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Abstract
Background
Early reperfusion after acute myocardial infarction is known to be effective in salvaging myocardium and hence improving early and late mortality and morbidity. The late reperfusion by percutaneous transluminal coronary angioplasty (PTC A) is also reported to be helpful in improving mortality and morbidity also, however the exact mechanism is not known when the salvage of myocardium is not expected.
Methods
In this study. 24 acute myocardial infarction patients who had not been undergone reperfusion therapy within 6 hours or those who had been failed to be recanalized were subjected to study. The patients were divided into two groups, group I. those who had little ischemic myocardium around the infarct(ll patients, all male, 59.1 ± 9.8years) and group II. those who had considerable ischemic area around the infarct zone(13 patients, M: F=33: 1. 60.9 ± 9.7 years) revealed by myocardial perfusion scanning with 201TI or 90mTc-MIBI. The area of ischemia and infarction, defect volume ratio and left ventricular dimensions and global functions were measured before and after PTCA. The mortality and morbidity were also observed.
Results
In group I the associated risk factors were hypertension in 5, hypercholesterolemia. 2 and smoking, 5 patients and in group II hypertension in 5, hypercholesterolemia, 4, smoking, 7 and diabetes mellitus, 2 patients.
The PTCA was peformed 10.2 ± 4.9days in group I and 10.5 ± 6.6days in group II after the admission. The infarct related arteries were left anterior descending artery in 12. left circumflex artery in 2 and right coronary artery in 10.
Echocardiographic variables, i.e. left ventricular end-diastolic volume, left ventricular end-systolic volume, ejection fraction of the left ventricle and the E to A ratio of mitral flow measured by doppler echocardiography were compared before and after PTCA in each group. The variables were not different between two groups and were not changed after PTCA.
Myocardial perfusion scanning revealed significantly decreased defect area(p<0.05). infarct area(p<0.005) and defect volume ratio(p<0.05) after PTCA in group II. In group I, 6 patients out of 11 showed improved infarct area and defect volume ratio, but the mean of the group was not different before and after PTCA. There was neither mortality nor nonfatal infarction during follow up period of 15.9 ± 3.8months in group I and 13.8 ± 3.8months in group II.
Conclusion
Above results suggested that the delayed PTCA was efficacious in reducing perfusion defect area, infarct area and defect volume ratio in group II and in some patients of group I also and that the delayed PTCA might be effective in preventing further dilation of the left ventricle and further deterioration of the left ventricular functions in either group of the patients.
References
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Fig. 1.
An example illustration of the angiographic(A and B), echocardiographic(C and D) and myocardial perfusion scanning findings(E and F) before and after percutaneous transluminal coronary angioplasty (PTCA) in a studied patient without peri-infarction ischemia. The totally occluded right coronary artery was completely recanalized by PTCA. The left ventricular dimension was not changrd after PTCA. Myocardial perfusion was improved after PTCA.
Fig. 2.
An example illustration of the angiographic(A and B). echocardiographic(C and D) and myocardial perfusion scanning findings(E and F) before and after percutaneous transluminal coronary angioplasty (PTCA) in a studied patient with pen-infarction ischemia. The totally occluded left anterior descending artery was completely recanalized by PTCA. No definitive change of the ventricular morphology was demonstrated. The myocardial perfusion was markedly improved after PTCA.
Fig. 3.
Left ventricular end-diastolic volume(LVEDV) and left ventricular end-systolic volume(LVESV) measured by echocardiographic examination before and after PTCA in group I showed no significant change.
Fig. 4.
Left ventricular end-diastolic volume(LVEDV) and left ventricular end-systolic volume(LVESV) measured by echocardiographic examination before and after PTCA in group II showed no significant change.
Fig. 5.
Left ventricular ejection fraction(EF) measured by echo-cardiographic examination before and after PTCA in group I and II showed no significant change.
Fig. 6.
The stress perfusion defect area(Defect), ischemic area(Ischemia) and infarct area(Infarction) measured by myocardial perfusion scan before and after PTCA in group I showed no significant change.
Fig. 7.
The stress perfusion defect area(Defect) and infarct area(lnfarction) measured by myocardial perfusion scan in group II, which were decreased significantly after PTCA(defect; p<0.05. infraction; p<0.005). But ischemic area(Ischemia) was not changed significantly after PTCA
Fig. 8.
The perfusion defect volume ratio(DVR) before and after PTCA in group I and II. The DVR was significantly decreased in group II after PTCA (p<0.05) but not in group I.
Table 1.
Comparison of the clinical and angiographic findings of two groups
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