Renal function in myocardial infarction: does serum creatinine tells the whole story?

Abstract

‘One more such victory and we are utterly undone’, Pyrrhus of Epirus was reportedly quoted after the battle of Asculum where he defeated the Romans at the cost of devastating losses to his army, hence the term pyrrhic victory. Considering the strong association of both chronic kidney disease (CKD) and acute kidney injury (AKI) with adverse clinical outcomes, physicians often perceive any drop in the serum creatinine level as a victory for their patients. In this issue of the journal, Khoury et al. present some intriguing evidence that at least in the context of ST-segment elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention (PCI), this may represent a pyrrhic victory.1 The study by Khoury et al. retrospectively reviewed 2339 consecutive STEMI patients treated with primary PCI at a single tertiary care centre. CKD stage 5 patients (with an estimated glomerular filtration rate <15 mL/min/1.73m2 or receiving renal replacement therapy) were not included in the analysis. The authors stratified the study population into three groups, according to the serum creatinine evolution: (a) post-PCI AKI, defined as a rise in serum creatinine of 0.3 mg/dL or greater within 48 hours of hospital admission; (b) improved renal function, defined as a continuous and gradual decrease in serum creatinine of 0.3 mg/dL or greater in total from admission to discharge; and (c) stable renal function, neither qualifying for post-PCI AKI or improved renal function. Unsurprisingly, patients with post-PCI AKI when compared to stable renal function had worse outcomes, including significantly increased all-cause mortality after a median follow-up of approximately 4 years (27% vs. 5%). Less intuitively clear, patients with improved versus stable renal function also seemed to fare worse as indicated by significantly higher rates of heart failure, arrhythmias, the need for coronary artery bypass grafting, as well as increased 30-day mortality. Although all-cause mortality was not significantly higher at final follow-up (8% vs. 5%), the study was underpowered to assess this and Kaplan-Meier curves seemingly indicate continued separation in favour of stable renal function at the end of follow-up. How do we explain the increased risk of patients with improved renal function in the current study? The authors point out that improved renal function did indicate prehospital AKI. Indeed, in support of this view, patients with improved versus stable renal function had higher serum creatinine levels on admission, but not at discharge, with otherwise no major differences in baseline characteristics (except for the slightly but significantly higher incidence of diabetes). Unfortunately, the lack of baseline serum creatinine values in stable conditions preceding hospital admission precludes conclusive evidence. However, even when considering that improved renal function in the study by Khoury et al. may have reflected the transient occurrence of AKI with an approximately 0.4 mg/dL rise in serum creatinine, the consequences of a nearly doubling risk for heart failure, fivefold increased risk for mechanical ventilation, threefold increased risk for incident ventricular arrhythmia and 3.5-fold increased risk for 30-day mortality seem somewhat out of proportion. The timing of these adverse events with respect to AKI occurrence would have provided insightful information that now remains unclear. If already present on hospital admission or immediately after PCI, the easy conclusion would be that improved renal function was a proxy for successfully treated cardiogenic shock with a large area of myocardium at risk, hence explaining the higher risk for early heart failure, arrhythmias and death. No haemodynamic data or indicators of heart failure severity on admission are provided to support this view. Yet, left ventricular ejection fraction after revascularisation was reportedly similar in patients with improved versus stable renal function. Alternatively, if the majority of adverse events occurred late during the index hospitalisation, after restoration of Renal function in myocardial infarction: does serum creatinine tells the whole story?