Effect of Infarct Site on Diastolic Time During Exercise: Limitations

There is a greater degree of shortening of the anterior than of the posterior wall during systole in the normal left ventricle, indicating that a similar degree of myocardial damage results in more impairment of left ventricular function after anterior MI. Furthermore, Wynne et al reported that abnormal regional ejection fraction in the segments remote from infarct zone was more frequent after anterior than in inferior MI. In this study, exercise testing revealed an exaggerated increase in pulmonary artery wedge pressure at peak exercise in anterior MI compared with those in inferior MI, despite nearly identical stroke volume index and HR. During exercise, important changes in left ventricular diastolic function occur frequently even in patients with preserved left ventricular systolic function. Therefore, in patients with anterior MI, a higher pulmonary artery wedge pressure with similar stroke volume index would suggest increased left ventricular stiffness.
Most coronary blood flow occurs in diastole, and earlier reports have demonstrated that the duration of diastole is the main determinant of subendocardial perfusion. In addition to decreased subendocardial coronary blood flow by increased left ventricular end-diastolic pressure in anterior MI, a disproportionate shortening of myocardial perfusion time permitted further reduction of subendocardial blood flow. Moreover, the presence of increased duration of systole may increase myocardial oxygen consumption. Thus, an extra burden placed on the residual functioning myocardium of the noninfarcted segments in anterior MI may have potential for initiating subendocardial ischemia in the residual functioning myocardium of the noninfarcted segments, which results in further abbreviation of DT and thereby may play a role in reduction of left ventricular function.
Two limitations of our study should be addressed. First, although none of our patients had obstructive lesions in epicardial coronary arteries supplying the noninfarcted area and only one patient in each group had a small transient defect in the infarct site by the necrotic zone, the results of the present study do not allow us to completely determine the primary cause of shortening of DT in anterior MI. That is, we do not know whether it was myocardial ischemia due to small vessel disease or weak myocardial response to inotropic stimulation. However, increased duration of systole and shortening of myocardial perfusion time undoubtedly play a role in oxygen supply and demand imbalance, leading to subendocardial ischemia. Second, since the patient population in this study was a highly selective group with good ejection fraction and a negative stress test results, further experience is necessary to evaluate that our conclusion about differences between anterior and inferior MI can be generalized to patients with ischemic response to exercise or clinical heart failure, or both.

This entry was posted in Cardiology and tagged anterior inferior, coronary arteries, ejection fraction, norepinephrine, pulmonary artery.