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N-Terminal Pro-Brain Natriuretic Peptide and Angiotensin-Converting Enzyme-2 Levels and Their Association With Postoperative Cardiac Complications After Emergency Orthopedic Surgery

https://doi.org/10.1016/j.amjcard.2011.12.032Get rights and content

The prognostic usefulness of the cardiac biomarkers N-terminal pro-brain natriuretic peptide (NT-proBNP) and angiotensin-converting enzyme 2 (ACE-2), in predicting adverse cardiac outcomes after orthopedic surgery is not well studied. The aim of our study was to determine the usefulness of perioperative NT-proBNP and ACE-2 for predicting cardiac events after emergency orthopedic surgery. The perioperative NT-proBNP and ACE-2 levels were determined in 187 consecutive patients aged >60 years who underwent orthopedic surgery with 1 year of follow-up for any cardiac complications (defined as acute myocardial infarction, congestive cardiac failure, atrial fibrillation, or major arrhythmia) and death. Of the 187 patients, 20 (10.7%) sustained an in-hospital postoperative cardiac complication. The total all-cause in-hospital and 1-year mortality rate was 1.6% (3 of 187) and 8.6% (16 of 187), respectively. The median preoperative and postoperative NT-proBNP level was greater in patients who sustained an in-hospital cardiac event than in those who had not (386 vs 2,273 pg/ml, p <0.001, and 605 vs 4,316 pg/ml, p <0.001, respectively). Similarly, the postoperative median ACE-2 levels were significantly greater in the patients with an in-hospital cardiac event than in those without (25.3 vs 39.5 pmol/ml/min, p = 0.012). A preoperative NT-proBNP level of ≥741 pg/ml (odds ratio 4.5, 95% confidence interval 1.3 to 15.2, p = 0.017), postoperative troponin elevation (odds ratio 4.9, 95% confidence interval 1.3 to 18.9, p = 0.022), and number of co-morbidities (odds ratio 1.8, 95% confidence interval 1.2 to 2.8, p = 0.009) independently predicted in-hospital cardiac complications on multivariate analysis. The pre- and postoperative NT-proBNP level independently predicted 1-year cardiovascular complications but not the ACE-2 levels. In conclusion, elevated perioperative NT-proBNP predicted in-hospital and 1-year cardiac events in an emergency orthopedic population but the ACE-2 levels did not, which requires additional study for validation.

Section snippets

Methods

The present study was performed in conjunction with a randomized controlled trial randomizing patients who sustained a troponin elevation to usual (standard) care or cardiology care (Australian New Zealand Clinical Trials Registry trial number ACTRN12608000165381). Ethics approval was given by the Northern Hospital Human Research and Ethics Committee, and patients were consecutively recruited from 2008 to 2009.

The patients were recruited from the orthopedic-geriatric unit at Northern Hospital

Results

A total of 383 patients were screened for the present study, and 187 eligible patients were included. The reason for exclusion for most patients was receiving high-level care, undergoing elective surgery, terminal illness, or coexisting severe dementia. Fifteen eligible patients declined involvement in the study. Most patients had preoperative blood samples stored for NT-proBNP analysis (161 [86.1%] of 187). Similarly, most patients had postoperative blood samples available for postoperative

Discussion

The present study found that perioperative NT-proBNP predicted in-hospital and 1-year cardiac events in patients undergoing emergency orthopedic surgery. A preoperative NT-proBNP level of ≥741 pg/ml and postoperative NT-proBNP level of ≥1,064 pg/ml were the optimal cutoff points predicting in-hospital cardiac events using ROC curve analysis. These results are similar to our other observational study of NT-proBNP that recruited patients undergoing lower limb emergency surgery.4 The AUC cutoff

Acknowledgments

We thank the Austin Pathology nurses and pathology staff at The Northern Hospital (Epping, Victoria, Australia), Beckman Coulter (Brea, California), and Austin Pathology (Epping, Victoria, Australia) for complimentary testing of troponin I.

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This study was sponsored by a Cardiovascular Lipid grant 2009 from Pfizer, Australia (West Ryde, Australia). Dr. Chong is a recipient of a National Health and Medical Research Council (Canberra, ACT, Australia) postgraduate research scholarship and has received research stipends from the University of Melbourne (Melbourne, Victoria, Australia) and the Northern Clinical Research Centre, Northern Health (Epping, Victoria, Australia).

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