Do we need a new definition for post-stress reduction in LVEF beyond the numerical values?
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Department of Cardiology, Al-Azhar School of Medicine, Cairo, Egypt Department of Nuclear Cardiology, Alexandria University, Alexandria, Egypt Department of Critical Care, Cairo University, Giza, Egypt
Received May 11, 2019; accepted May 13, 2019 doi:10.1007/s12350-019-01799-5
See related article, https://doi.org/10.10 07/s12350-019-01725-9. In this issue of the Journal, Obiedate et al. highlighted the prognostic value of post-adenosine reduction in LVEF among Jordanian population with negative myocardial perfusion imaging (MPI) studies. The principal conclusion emerging from this excellent work is that post-adenosine reduction in LVEF in the setting of normal MPI was not associated with higher cardiac event rate at 2 years of follow-up: a finding that correlates with similar reports which concluded the same finding in relation to treadmill exercise, Dipyridamole, and recently regadenoson stress as well.1–4 The current study has evoked a series of thoughtful ideas and highlighted some important concepts. Some of these thoughts and concepts are revisited below: PATHOPHYSIOLOGIC MECHANISMS OF POSTSTRESS REDUCTION IN LVEF The finding of post-stress reduction in LVEF was initially suggested as a high-risk finding related to significant CAD. However, the true pathophysiologic mechanism is still a matter of debate. Below are discussed the relevant pathophysiologic mechanisms and their impacts:
Reprint requests: Mohamed Mandour Ali, MD, Department of Cardiology, Al-Azhar School of Medicine, Cairo, Egypt; [email protected] J Nucl Cardiol 1071-3581/$34.00 Copyright 2019 American Society of Nuclear Cardiology.
• First, it could be due to persistent changes in LV loading pressure with subsequent higher LV volumes and reduced LVEF (Volumetric theory).5 This could be the main explanation of such a phenomenon in case of dilated cardiomyopathy or even subclinical heart muscle disease. It is unlikely to occur in a heart with normal volume and LVEF. This situation should be considered as a different phenomenon from the transient ‘‘ischemic’’ LV cavity dilation with a different spectrum of MACEs from the true ischemic category.5 • Second, inducible myocardial ischemia leads to transient (post-stress) LV dilatation. As a matter of fact, we do not see the actual endocardium on SPECT imaging. We usually rely upon the edge of the tracer distribution, so that if there is reduction in tracer uptake in the subendocardial rim, this will be reflected as higher cavity size and lower LVEF (indeed, without true change in LV volumes). Here, stressinduced LV dilatation is simply a reflection of ischemia (Subendocardial ischemia theory).5 Its utility in clinical imaging may bring attention to larger, primarily subendocardial regions of inducible ischemia, rather than an unremarkably normal MPI study in these discreet cases of subendocardial ischemia.5–7 • Third, the last possibility is that severe inducible ischemia led to unstable LV pressure and volume (a mixture of reversible ischemia and actual volume changes). In such a situation,
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