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Editor,—Rinaldi et alperformed an important study, demonstrating for the first time in patients with coronary disease that protection against postexercise “stunning” occurs in association with the warm-up effect when exercise tests are separated by 30 minutes.1 Cumulative stunning occurs when tests are separated by 60 minutes. Moreover, previous reports have failed to demonstrate persistent impairment ofglobal left ventricular function, even using radionuclide ventriculography.2 The study illustrates the difficulty of applying concepts defined in highly instrumented animal preparations to a rather less controllable human model. The warm-up effect in angina is a complex phenomenon and probably represents an interplay of protective mechanisms including a short term training effect and improved myocardial perfusion via collaterals, as well as ischaemic preconditioning. In patients exercising on a treadmill it is impossible to monitor all of the variables necessary to identify the exact contribution of each of these mechanisms. Thus there are a number of issues that complicate the interpretation of the study data.
Patients were not required to perform practice exercise tests before the study. The increase in the times to peak exercise, angina, and 1 mm ST depression observed during the second of two tests 30 minutes apart might simply have been due to a slower rate of rise of rate–pressure product (RPP)—that is, an autonomic training effect. The component of the warm-up effect most likely to be due to ischaemic preconditioning involves an increase in the RPP required to provoke a given degree of ischaemia.3 It is therefore important to know the RPP at the onset of angina and at 1 mm ST depression.
The authors conclude that equivalent maximum ST depression for two sequential exercise tests implies “an equivalent ischaemic burden on both occasions”. However this takes no account of the overallduration of ischaemia, which may vary if the exercise time at which ST depression begins or the subsequent period over which it develops changes. The integral of the ST depressionv time relation would therefore be a better index of the “amount” of ischaemia, although this is difficult to measure. Some workers have proposed the total time for which there is more than 1 mm ST depression during both exercise and recovery as a useful index.4
Echocardiograms were not obtained during exercise, nor are the measurements from the immediate postexercise period quoted. The improved recovery of function observed after the second of two exercise tests 30 minutes apart is presented as evidence of protection againststunning. In reality, this observation is more likely to be a consequence of protection againstischaemic left ventricular dysfunction during exercise. In addition, variations in afterload or preload rather than the contractile state of the myocardium might account for some of the observed changes in echocardiographic indices.
In dogs, myocardial contractile function is largely dependent on subendocardial blood flow, which is disproportionately vulnerable to a reduction in transmural blood flow.5 6 Thus a 25% reduction in transmural flow may lead to a 50% reduction in subendocardial blood flow causing significant contractile dysfunction. Such a reduction of transmural blood flow would be barely detectable using SPECT perfusion imaging. Moreover, subendocardial ischaemia may persist after transmural ischaemia has apparently resolved due to a transmural steal effect. Thus the authors’ assertion that they have “simultaneously demonstrated myocardial dysfunction in the presence of normal perfusion at 30 minutes postexercise” confirming stunning must be approached with caution. It is likely to be some time before technology is available to exclude persistent subendocardial ischaemia as the cause of postexercise “stunning” in patients with coronary disease.
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