Risk of contrast-induced acute kidney injury in ST-elevation myocardial infarction patients undergoing multi-vessel intervention-meta-analysis of randomized trials and risk prediction modeling study using observational data.

OBJECTIVES: Ascertaining risk of contrast induced acute kidney injury (CI-AKI) in ST-segment elevation myocardial infarction (STEMI) patients undergoing multi-vessel percutaneous coronary intervention (MV-PCI). BACKGROUND: Complete revascularization may improve outcomes in STEMI patients with multi-vessel disease. However, a practice of MV-PCI may be associated with a higher risk of CI-AKI. We aimed to evaluate the risk of CI-AKI in patients with STEMI and MV-PCI and examine the accuracy of a validated risk score. METHODS: We searched PubMed, Cochrane Library, EMBASE, EBSCO, Web of Science, and CINAHL databases from inception through August 31, 2016 for randomized studies comparing CI-AKI rates with MV-PCI and infarct-related artery (IRA) only PCI during index hospitalization. A random effects model was used to estimate the risk ratio (RR) and respective 95% confidence intervals (CI). We queried the Nationwide Inpatient Sample (NIS) to assess the ability of the Mehran risk score to accurately predict the incidence of CI-AKI in patients undergoing MV-PCI. RESULTS: Four randomized studies (N = 1,602) were included in the final analysis. The risk of CI-AKI was low and no difference was observed with MV-PCI (1.45%) compared with IRA-only (1.94%) (RR 0.73, 95% CI 0.34-1.57; P = 0.57). From 2009 to 2012, excluding shock, there were 11,454 MV-PCI for STEMI patients in the NIS. The Mehran risk score accurately discriminated 78% of the patients who developed CI-AKI in this cohort (c-statistic of 0.78, P = 0.002). CONCLUSIONS: MV-PCI in STEMI is not associated with a higher risk of CI-AKI and the Mehran risk score can identify patients at higher risk for this complication. © 2017 Wiley Periodicals, Inc.

The National Cardiovascular Data Registry Data Quality Program 2020: JACC State-of-the-Art Review.

The National Cardiovascular Data Registry is a group of registries maintained by the American College of Cardiology Foundation. These registries are used by a diverse constituency to improve the quality and outcomes of cardiovascular care, to assess the safety and effectiveness of new therapies, and for research. To achieve these goals, registry data must be complete and reliable. In this article, we review the process of National Cardiovascular Data Registry data collection, assess data completeness and integrity, and report on the current state of the data. Registry data are complete. Accuracy is very good but variable, and there is room for improvement. Knowledge of the quality of data is essential to ensuring its appropriate use.

Calpain inhibition improves collateral-dependent perfusion in a hypercholesterolemic swine model of chronic myocardial ischemia.

PURPOSE: Calpain overexpression is implicated in aberrant angiogenesis. We hypothesized that calpain inhibition (MDL28170) would improve collateral perfusion in a swine model with hypercholesterolemia and chronic myocardial ischemia. METHODS: Yorkshire swine fed a high cholesterol diet for 4 weeks underwent surgical placement of an ameroid constrictor to their left circumflex coronary artery. Three weeks later, animals received no drug, high cholesterol control group (n = 8); low-dose calpain inhibition (0.12 mg/kg; n = 9); or high-dose calpain inhibition (0.25 mg/kg; n = 8). The heart was harvested after 5 weeks. RESULTS: Myocardial perfusion in ischemic myocardium significantly improved with high-dose calpain inhibition at rest and with demand pacing (P = .016 and .011). Endothelium-dependent microvessel relaxation was significantly improved with low-dose calpain inhibition (P = .001). There was a significant increase in capillary density, with low-dose calpain inhibition and high-dose calpain inhibition (P = .01 and .01), and arteriolar density with low-dose calpain inhibition (P = .001). Calpain inhibition significantly increased several proangiogenic proteins, including vascular endothelial growth factor (P = .02), vascular endothelial growth factor receptor 1 (P = .003), vascular endothelial growth factor receptor 2 (P = .003), and talin, a microvascular structural protein (P = .0002). There was a slight increase in proteins implicated in endothelial-dependent (nitric oxide mediated) relaxation, including extracellular signal-regulated kinase, phosphorylated extracellular signal-regulated kinase, and inducible nitric oxide synthase with calpain inhibition. CONCLUSIONS: In the setting of hypercholesterolemia, calpain inhibition improved perfusion, with a trend toward increased collateralization on angiography and increased capillary and arteriolar densities in ischemic myocardium. Calpain inhibition also improved endothelium-dependent microvessel relaxation and increased expression of proteins implicated in angiogenesis and vasodilatation.