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      Plasma ProBNP Is Not a Specific Marker for Transient Myocardial Ischemia

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          Abstract

          Background

          Plasma proBNP levels are increased in patients with acute myocardial infarction. Previous studies have shown conflicting data on the effect of transient myocardial ischemia on plasma BNP levels. We designed the current study to examine plasma proBNP levels in patients with transient myocardial ischemia during a percutaneous coronary intervention (PCI). This study was to study plasma proBNP as a marker of transient myocardial ischemia.

          Methods

          We enrolled 49 consecutive patients with a history of angina or abnormal stress test who presented for cardiac catheterization. We obtained plasma proBNP levels in all patients at 1) arterial access (proBNP-1), 2) the end of the procedure (proBNP-2) and 3) 4 hours after procedure (proBNP-3). Hotelling’s T-squared test was used to evaluate the equality of means. Log transforms of proBNP were used to impart data normality.

          Results

          Twenty-two patients underwent diagnostic catheterization (DCA group) and 27 underwent PCI (PCI group). Both groups had normal left ventricular function and a baseline creatinine < 2 mg/dL. Baseline log (proBNP) was 4.7 + 0.99 (units) and rose significantly at 4 hours in both groups (P < 0.02), with no difference in rate of change.

          Conclusions

          Plasma proBNP was increased in both DCA and PCI groups which limits its utility to identify transient myocardial ischemia. The etiology of increase in proBNP in both groups is speculative and may be related to injection of radiographic contrast media into the coronary artery which leads to microcirculatory impairment resulting in myocardial tissue hypoxia and transient increase in left ventricular pressure; however, further evaluation is required.

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          Most cited references39

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          Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure.

          B-type natriuretic peptide is released from the cardiac ventricles in response to increased wall tension. We conducted a prospective study of 1586 patients who came to the emergency department with acute dyspnea and whose B-type natriuretic peptide was measured with a bedside assay. The clinical diagnosis of congestive heart failure was adjudicated by two independent cardiologists, who were blinded to the results of the B-type natriuretic peptide assay. The final diagnosis was dyspnea due to congestive heart failure in 744 patients (47 percent), dyspnea due to noncardiac causes in 72 patients with a history of left ventricular dysfunction (5 percent), and no finding of congestive heart failure in 770 patients (49 percent). B-type natriuretic peptide levels by themselves were more accurate than any historical or physical findings or laboratory values in identifying congestive heart failure as the cause of dyspnea. The diagnostic accuracy of B-type natriuretic peptide at a cutoff of 100 pg per milliliter was 83.4 percent. The negative predictive value of B-type natriuretic peptide at levels of less than 50 pg per milliliter was 96 percent. In multiple logistic-regression analysis, measurements of B-type natriuretic peptide added significant independent predictive power to other clinical variables in models predicting which patients had congestive heart failure. Used in conjunction with other clinical information, rapid measurement of B-type natriuretic peptide is useful in establishing or excluding the diagnosis of congestive heart failure in patients with acute dyspnea. Copyright 2002 Massachusetts Medical Society.
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            Natriuretic peptides.

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              The N-terminal Pro-BNP investigation of dyspnea in the emergency department (PRIDE) study.

              The utility of aminoterminal pro-brain natriuretic peptide (NT-proBNP) testing in the emergency department to rule out acute congestive heart failure (CHF) and the optimal cutpoints for this use are not established. We conducted a prospective study of 600 patients who presented in the emergency department with dyspnea. The clinical diagnosis of acute CHF was determined by study physicians who were blinded to NT-proBNP results. The primary end point was a comparison of NT-proBNP results with the clinical assessment of the managing physician for identifying acute CHF. The median NT-proBNP level among 209 patients (35%) who had acute CHF was 4,054 versus 131 pg/ml among 390 patients (65%) who did not (p 450 pg/ml for patients 900 pg/ml for patients >or=50 years of age were highly sensitive and specific for the diagnosis of acute CHF (p <0.001). An NT-proBNP level <300 pg/ml was optimal for ruling out acute CHF, with a negative predictive value of 99%. Increased NT-proBNP was the strongest independent predictor of a final diagnosis of acute CHF (odds ratio 44, 95% confidence interval 21.0 to 91.0, p <0.0001). NT-proBNP testing alone was superior to clinical judgment alone for diagnosing acute CHF (p = 0.006); NT-proBNP plus clinical judgment was superior to NT-proBNP or clinical judgment alone. NT-proBNP measurement is a valuable addition to standard clinical assessment for the identification and exclusion of acute CHF in the emergency department setting.
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                Author and article information

                Journal
                J Clin Med Res
                J Clin Med Res
                Elmer Press
                Journal of Clinical Medicine Research
                Elmer Press
                1918-3003
                1918-3011
                July 2015
                08 May 2015
                : 7
                : 7
                : 506-510
                Affiliations
                [a ]Department of Cardiology, Baystate Medical Center, Tufts University School of Medicine, Springfield, MA, USA
                [b ]Department of Medicine, Baystate Medical Center, Tufts University School of Medicine, Springfield, MA, USA
                Author notes
                [c ]Corresponding Author: Khawar Maqsood, Department of Cardiology, Baystate Medical Center, Tufts University School of Medicine, 759 Chestnut Street, Springfield, MA 01199, USA. Email: dockmaq@ 123456gmail.com
                Article
                10.14740/jocmr2024w
                4432891
                26015814
                8e8124c8-ed45-4546-952d-ae75a7f9c5f1
                Copyright 2015, Maqsood et al.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 06 November 2014
                Categories
                Original Article

                Medicine
                probnp,acute myocardial ischemia
                Medicine
                probnp, acute myocardial ischemia

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