Predicting acute kidney injury in post-operative hypertrophic cardiomyopathy myectomy patients and its relation to the phenotype

IntroductionHypertrophic obstructive cardiomyopathy (HOCM) is a disease characterised by left ventricular hypertrophy and outflow tract obstruction (LVOTO). Symptomatic HOCM can be treated with surgical septal myectomy. Prior research has identified that cardiac surgery-associated acute kidney injury (CSA-AKI) is a common complication after cardiac surgery, associated with increased morbidity and mortality. There is limited information on the development of CSA-AKI after myectomy. Furthermore, the ‘acute kidney injury following cardiac surgery’ (AKICS) score, developed for patients undergoing coronary artery bypass grafting (CABG), has not been tested in myectomy patients. Therefore, the objectives are to (i) evaluate the prevalence of CSA-AKI in myectomy patients, (ii) identify surgical factors which may lead to CSA-AKI, and (iii) identify factors related to the phenotype which may contribute to CSA-AKI.MethodsCSA-AKI was categorized according to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines. The patients were assessed based on their cardiac phenotype, and relevant intraoperative variables were examined to identify concomitant perioperative risk factors that might contribute to CSA-AKI development. Subsequently, multivariable logistic regression was employed to analyse significant results. A receiver operating characteristic curve (ROC) was used to evaluate the discriminative capacity of those significant findingsResultsPerioperative clinical data was available for 242 myectomy patients from a single centre between 2005-2022. A majority of HOCM patients were sarcomere-negative (69%). CSA-AKI developed in 45% of patients (55% KDIGO stage 1, 45% stage 2). The AKICS score was significantly higher in the CSA-AKI group as opposed to the non-CSA-AKI group (p=0.02), with an effect size (h2) of 0.022. Genotype and cardiac parameters such as intraventricular septal thickness or LVOTO severity did not predict CSA-AKI development, neither did the operation duration or intra-operative blood loss. Arterial hypertension (34% in non-CSA-AKI vs. 39% in CSA-AKI, p=0.04), coronary artery disease (5% vs. 14%, p=0.02) and the use of beta blockers (70% vs. 87%, p=0.001) were more prevalent in the CSA-AKI cohort. Multivariable logistic regression was used to investigate the association between beta blockers and the incidence of CSA-AKI. This regression revealed a significant model (X2(12)=34.521, p<0.001), with a correct classification rate of 67%, explaining 22% (Nagelkerke R2) of the variance in CSA-AKI (Table 1). Interestingly, while beta blocker use was not found to be an independent predictor of CSA-AKI as shown in table 1, its use in addition to the other covariates in an ROC analysis revealed moderate discriminatory power with an area under the curve of 0.702 (standard error: 0.035, p<0.0001) (Figure 1).DiscussionCSA-AKI occurred in 45% of patients after myectomy, but was transient and kidney function recovered in all patients. Even though the AKICS score was significantly higher in the CSA-AKI group, the effect size was very small, resulting in negligible discriminatory power. The sole use of beta-blockers was not related to the development of CSA-AKI, however, the model built did have a moderate discriminatory power. Further research is warranted to investigate the mechanisms and possible causal effects of CSA-AKI in this cohort, as it is associated with increased morbidity and mortality.