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Correspondence Letters Regarding Article by Bibbons-Domingo et al, “B-Type Natriuretic Peptide and Ischemia in Patients With Stable Coronary Disease: Data From the Heart and Soul Study” 1. Bibbins-Domingo K, Ansari M, Schiller NB, et al. B-type natriuretic peptide and ischemia in patients with stable coronary disease: data from the Heart and Soul study. Circulation. 2003;108:2987–2992. 2. Gill JS, Prasad K, Stewart JT, et al. Acute changes in atrial natriuretic peptide, insulin-like growth factor-1, and lactate levels during left anterior descending coronary artery angioplasty. Am Heart J. 1995;130:717–722. 3. Malatino LS, Leonardi C, Stancanelli B, et al. Transient myocardial ischemia stimulates atrial natriuretic factor release. Am Heart J. 1992; 123:693– 698. 4. Prachar H, Ogris E, Dittel M, et al. Rapid changes of atrial natriuretic peptide concentration during percutaneous transluminal coronary angioplasty. Am Heart J. 1991;122:157–163. 5. Nishikimi T, Mori Y, Ishimura K, et al. Association of plasma atrial natriuretic peptide, N-terminal proatrial natriuretic peptide, and brain natriuretic peptide levels with coronary artery stenosis in patients with normal left ventricular systolic function. Am J Med. 2004;116:517-523. The following correspondence pertains to an original article published in 2003 by Bibbons-Domingo et al (Circulation. 2003;108:2987–2992). The first letter, by Nishikimi et al, was originally published in the June 29, 2004, issue of Circulation. It is reprinted here for readers’ convenience. Subsequently, a letter was received from Nielsen and Goetze, published below. A final response from Nishikimi et al follows the Nielsen/Goetze letter. Downloaded from http://circ.ahajournals.org/ by guest on June 12, 2017 To the Editor: We read with great interest the recent article by BibbinsDomingo et al1 on plasma brain natriuretic peptide (BNP) in outpatients with stable coronary disease. They concluded that elevated levels of BNP are independently associated with inducible ischemia in outpatients with stable coronary disease, particularly among those who have a history of myocardial infarction. Previous studies have demonstrated that transient myocardial ischemia stimulates the secretion of atrial natriuretic peptide (ANP) and N-terminal ProANP (N-ANP); because of its longer half-life, N-ANP may be a better marker than ANP for the detection of high-grade coronary artery stenosis.2– 4 However, whether plasma BNP levels are increased in patients with coronary artery stenosis who have normal left ventricular function remains unknown. To examine whether coronary artery stenosis affects plasma ANP, N-ANP, and BNP levels, we recently measured these peptide levels in 104 patients with normal left ventricular systolic function who had a suspected diagnosis of angina pectoris.5 Plasma levels of all 3 of these natriuretic peptides were higher in patients with coronary artery stenosis (major coronary artery stenosis ⬎75%) (n⫽65) than in those without stenosis (n⫽39), whereas hemodynamic variables were similar. Multiple logistic regression analysis revealed that N-ANP (per 100 fmol/mL increase; odds ratio⫽1.9 [95% CI⫽1.2 to 2.6], P⬍0.01), but not ANP (per 10 pg/mL increase; odds ratio⫽0.9 [95% CI⫽0.5 to 1.2], P⫽0.41) or BNP (per 10 pg/mL increase; odds ratio⫽1.1 [95% CI⫽0.8 to 1.4], P⫽0.73), was independently associated with coronary artery stenosis after adjusting for clinical and demographic variables. Furthermore, we measured these natriuretic peptides before and 3 to 6 months after percutaneous coronary intervention in patients with myocardial infarction of recent onset (n⫽58). Plasma levels of ANP, N-ANP, and BNP significantly decreased in patients without restenosis (n⫽46) (ANP, 91⫾15 to 39⫾7 pg/mL; BNP, 134⫾28.9 to 41⫾9 pg/mL; N-ANP, 688⫾81 to 407⫾52 fmol/mL; all P⬍0.05). In contrast, these natriuretic peptide levels did not change after coronary intervention in patients with restenosis (n⫽12) (ANP, 57⫾19 to 50⫾20; BNP, 102⫾35 to 57⫾13; N-ANP, 567⫾178 to 508⫾126; all NS). Our results support the findings of Bibbins-Domingo et al1; however, we propose that N-ANP may be more useful for the discrimination of clinically significant coronary artery stenosis than BNP because of its different sites of production, mechanisms of release, and metabolic characteristics. To the Editor: We read the correspondence1 about the article by BibbinsDomingo et al2 with great interest. The report by BibbinsDomingo et al2 demonstrated elevated plasma concentrations of B-type natriuretic peptide (BNP) associated with inducible ischemia in patients with stable coronary artery disease. In contrast, Nishikimi and Matsuoka1 suggested that N-terminal proANP (atrial natriuretic peptide) might be a more sensitive plasma marker of stable coronary artery disease than are ANP and BNP. We recently measured the plasma concentrations of BNP as well as its biosynthetic precursor, proBNP, in patients with coronary artery disease and normal left ventricular systolic function.3 Both BNP and proBNP were markedly elevated (5and 10-fold, respectively) in those patients as compared with individuals without coronary artery disease. Moreover, the BNP and proBNP plasma concentrations were closely associated. Interestingly, within a group of patients undergoing coronary artery bypass surgery, the extent of elevation of both plasma BNP and proBNP concentrations in each patient was positively associated with the ventricular BNP mRNA content.3 These data suggest that both BNP and proBNP are sensitive markers of chronic cardiac ischemia and that the elevated plasma concentrations reflect an increased BNP gene transcription. In studies of pigs, we recently found that even acute cardiac hypoxia induces BNP gene expression in the ventricular myocardium and an increase of the plasma proBNP concentration.4 Moreover, only proBNP (not BNP) was rapidly released from ventricular myocytes when subjected to hypoxia in vitro.4 These experimental data are in accord with another recent clinical observation that coronary arteriography results in a rapid but transient rise in the plasma proBNP but not BNP concentrations.5 We suggest that plasma measurement of both BNP and proBNP is useful in detecting chronic ischemia associated with coronary artery disease, whereas proBNP may be a more sensitive marker of acute cardiac ischemia. Lars B. Nielsen, MD, PhD, DMSc Jens P. Goetze, MD Department of Clinical Biochemistry Rigshospitalet, University of Copenhagen Copenhagen, Denmark 1. Nishikimi T, Matsuoka H. Are plasma levels of atrial natriuretic peptide, N-terminal ProANP, and brain natriuretic peptide affected by the presence of coronary artery disease? Circulation. 2004;109:e331. 2. Bibbins-Domingo K, Ansari M, Schiller NB, Massie B, Whooley MA. B-type natriuretic peptide and ischemia in patients with stable coronary disease: data from the Heart and Soul study. Circulation. 2003;108: 2987–2992. 3. Goetze JP, Christoffersen C, Perko M, Arendrup H, Rehfeld JF, Kastrup J, Nielsen LB. Increased cardiac BNP expression associated with myocardial ischemia. FASEB J. 2003;17:1105–1107. Toshio Nishikimi, MD, PhD Hiroaki Matsuoka, MD, PhD Department of Hypertension and Cardiorenal Medicine Dokkyo University Medical School Mibu, Tochigi, Japan e15 16 Correspondence 4. Goetze JP, Gore A, Møller CH, Steinbrüchel DA, Rehfeld JF, Nielsen LB. Acute myocardial hypoxia increases BNP gene expression. FASEB J. 2004;18:1928 –1930. 5. Goetze JP, Yongzhong W, Rehfeld JF, Jorgensen E, Kastrup J. Coronary angiography transiently increases plasma pro-B-type natriuretic peptide. Eur Heart J. 2004;25:759 –764. Response Downloaded from http://circ.ahajournals.org/ by guest on June 12, 2017 We thank Drs Nielsen and Goetze for their interest in our recently published correspondence.1 In our study, we measured levels of N-terminal proatrial natriuretic peptide (N-ANP), atrial natriuretic peptide (ANP), and brain natriuretic peptide (BNP) in patients with normal left ventricular function (ejection fraction ⱖ60%) who were suspected of having coronary artery disease (CAD).1,2 Our main objective was to determine whether coronary artery stenosis affects plasma natriuretic peptide levels. Our findings suggested that N-ANP is associated with the presence of coronary artery stenosis in patients with normal left ventricular systolic function because transient myocardial ischemia stimulates the secretion of ANP and N-ANP3 and increased plasma N-ANP levels may last for a longer time than ANP because the former has a longer half-life. Goetze et al4 showed that plasma BNP and proBNP levels are higher than controls in patients who have CAD with normal systolic function. Although left ventricular ejection fraction (LVEF) was similar in the CAD and the control groups in their study, the CAD group included patients with an LVEF of ⱕ50 (5 of 13 patients undergoing CABG and 5 of 10 undergoing percutaneous coronary intervention). The figures seem to indicate that patients with good systolic function (LVEF ⱖ60%) had normal BNP levels and low BNP mRNA levels. Thus, plasma BNP and proBNP levels may increase in patients with minimal degrees of impaired systolic function, wall motion abnormality, or both. In these patients, hypoxia may be an important stimulus for BNP mRNA expression, as Goetze et al suggest. Thus, ANP, N-ANP, BNP, and proBNP all are useful biochemical markers for cardiovascular diseases, including CAD, but their clinical implications differ slightly because they have different sites of production, mechanisms of release, and metabolic characteristics. Finally, we would like to comment on the plasma BNP levels measured by Goetze et al4 using a Shionoria BNP kit (Shionogi Inc). This kit uses 2 monoclonal antibodies, which recognize the ring structure and carboxyterminal sequence. Therefore, BNP levels measured with this kit indicate the sum of BNP (77–108) plus proBNP(1–108,) not BNP (77–108) alone. Toshio Nishikimi, MD, PhD Hiroaki Matsuoka, MD, PhD Department of Hypertension and Cardiorenal Medicine Dokkyo University School of Medicine Tochigi, Japan 1. Nishikimi T, Matsuoka H. Are plasma levels of atrial natriuretic peptide, N-terminal ProANP, and brain natriuretic peptide affected by the presence of coronary artery disease? Circulation. 2004;109:e331. 2. Nishikimi T, Mori Y, Ishimura K, Tadokoro K, Yagi H, Yabe A, Horinaka S, Matsuoka H. Association of plasma atrial natriuretic peptide, N-terminal proatrial natriuretic peptide, and brain natriuretic peptide levels with coronary artery stenosis in patients with normal left ventricular systolic function. Am J Med. 2004;116:517–523. 3. Malatino LS, Leonardi C, Stancanelli B, Polizzi G, Grassi R, Tamburino C, Tamburino G. Transient myocardial ischemia stimulates atrial natriuretic factor release. Am Heart J. 1992;123:693– 698. 4. Goetze JP, Christoffersen C, Perko M, Arendrup H, Rehfeld JF, Kastrup J, Nielsen LB. Increased cardiac BNP expression associated with myocardial ischemia. FASEB J. 2003;17:1105–1107. Letters Regarding Article by Bibbons-Domingo et al, ''B-Type Natriuretic Peptide and Ischemia in Patients With Stable Coronary Disease: Data From the Heart and Soul Study'' Toshio Nishikimi and Hiroaki Matsuoka Downloaded from http://circ.ahajournals.org/ by guest on June 12, 2017 Circulation. 2005;111:e15 doi: 10.1161/01.CIR.0000152484.15271.A8 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2005 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/111/2/e15.1 Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Circulation is online at: http://circ.ahajournals.org//subscriptions/