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In a study by Jellis et al. [ 59], who defined abnormal E′ (septal E′) at rest as <2SD of normal for age and abnormal E′ at peak exercise stress as <−9.9 cm/s, E′ at stress was abnormally low in 49%% of the T2DM patients with normal E′ at rest.
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Participants then completed a peak graded cardiopulmonary exercise stress test that was used to determine the workload of the two experimental exercise sessions.
This was almost entirely due to a smaller increase (P < 0.01) in ELVI from rest to peak exercise in exercise and dobutamine stress); interestingly, despite a blunted increase in contractility in dipyridamole tests, coupling differences were still present for a greater negative arterial elastance reserve in dipyridamole group patients with follow-up events.
We measured cTnT with a sensitive assay before, immediately after peak exercise and 1.5 and 4.5 h after exercise stress testing in 198 patients referred for MPI.
Injection of the radiopharmaceutical was done at peak exercise, or in the third minute of pharmacological stress induction.
The stress echocardiogram images were acquired immediately at peak exercise, and focused on LV outflow gradients, degree of mitral regurgitation and wall motion.
Several previous studies have reported an association between pulmonary regurgitation and exercise impairment, as testified by reduced exercise time, VO2 peak, and maximum achieved METs in comparison with healthy controls during exercise stress testing [ 9].
A graded exercise stress test was also performed on a treadmill or cycle ergometer with measurement of peak oxygen uptake.
RPE scores were recorded at peak exercise.
Arterial blood was sampled at rest and at peak exercise.
Poor exercise capacity was defined as<5 METS at peak exercise [17].
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