Key result
Increasing afterload with methoxamine in 15 patients with old MI and ventricular aneurysm decreased wall motion in non-infarcted regions and increased it in aneurysmal regions.
Why the study?
Does increased afterload with methoxamine alter regional left ventricular wall motion in patients with old myocardial infarction and ventricular aneurysm?
Observational (n=15)
Does increased afterload with methoxamine alter regional left ventricular wall motion in patients with old myocardial infarction and ventricular aneurysm?
In patients with old myocardial infarction and left ventricular aneurysm, increasing afterload paradoxically improves wall motion in the aneurysmal region while decreasing it in remote non-infarcted regions due to shifts in pressure-length loops.
Should not change afterload management in post-MI aneurysm; hypothesis-generating for regional mechanics in larger studies.
The functional response of the left ventricle with scar to increased afterload, was examined in 15 patients with old myocardial infarction and left ventricular aneurysm (OMI). Interventional cine left ventriculography during elevating left ventricular pressure with methoxamine. Wall motion was assessed by the radial and the centerline method. Augmented afterload didn't change ejection fraction in patients with OMI, but normalized wall motion (Z) increased in the aneurysmal region and decreased in the remote region in both methods. In the remote region in patients with OMI, afterload stress shortened left ventricular pressure-radial length (P-L) loops along length axis, and reduced percent systolic radial shortening (SS). In the aneurysmal region, P-L loops showed systolic elongation of length at rest and the slope of end-diastolic point to end-systolic point became steeper with increased afterload, resulting in a decrease of aneurysmal expansion. In summary, with increasing afterload, wall motion decreased in non-infarcted regions and increased in aneurysmal regions, in left ventricles with aneurysm. This mechanism may be interpreted as afterload-induced shifts of P-L loops in each region.
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Miyawaki et al. (1991) conducted an observational in Old myocardial infarction and left ventricular aneurysm (n=15). Increased afterload via methoxamine vs. Baseline (rest) was evaluated on Left ventricular regional function (wall motion and ejection fraction). Increasing afterload with methoxamine in 15 patients with old MI and ventricular aneurysm decreased wall motion in non-infarcted regions and increased it in aneurysmal regions.
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