TY - JOUR
T1 - The importance of defining left ventricular area at risk in vivo during acute myocardial infarction
T2 - An experimental evaluation with myocardial contrast two-dimensional echocardiography
AU - Kaul, S.
AU - Glasheen, W.
AU - Ruddy, T. D.
AU - Pandian, N. G.
AU - Weyman, A. E.
AU - Okada, R. D.
PY - 1987
Y1 - 1987
N2 - Because the left ventricular 'area at risk' is the most important determinant of ultimate infarct size, it would be useful to know the size of the area at risk during acute myocardial infarction to make therapeutic decisions. We therefore performed a series of experiments in four groups of dogs. In group I dogs (n = 15) we attempted to determine whether current methods of assessing left ventricular function during acute myocardial infarction reflect the true size of the area at risk. At each of two to five sequential stages, a more proximal coronary occlusion was performed to produce a larger area at risk until cardiovascular collapse occurred. At each stage, the area at risk (measured by myocardial contrast echocardiography), hemodynamic variables, and left ventricular ejection fraction (LVEF) were measured. Hemodynamic variables became abnormal when the area at risk was large (25% to 40% of the left ventricle), whereas LVEF became abnormal when the area at risk was of moderate size (18%). When cardiac output and LVEF were normalized to baseline values, a close inverse relationship was noted between these variables and area at risk. In contrast, there was a poor relationship between normalized mean arterial pressure and area at risk (r = .42). In group II dogs (n = 9) the area at risk was measured serially over 6 hr after coronary occlusion. The size of the area at risk remained unchanged regardless of the transmural extent of the ultimate infarct. The circumferential endocardial extent of the area at risk closely predicted the circumferential endocardial extent of the infarct at 6 hr in eight of nine dogs that developed an infarct. Group III dogs (n = 7) underwent the same protocol as group II dogs, but the duration of occlusion was 3 hr. The circumferential endocardial extent of the area at risk closely predicted the circumferential endocardial extent of the infarct. Group IV dogs (n = 5) underwent subtotal coronary occlusion. Although regional wall motion abnormalities were noted in this group, no area at risk could be defined. We conclude that (1) although a close inverse relationship is noted between normalized cardiac output and area at risk, the absolute values for cardiac output and other hemodynamic variables become abnormal only when the area at risk is large (25% to 40%); (2) measurement of LVEF may provide a better assessment of the size of the area at risk than hemodynamic variables; (3) the circumferential endocardial extent of the area at risk closely predicts that of the ultimate infarct at both 3 and 6 hr after occlusion; (4) although abnormal wall motion is always present in the region of the area at risk, the converse is not true; and (5) a direct method of measuring area at risk such as myocardial contrast echocardiography would have several advantages in this era of interventional cardiology.
AB - Because the left ventricular 'area at risk' is the most important determinant of ultimate infarct size, it would be useful to know the size of the area at risk during acute myocardial infarction to make therapeutic decisions. We therefore performed a series of experiments in four groups of dogs. In group I dogs (n = 15) we attempted to determine whether current methods of assessing left ventricular function during acute myocardial infarction reflect the true size of the area at risk. At each of two to five sequential stages, a more proximal coronary occlusion was performed to produce a larger area at risk until cardiovascular collapse occurred. At each stage, the area at risk (measured by myocardial contrast echocardiography), hemodynamic variables, and left ventricular ejection fraction (LVEF) were measured. Hemodynamic variables became abnormal when the area at risk was large (25% to 40% of the left ventricle), whereas LVEF became abnormal when the area at risk was of moderate size (18%). When cardiac output and LVEF were normalized to baseline values, a close inverse relationship was noted between these variables and area at risk. In contrast, there was a poor relationship between normalized mean arterial pressure and area at risk (r = .42). In group II dogs (n = 9) the area at risk was measured serially over 6 hr after coronary occlusion. The size of the area at risk remained unchanged regardless of the transmural extent of the ultimate infarct. The circumferential endocardial extent of the area at risk closely predicted the circumferential endocardial extent of the infarct at 6 hr in eight of nine dogs that developed an infarct. Group III dogs (n = 7) underwent the same protocol as group II dogs, but the duration of occlusion was 3 hr. The circumferential endocardial extent of the area at risk closely predicted the circumferential endocardial extent of the infarct. Group IV dogs (n = 5) underwent subtotal coronary occlusion. Although regional wall motion abnormalities were noted in this group, no area at risk could be defined. We conclude that (1) although a close inverse relationship is noted between normalized cardiac output and area at risk, the absolute values for cardiac output and other hemodynamic variables become abnormal only when the area at risk is large (25% to 40%); (2) measurement of LVEF may provide a better assessment of the size of the area at risk than hemodynamic variables; (3) the circumferential endocardial extent of the area at risk closely predicts that of the ultimate infarct at both 3 and 6 hr after occlusion; (4) although abnormal wall motion is always present in the region of the area at risk, the converse is not true; and (5) a direct method of measuring area at risk such as myocardial contrast echocardiography would have several advantages in this era of interventional cardiology.
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U2 - 10.1161/01.CIR.75.6.1249
DO - 10.1161/01.CIR.75.6.1249
M3 - Article
C2 - 3032476
AN - SCOPUS:0023189113
SN - 0009-7322
VL - 75
SP - 1249
EP - 1260
JO - Circulation
JF - Circulation
IS - 6
ER -