These results suggest that TCA cycle activity is not persistently decreased in dysfunctional reperfused myocardium after a brief ischemic episode and therefore cannot account for the reduced contractile function at that time.
Background-Left ventricular (LV) function is the most important determinant of outcome after a myocardial infarction. Global LV function after a myocardial infarction is affected not only by wall motion in the infarct zone but also by regional function in the contralateral territory. It was hypothesised that the presence of significant stenoses in coronary arteries supplying the contralateral territory might influence the ability of this region to compensate for damaged myocardium after a myocardial infarction. Methods and results-79 patients treated with thrombolysis for acute myocardial infarction had coronary and ventricular angiograms within 24 h and at a mean follow up of 12 months after myocardial infarction. Wall motion in the contralateral territory was analysed and scored by the centre line method and the change over time was correlated with the presence or absence of significant (>70%) diameter stenoses in the non-infarct-related artery. Mean (SD) contralateral territory motion worsened, from 0 74 (1.78) to -1-55 (2.06) SD chord (p < 0.001) in 40 patients with stenoses, whereas contralateral territory motion improved from -0-02 (2. Global function after infarction, however, is affected not only by changes in the wall motion of the infarct zone but also by regional function in the contralateral, noninfarct territory.56 After acute infarction hyperkinesis in the non-infarct area can normalise overall global ventricular function7 and such hyperkinesia is significantly related to improved in-hospital survival both in patients who have undergone successful thrombolysis and in those who have not.68 Less is known, however, about the importance of non-infarct regional function during the long-term follow up of post-infarction patients and about the factors which influence that performance.It is conceivable that increased demand is placed on the non-infarct zone after a transmural infarction. After a coronary artery is occluded flow to the contralateral myocardium increases to match the increased oxygen requirements in that area caused by a higher regional workload.
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