Key result
Exercise stress, but not short-acting pharmacological stress, significantly decreased left ventricular ejection fraction compared to rest in patients with perfusion abnormalities (P<0.01).
Why the study?
Does short-acting pharmacological stress (adenosine triphosphate) induce transient left ventricular dysfunction compared to exercise stress in patients suspected of having ischaemic heart disease?
Observational (n=362)
Does short-acting pharmacological stress (adenosine triphosphate) induce transient left ventricular dysfunction compared to exercise stress in patients suspected of having ischaemic heart disease?
p-value: p=<0.01
Transient left ventricular dysfunction is observed following exercise stress but not short-acting pharmacological stress in patients with perfusion abnormalities, suggesting it results from post-exercise stunning rather than subendocardial hypoperfusion.
Post-stress LVEF changes require stress-modality consideration in perfusion imaging; hypothesis-generating for stunning mechanisms and needs prospective validation.
In ischaemic heart disease patients, transient left ventricular dysfunction is observed due to post-exercise stunning. The aim of this study was to determine whether transient left ventricular dysfunction could also be seen after short-acting pharmacological stress (adenosine triphosphate). A 1 day rest/stress gated myocardial single photon emission computed tomography was performed on 362 patients suspected of having ischaemic heart disease by exercise (n=199) or short-acting pharmacological stress (n=163). Left ventricular ejection fraction were estimated both at rest and stress. Based on perfusion findings, patients were subdivided into ischaemia, fixed defect and normal group. For the ischaemia and fixed defect group, left ventricular ejection fraction after stress was significantly decreased compared with the resting value by exercise stress (ischaemia group, 57.5+/-11.0 vs 60.4+/-10.4; fixed defect group, 47.7+/-16.7 vs 49.6+/-16.8; P<0.01), but not by pharmacological stress (ischaemia group, 55.8+/-13.4 vs 57.1+/-13.8; fixed defect group, 50.8+/-13.5 vs 50.6+/-13.1; P=NS). In the normal group, left ventricular ejection fraction after stress was not significantly changed by either exercise (65.7+/-10.4 vs 66.8+/-10.2; P=NS) or pharmacological stress (63.0+/-11.7 vs 64.0+/-12.1; P=NS). It is concluded that a transient decrease in left ventricular ejection fraction after stress was observed following post-exercise, not following a short-acting pharmacological stress in patients showing perfusion abnormalities. Transient left ventricular dysfunction may be the result of post-exercise stunning, not from subendocardial hypoperfusion induced by short-acting pharmacological stress.
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Iwado et al. (2003) conducted an observational in Ischaemic heart disease (n=362). Exercise stress vs. Short-acting pharmacological stress (adenosine triphosphate) was evaluated on Change in left ventricular ejection fraction from rest to stress (p=<0.01). Exercise stress, but not short-acting pharmacological stress, significantly decreased left ventricular ejection fraction compared to rest in patients with perfusion abnormalities (P<0.01).
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