Utility of the oxygen pulse in the diagnosis of obstructive coronary artery disease in physically fit patients

Cardiopulmonary exercise testing (CPET) guidelines recommend analysis of the oxygen (O-2) pulse for a late exercise plateau in evaluation for obstructive coronary artery disease (OCAD). However, whether this O-2 pulse trajectory is within the range of normal has been debated, and the diagnostic performance of the O-2 pulse for OCAD in physically fit individuals, in whom (V) over dotO(2) may be more likely to plateau, has not been evaluated. Using prospectively collected data from a sports cardiology program, patients were identified who were free of other cardiac disease and underwent clinically-indicated CPET within 90 days of invasive or computed tomography coronary angiography. The diagnostic performance of quantitative O-2 pulse metrics (late exercise slope, proportional change in slope during late exercise) and qualitative assessment for O-2 pulse plateau to predict OCAD was assessed. Among 104 patients (age:56 +/- 12 years, 30% female, peak (V) over dotO(2) 119 +/- 34% predicted), the diagnostic performance for OCAD (n = 24,23%) was poor for both quantitative and qualitative metrics reflecting an O-2 pulse plateau (late exercise slope: AUC = 0.55, sensitivity = 68%, specificity = 41%; proportional change in slope: AUC = 0.55, sensitivity = 91%, specificity = 18%; visual plateau/decline: AUC = 0.51, sensitivity = 33%, specificity = 67%). When O-2 pulse parameters were added to the electrocardiogram, the change in AUC was minimal (-0.01 to +0.02, p >= 0.05). Those patients without OCAD with a plateau or decline in O-2 pulse were titter than those with linear augmentation (peak (V) over dotO(2) 133 +/- 31% vs. 114 +/- 36% predicted, p < 0.05) and had a longer exercise ramp time (9.5 +/- 3.2 vs. 8.0 +/- 2.5 min. p < 0.05). Overall, a plateau in O-2 pulse was not a useful predictor of OCAD in a physically fit population, indicating that the O-2 pulse should be integrated with other CPET parameters and may reflect a physiologic limitation of stroke volume and/or O-2 extraction during intense exercise.