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Comparison of cardiopulmonary‐based risk models with a clinical heart failure risk model

In this issue of the Journal, Agostoni and colleagues1 compared the newer cardiopulmonary exercise testing (CPET) risk model [Metabolic Exercise test data combined with Cardiac and Kidney Indexes (MECKI)],2 an older CPET model [Heart Failure Survival Score (HFSS)]3 and a clinical risk model [Seattle Heart Failure Model (SHFM)]4 in predicting the 2and 4-year risk of cardiovascular death, left ventricular assist device (LVAD) implantation, and urgent cardiac transplant in 6112 patients. They found the newer CPET model was superior for this endpoint as measured by the area under the receiver operating curve (AUC) (all three models ≥0.72) and the calibration was appropriate for all models. This is a large cohort of patients undergoing CPET and the authors are congratulated on deriving and very importantly validating the MECKI risk model. Identifying ambulatory patients for listing for cardiac transplant is a difficult decision and often relies on CPET. CPET [specifically peak oxygen consumption (pVO2)] remains a 2016 International Society for Heart and Lung Transplantation (ISHLT) class 1 recommendation for listing for cardiac transplant with a pVO2 of ≤14 mL/kg/min if intolerant of a beta-blocker and ≤12 mL/kg/min if on a beta-blocker,5 which corresponds to an annual mortality of ∼15–20% in a large cohort of 2105 patients from the Cleveland Clinic Foundation in the 2005 era (Figure 1),6 similar to results we published.7 In the HF-ACTION cohort, the annual mortality was much lower for men and women with a pVO2 12 mL/kg/min, corresponding to an annual mortality of∼10% in men and∼5% in women (Figure 1).8 This lower mortality has recently been confirmed in 630 patients with heart failure and reduced ejection fraction (HFrEF) with a 1-year ∼9% risk of death/LVAD/urgent transplant for a pVO2 of 12 mL/kg/min.9 This illustrates the difficulty and complexity of using pVO2 as a single variable in making decisions for transplant listing along with the interaction of gender and beta-blockers on the absolute risk of death for any pVO2.