Effect of Infarct Site on Diastolic Time During Exercise: Discussion

Effect of Infarct Site on Diastolic Time During Exercise: DiscussionClinical Findings
The extent of myocardial necrosis is of primary importance in determining left ventricular function. Peak creatine kinase is reported to correlate with total creatine kinase and with infarct size at autopsy, but this method has certain limitations. After inferior MI, peak level of creatine kinase may not accurately reflect the extent of necrosis of the left ventricle because the right ventricle may have contributed to enzyme release. Radionuclide ventriculography allows noninvasive measurement of left ventricular function and thereby estimates the impact of MI on ventricular performance. In this study, none of the patients had prior MI or electrocardiographically evidenced right ventricular MI. Furthermore, peak creatine kinase and lactate dehydrogenase levels, left ventricular end-diastolic volume index, and ejection fraction were nearly identical between anterior and inferior MI. Although anatomic infarct size could be different if it was measured with more sensitive methods, our data indicate that the infarct size between patients with anterior and inferior MI could not have been clinically different.
Results of Present Study
The present study carefully assessed systolic and diastolic function during supine exercise and their relationship to infarct site 6 to 8 weeks after acute MI in patients with nearly identical left ventricular function at rest. As a result, despite no significant differences in HR and blood pressure response to exercise, the DT-HR relationship in anterior MI differed significantly from that in inferior MI, ie, patients with anterior MI showed a disproportionate shortening of DT at any given HR at peak exercise. The duration of diastole is determined by HR and QS2; an increase in HR and lengthening of QS2 shorten DT. During exercise, HR increases and QS2 shortens, reflecting the chronotropic and inotropic response to exercise-induced catecholamine release. In anterior MI, QS2 was longer at any given HR compared with inferior MI at peak exercise. Furthermore, in contrast to inferior MI, QS2 did not shorten with increasing norepinephrine levels in anterior MI. An increase in catecholamine during exercise abbreviates duration of systole, and hence prolongs duration of diastole, the relative prolongation of QS2 in anterior MI may be due to the inability of the left ventricle to respond to inotropic stimulation.

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