Jr., MD, Thorndike Memorial Laboratory, Boston City Hospital and Boston University, Boston, Massachusetts Reperfusion after myocardial ischemia does not always prevent irreversible injury. In order to study those factors which limit the potential of reperfusion, isolated rat hearts were subjected to 30 min of complete global ischemia and reperfused. Coronary vascular resistance was measured by monitoring mean aortic pressure (AoP) in the cannulated and retrogradely perfused aortic stump which received oxygenated Krebs-Henseleit buffer (95% 02 - 5% CO2) at a constant coronary flow rate of 8 ml/min. Preischemic mean AoP was 6527 mm Hg; in the early post-ischemic reperfusion period mean AoP increased to 119+11 mm Hg (p(O.001) and then progressively declined. The ieft ventricular dry:wet weight ratio did not change between the pre- and post-ischemic periods (0.214+0.007, n=9, vs. 0.215-H).004, n=6); therefore tissue edema did not cause the increased coronary vascular resistance. Left ventricular contracture (measured with a non-compressible intraLV balloon) increased in parallel with the mean AoP and coronary vascular resistance during reperfusion. Less severe ischemia caused smaller increases in contracture and coronary vascular resistance: reperfusion coronary vascular resistance increased by 93%, 47%, 38%, and 12% after 30 min coronary flow reductions of lOO%, 99.5%, 95%, and 90% respectively. An increased coronary vascular resistance due to contracture after severe ischemia may shunt flow away from an ischemic region and hinder the restoration of nutritive coronary flow. Small increments of 02 delivery during the ischemic period prevented a marked increase in contracture and coronary vascular resistance.
118
January 1978
The AmerlcanJournalof
CARDIOLOGY
Volume
MECHANISM OF REDUCTION OF MYOCARDIAL INJURY BY HYALURONIDASE. Joseph Askenazi MD, L David Hillis MD, Pablo E Diaz MD, Michael A Davis DSc, Eugene Braunwald MD FACC, Peter R Maroko MD FACC. Depts Med, Harvard Med Sch & Peter B Brigham Hosp, Boston, MA. To study the mechanism by which hyaluronidase(H) decreases myocardial injury after coronary artery occlusion, myocardial flow was determined using radiolabeled microspheres(7-10u) in 18 open chest dogs with left anterior descending coronary artery occlusion. Nine served as controls(Cont) and 9 received H(5OONF units/kg) intravenously 20 min after occlusion. Fifteen min and 6 hrs after occlusion, 2~10~ microspheres("'Ce or 85Sr) were injected into the left atrium and reference samples were collected from the femoral artery. After 6 hrs, 8 transmural(TM) biopsies (2.202.07g) were obtained from the left ventricle and divided into endocardial(Endo) and epicardial (Epi) portions for determination of radioactivity. Mean arterial pressure, heart rate, cardiac output and flow in the nonischemic myocardium, both in the Cont and the H treated dogs, were similar 15 min and 6 hrs after occlusion, averaging 116?4mmHg, 141+5beats/min, 2.67?.3L/min and 101~3m1/100g/min, respectively. At 15 min the flow to the ischemic myocardium in Cont was: TM 28.9?4.1(+SE), Endo 18.8f2.6, Epi 39.5?5.4ml/IOOg/min and Endo/Epi 0.6? .07 (n=24), which was not significantly different than in the H treated dogs: 3O.lt3.4, 21.3t3.0, 38.5t4.5 and 0.5? .06, respectively. In the Cont after 6 hrs flow fell: TM 18.6'4.O(p<.OOl), Endo 10.3'3.3(~<.05), Epi 30.0+5.3"1/ lOOg/min(pi.OS) and Endo/Epi 0.3?.05(~<.01). In contrast, H treated dogs showed no fall in flow after 6 hrs: TM 33.2+3.5(NS), Endo 23.8+3.O(NS), Epi 42.4?4.6ml/lOOg/min (NS) and Endo/Epi 0.6?.06(NS). All these values were significantly higher than those of the Cont at 6 hrs. Thus, salvage of ischemic myocardium by hyaluronidase may be explained by its beneficial effect on collateral blood flow to the injured area.
DETECTION OF CORONARY ARTERY DISEASE AND MYOCARDIAL ISCHEMIA BY ELECTROCARDIOGRAPHY AND MYOCARDIAL PERFUSION SCANNING WITH THALLIUM 201. Ion K. Bailey, MD; Lawrence S.C. Griffith, MD; H. William Strauss,MD; Bertram Pitt, MD, The Johns Hopkins Medical Institutions, B;lltimore, Maryland. The sensitivity of rest and exercise myocardial perfusion scanning with thallium 201 for the detection of anatomic coronary artery disease and myocardial ischemia was compared to rest and maximum stress electrocardiography. Of 43 patients with angiographical ly proven coronary artery disease (narrowing2 70% in at least 1 vessel), 33 (77%) patients had an abnormal rest or stress perfusion scan (presence of a local perfusion defect). Twenty-six (60%) had an abnormal rest or stress electrocardiogram (presence of significant Q waves at rest or ST depression of ~1 mm during stress compared to rest) (p <. 05). Abnormal thallium perfusion scan at exercise suggesting ischemia (appearance of a new perfusion defect not present at rest) was found in 26 (60%). Abnormal exercise electrocardiogram was present in 14 (33%) (p<.OOl). Of 21 patients with single vessel disease perfusion scanning at rest and stress detected 15 while rest and stress electrocardiography detected 8 (p <. 01). Of 22 patients with double or triple vessel disease scanning detected 18 while electrocardiography also detected 18 (not significant). Thus myocardial perfusion scanning with thallium 201 is more sensitive than electrocardiography in detecting coronary artery disease and stress induced ischemia, although the specificity is yet to be evaluated. Thallium 201 scanning may be of particular value in patients with single vessel disease. Neither technique, however, is sufficient to completely exclude significant coronary artery disease.
37
ACCURATE DETECTION OF ELEVAT‘ED LEFT VENTRICULAR FILLING PRESSURE IN ACUTE MYOCARDIAL INFARCTION BY ECHOCARDIOGRAPHY: COMPARISON OF NON-INVASIVE TECHNIQUES WITH CARDIAC CATHETERIZATION. Juan Angel, MD, Ezra A. Amsterdam, MD, FACC, Dean T. Mason, MD, FACC, Lynn Weinnert, BS, and Anthony N. DeUniversity of California, Davis, CA. Maria, MD, FACC. Since left ventricular filling pressure (LVFP) is of quantitative, prognostic and therapeutic significance in acute myocardial infarction (AMI), the reliable identification of increased LVFP by atraumatic means would be of considerable clinical value. Thus this study compared the ability of chest x-ray (CXR), physical examination (PE), ECG, serum creatine phosphokinase (CPK), and echocardiography (U), to detect increased LVFP in 25 AM1 patients (pts) as determined by pulmonary artery wedge pressure. Of 51 determinations of LVFP by cardiac catheterization, 26 were elevated (E) (>16 mm Hg, mean 24) while 25 were normal (N) (mean 9 mm Hg). CXR and PE were scored from 1 to 5 for progressive signs of heart failure. Only minor differences existed between E and N by CXR (2.8 vs 1.7, pc.02) and PE (2.2 vs 1.8, pc.05). The number of Q waves (mean 3) and peak CPK (mean 1221) were similar in both the E and N groups. Although U stroke index and fiber shortening velocity were similar (mean 42 vs 0.98 circumference/sec), U end-diastolic dimension (EdD) was larger (6.43 vs 5.18 cm, pc.001) and ejection fraction smaller (39 vs 55%, pc.001) in E than N. Moreover, of 24 determinations with EdD >6 cm, 22 (88%) had elevated LVFP, whereas LVFP was elevated in only 5/27 (18%) instances From these comparative observations, it with EdD (6 cm. is concluded that echocardiography is superior to other non-invasive modalities in detection of elevated LVFP in AIiI. Importantly, an echographic end-diastolic dimension of 6 cm or more indicates that left ventricular end-diastolic pressure is + in nearly all such AM1 pts.
INCREASE IN POST-ISCHEMIC (EPERFUSION) CORONARY VASCULAR RESISTANCE DUE TO CARDIAC CONTRACTURE Carl S. Apstein, MD; Marc Mueller, BS; William B. Hood, Jr., MD, Thorndike Memorial Laboratory, Boston City Hospital and Boston University, Boston, Massachusetts Reperfusion after myocardial ischemia does not always prevent irreversible injury. In order to study those factors which limit the potential of reperfusion, isolated rat hearts were subjected to 30 min of complete global ischemia and reperfused. Coronary vascular resistance was measured by monitoring mean aortic pressure (AoP) in the cannulated and retrogradely perfused aortic stump which received oxygenated Krebs-Henseleit buffer (95% 02 - 5% CO2) at a constant coronary flow rate of 8 ml/min. Preischemic mean AoP was 6527 mm Hg; in the early post-ischemic reperfusion period mean AoP increased to 119+11 mm Hg (p(O.001) and then progressively declined. The ieft ventricular dry:wet weight ratio did not change between the pre- and post-ischemic periods (0.214+0.007, n=9, vs. 0.215-H).004, n=6); therefore tissue edema did not cause the increased coronary vascular resistance. Left ventricular contracture (measured with a non-compressible intraLV balloon) increased in parallel with the mean AoP and coronary vascular resistance during reperfusion. Less severe ischemia caused smaller increases in contracture and coronary vascular resistance: reperfusion coronary vascular resistance increased by 93%, 47%, 38%, and 12% after 30 min coronary flow reductions of lOO%, 99.5%, 95%, and 90% respectively. An increased coronary vascular resistance due to contracture after severe ischemia may shunt flow away from an ischemic region and hinder the restoration of nutritive coronary flow. Small increments of 02 delivery during the ischemic period prevented a marked increase in contracture and coronary vascular resistance.
118
January 1978
The AmerlcanJournalof
CARDIOLOGY
Volume
MECHANISM OF REDUCTION OF MYOCARDIAL INJURY BY HYALURONIDASE. Joseph Askenazi MD, L David Hillis MD, Pablo E Diaz MD, Michael A Davis DSc, Eugene Braunwald MD FACC, Peter R Maroko MD FACC. Depts Med, Harvard Med Sch & Peter B Brigham Hosp, Boston, MA. To study the mechanism by which hyaluronidase(H) decreases myocardial injury after coronary artery occlusion, myocardial flow was determined using radiolabeled microspheres(7-10u) in 18 open chest dogs with left anterior descending coronary artery occlusion. Nine served as controls(Cont) and 9 received H(5OONF units/kg) intravenously 20 min after occlusion. Fifteen min and 6 hrs after occlusion, 2~10~ microspheres("'Ce or 85Sr) were injected into the left atrium and reference samples were collected from the femoral artery. After 6 hrs, 8 transmural(TM) biopsies (2.202.07g) were obtained from the left ventricle and divided into endocardial(Endo) and epicardial (Epi) portions for determination of radioactivity. Mean arterial pressure, heart rate, cardiac output and flow in the nonischemic myocardium, both in the Cont and the H treated dogs, were similar 15 min and 6 hrs after occlusion, averaging 116?4mmHg, 141+5beats/min, 2.67?.3L/min and 101~3m1/100g/min, respectively. At 15 min the flow to the ischemic myocardium in Cont was: TM 28.9?4.1(+SE), Endo 18.8f2.6, Epi 39.5?5.4ml/IOOg/min and Endo/Epi 0.6? .07 (n=24), which was not significantly different than in the H treated dogs: 3O.lt3.4, 21.3t3.0, 38.5t4.5 and 0.5? .06, respectively. In the Cont after 6 hrs flow fell: TM 18.6'4.O(p<.OOl), Endo 10.3'3.3(~<.05), Epi 30.0+5.3"1/ lOOg/min(pi.OS) and Endo/Epi 0.3?.05(~<.01). In contrast, H treated dogs showed no fall in flow after 6 hrs: TM 33.2+3.5(NS), Endo 23.8+3.O(NS), Epi 42.4?4.6ml/lOOg/min (NS) and Endo/Epi 0.6?.06(NS). All these values were significantly higher than those of the Cont at 6 hrs. Thus, salvage of ischemic myocardium by hyaluronidase may be explained by its beneficial effect on collateral blood flow to the injured area.
DETECTION OF CORONARY ARTERY DISEASE AND MYOCARDIAL ISCHEMIA BY ELECTROCARDIOGRAPHY AND MYOCARDIAL PERFUSION SCANNING WITH THALLIUM 201. Ion K. Bailey, MD; Lawrence S.C. Griffith, MD; H. William Strauss,MD; Bertram Pitt, MD, The Johns Hopkins Medical Institutions, B;lltimore, Maryland. The sensitivity of rest and exercise myocardial perfusion scanning with thallium 201 for the detection of anatomic coronary artery disease and myocardial ischemia was compared to rest and maximum stress electrocardiography. Of 43 patients with angiographical ly proven coronary artery disease (narrowing2 70% in at least 1 vessel), 33 (77%) patients had an abnormal rest or stress perfusion scan (presence of a local perfusion defect). Twenty-six (60%) had an abnormal rest or stress electrocardiogram (presence of significant Q waves at rest or ST depression of ~1 mm during stress compared to rest) (p <. 05). Abnormal thallium perfusion scan at exercise suggesting ischemia (appearance of a new perfusion defect not present at rest) was found in 26 (60%). Abnormal exercise electrocardiogram was present in 14 (33%) (p<.OOl). Of 21 patients with single vessel disease perfusion scanning at rest and stress detected 15 while rest and stress electrocardiography detected 8 (p <. 01). Of 22 patients with double or triple vessel disease scanning detected 18 while electrocardiography also detected 18 (not significant). Thus myocardial perfusion scanning with thallium 201 is more sensitive than electrocardiography in detecting coronary artery disease and stress induced ischemia, although the specificity is yet to be evaluated. Thallium 201 scanning may be of particular value in patients with single vessel disease. Neither technique, however, is sufficient to completely exclude significant coronary artery disease.
37