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Article ; Online: Neuregulin-1 signaling in the pathogenesis of chemotherapy-induced heart failure.

Lenneman, Carrie Geisberg

2014 Volume 11, Issue 2, Page(s) 134–138

Abstract: The National Cancer Institute estimates that approximately 13.7 million Americans with a history of cancer were alive on January 1, 2012. With the rising number of cancer survivors, there is an increased focus on how chemotherapy agents modulate the ... ...

Abstract	The National Cancer Institute estimates that approximately 13.7 million Americans with a history of cancer were alive on January 1, 2012. With the rising number of cancer survivors, there is an increased focus on how chemotherapy agents modulate the cardiovascular biology and cause chemotherapy-related heart failure in certain patients. Neuregulin-1 (NRG-1) is an important cardiac growth factor that is essential for normal myocardial development and maintenance. Certain chemotherapy agents perturb the normal NRG-1 signaling in the cardiovascular system and cause cardiac dysfunction and, in some cases, symptomatic heart failure. As researchers have learned the critical importance of NRG-1 within the cardiovascular system, more attention has been focused on the potential use of NRG-1 as biomarker and therapy for the treatment of heart failure. This review will highlight the biology of NRG-1 within the cardiovascular system, its role in chemotherapy-induced heart failure, and the translational potential of NRG-1 as treatment for heart failure.
MeSH term(s)	Antineoplastic Agents/adverse effects ; Biomarkers/metabolism ; Cardiotoxicity/drug therapy ; Cardiotoxicity/physiopathology ; Heart Failure/chemically induced ; Heart Failure/drug therapy ; Heart Failure/physiopathology ; Humans ; Neuregulin-1/metabolism ; Neuregulin-1/physiology ; Neuregulin-1/therapeutic use ; Recombinant Proteins/therapeutic use ; Signal Transduction/drug effects ; Signal Transduction/physiology
Chemical Substances	Antineoplastic Agents ; Biomarkers ; NRG1 protein, human ; Neuregulin-1 ; Recombinant Proteins
Language	English
Publishing date	2014-03-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2151202-4
ISSN	1546-9549 ; 1546-9530
ISSN (online)	1546-9549
ISSN	1546-9530
DOI	10.1007/s11897-014-0193-9
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Zs.A 5936: Show issues

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Article ; Online: Mechanisms of anthracycline cardiotoxicity and strategies to decrease cardiac damage.

Geisberg, Carrie Anna / Sawyer, Douglas B

Current hypertension reports

2010 Volume 12, Issue 6, Page(s) 404–410

Abstract: Anthracyclines are common chemotherapeutic agents used to treat many different types of cancer. Unfortunately, the use of anthracyclines is limited by their cardiotoxic effects, which may become manifest as late as 20 years from initial exposure. Studies ...

Abstract	Anthracyclines are common chemotherapeutic agents used to treat many different types of cancer. Unfortunately, the use of anthracyclines is limited by their cardiotoxic effects, which may become manifest as late as 20 years from initial exposure. Studies in cells and animals suggest that the mechanism of anthracycline-induced cardiotoxicity (AIC) is multifactorial. Anthracyclines induce multiple forms of cellular injury by free radical production. In addition, anthracyclines alter nucleic acid biology by intercalation into DNA and modulate intracellular signaling, leading to cell death and the disruption of homeostatic processes such as sarcomere maintenance. In an effort to decrease AIC, many strategies have been tested, but no specific therapies are universally acknowledged to prevent or treat anthracycline-induced cardiac dysfunction. Newer imaging modalities and cardiac biomarkers may be useful in improving early detection of cardiac injury and dysfunction. As long as there is no cardiac-specific therapy for AIC, evidence suggests that high-risk patients will benefit from prophylactic treatment with neurohormonal blockade by angiotensin-converting enzyme inhibitors and beta-adrenergic receptor blockers.
MeSH term(s)	Adrenergic beta-Antagonists/therapeutic use ; Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; Animals ; Anthracyclines/adverse effects ; Anthracyclines/therapeutic use ; Antibiotics, Antineoplastic/adverse effects ; Antibiotics, Antineoplastic/therapeutic use ; Antineoplastic Protocols ; Cardiotonic Agents/therapeutic use ; Cardiotoxins/adverse effects ; Cardiotoxins/therapeutic use ; Cell Death ; Heart Diseases/chemically induced ; Heart Diseases/metabolism ; Heart Diseases/mortality ; Heart Diseases/physiopathology ; Heart Diseases/therapy ; Humans ; Models, Animal ; Neoplasms/drug therapy ; Oxidative Stress ; Risk Factors ; Sarcomeres/drug effects ; Sarcomeres/metabolism ; Sarcomeres/pathology ; Time
Chemical Substances	Adrenergic beta-Antagonists ; Angiotensin-Converting Enzyme Inhibitors ; Anthracyclines ; Antibiotics, Antineoplastic ; Cardiotonic Agents ; Cardiotoxins
Language	English
Publishing date	2010-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2057367-4
ISSN	1534-3111 ; 1522-6417
ISSN (online)	1534-3111
ISSN	1522-6417
DOI	10.1007/s11906-010-0146-y
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Article ; Online: Cardiac side effects of anticancer treatments: new mechanistic insights.

Geisberg, Carrie / Pentassuglia, Laura / Sawyer, Douglas B

Current heart failure reports

2012 Volume 9, Issue 3, Page(s) 211–218

Abstract: Damage to heart cells leading to heart failure is a known complication of well-established cancer therapies including anthracycline antibiotics and radiation therapy, and the cardiovascular complications of these therapies has been controlled in large ... ...

Abstract	Damage to heart cells leading to heart failure is a known complication of well-established cancer therapies including anthracycline antibiotics and radiation therapy, and the cardiovascular complications of these therapies has been controlled in large part through dose limitations and modifications of delivery methods. Recent research into the cellular and molecular mechanisms for the cardiovascular effects of these therapies may lead to other cardioprotective strategies that improve effectiveness of cancer treatments. Newer cancer therapies that have been developed based upon specifically targeting oncogene signaling also have been associated with heart failure. Rapid development of a detailed understanding of how these agents cause cardiac dysfunction promises to improve outcomes in cancer patients, as well as stimulate concepts of cardiovascular homeostasis that will likely accelerate development of cardiovascular therapies.
MeSH term(s)	Anthracyclines/adverse effects ; Antibiotics, Antineoplastic/adverse effects ; Antibodies, Monoclonal, Humanized/adverse effects ; Antineoplastic Agents/adverse effects ; Benzenesulfonates/adverse effects ; Daunorubicin/adverse effects ; Doxorubicin/adverse effects ; Heart Failure/chemically induced ; Humans ; Indoles/adverse effects ; Myocardial Contraction/drug effects ; Myocytes, Cardiac/drug effects ; Niacinamide/analogs & derivatives ; Phenylurea Compounds ; Pyridines/adverse effects ; Pyrroles/adverse effects ; Sorafenib ; Sunitinib ; Trastuzumab
Chemical Substances	Anthracyclines ; Antibiotics, Antineoplastic ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents ; Benzenesulfonates ; Indoles ; Phenylurea Compounds ; Pyridines ; Pyrroles ; Niacinamide (25X51I8RD4) ; Doxorubicin (80168379AG) ; Sorafenib (9ZOQ3TZI87) ; Trastuzumab (P188ANX8CK) ; Sunitinib (V99T50803M) ; Daunorubicin (ZS7284E0ZP)
Language	English
Publishing date	2012-06-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2151202-4
ISSN	1546-9549 ; 1546-9530
ISSN (online)	1546-9549
ISSN	1546-9530
DOI	10.1007/s11897-012-0098-4
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Article ; Online: Bortezomib-Induced Cardiac Tamponade in a 49-Year-Old Man.

Burkhart, Taylor / Keith, Matthew Cody Lee / Lenneman, Carrie Ann Geisberg / Fernando, Rajeev Ruben

Texas Heart Institute journal

2018 Volume 45, Issue 4, Page(s) 260–263

Abstract: Proteasome inhibitors such as bortezomib and carfilzomib have been used effectively to treat patients who have certain hematologic malignancies. Proteasome activity is elevated in the heart, and potent inhibition results in accumulation of misfolded ... ...

Abstract	Proteasome inhibitors such as bortezomib and carfilzomib have been used effectively to treat patients who have certain hematologic malignancies. Proteasome activity is elevated in the heart, and potent inhibition results in accumulation of misfolded intracellular protein aggregates and apoptosis. Heart failure, conduction disturbances, and premature atherosclerosis have been associated with bortezomib therapy. We describe the case of a 49-year-old man who was taking bortezomib for graft-versus-host disease, when he developed cardiac tamponade and needed emergency pericardiocentesis. At that time, there was no evidence of graft-versus-host disease. To our knowledge, this is the first time that a pericardial effusion without underlying cardiac dysfunction has been reported in relation to bortezomib therapy. The diagnosis of pericardial effusion during bortezomib therapy, the absence of other causative agents-including graft-versus-host disease-and no recurrence of pericardial effusion after discontinuing bortezomib therapy suggest that bortezomib caused our patient's tamponade.
MeSH term(s)	Antineoplastic Agents/adverse effects ; Antineoplastic Agents/therapeutic use ; Bortezomib/adverse effects ; Bortezomib/therapeutic use ; Cardiac Tamponade/chemically induced ; Cardiac Tamponade/diagnosis ; Cardiac Tamponade/surgery ; Echocardiography, Doppler ; Fluoroscopy ; Follow-Up Studies ; Graft vs Host Disease/drug therapy ; Hematopoietic Stem Cell Transplantation/adverse effects ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/therapy ; Male ; Middle Aged ; Pericardiocentesis/methods ; Surgery, Computer-Assisted/methods
Chemical Substances	Antineoplastic Agents ; Bortezomib (69G8BD63PP)
Language	English
Publishing date	2018-08-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	604761-0
ISSN	1526-6702 ; 0730-2347
ISSN (online)	1526-6702
ISSN	0730-2347
DOI	10.14503/THIJ-17-6242
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Zs.A 1452: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Addressing the challenges of cardiorenal syndrome.

Geisberg, Carrie / Butler, Javed

Cleveland Clinic journal of medicine

2006 Volume 73, Issue 5, Page(s) 485–491

Abstract: In heart failure, as the heart gets worse, often so do the kidneys, complicating the treatment of heart failure and worsening the prognosis. This article addresses challenges in the use of diuretics, angiotensin-converting enzyme (ACE) inhibitors, and ... ...

Abstract	In heart failure, as the heart gets worse, often so do the kidneys, complicating the treatment of heart failure and worsening the prognosis. This article addresses challenges in the use of diuretics, angiotensin-converting enzyme (ACE) inhibitors, and other therapies in the cardiorenal syndrome, as well as novel therapies that hold promise, such as arginine vasopressin antagonists, adenosine A1 receptor antagonists, and ultrafiltration.
MeSH term(s)	Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; Diuretics/therapeutic use ; Glomerular Filtration Rate ; Heart Failure/complications ; Heart Failure/physiopathology ; Humans ; Prognosis ; Renal Insufficiency/etiology ; Renal Insufficiency/physiopathology ; Syndrome
Chemical Substances	Angiotensin-Converting Enzyme Inhibitors ; Diuretics
Language	English
Publishing date	2006-05-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	639116-3
ISSN	0891-1150
ISSN	0891-1150
DOI	10.3949/ccjm.73.5.485
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Article ; Online: ERBB signaling attenuates proinflammatory activation of nonclassical monocytes.

Ryzhov, Sergey / Matafonov, Anton / Galindo, Cristi L / Zhang, Qinkun / Tran, Truc-Linh / Lenihan, Daniel J / Lenneman, Carrie Geisberg / Feoktistov, Igor / Sawyer, Douglas B

American journal of physiology. Heart and circulatory physiology

2017 Volume 312, Issue 5, Page(s) H907–H918

Abstract: Immune activation in chronic systolic heart failure (HF) correlates with disease severity and prognosis. Recombinant neuregulin-1 (rNRG-1) is being developed as a possible therapy for HF, based on the activation of ERBB receptors in cardiac cells. Work ... ...

Abstract	Immune activation in chronic systolic heart failure (HF) correlates with disease severity and prognosis. Recombinant neuregulin-1 (rNRG-1) is being developed as a possible therapy for HF, based on the activation of ERBB receptors in cardiac cells. Work in animal models of HF led us to hypothesize that there may be direct effects of NRG-1 on immune system activation and inflammation. We investigated the expression of ERBB receptors and the effect of rNRG-1 isoform glial growth factor 2 (GGF2) in subpopulations of peripheral blood mononuclear cells (PB MNCs) in subjects with HF. We found that human monocytes express both ERBB2 and ERBB3 receptors, with high interindividual variability among subjects. Monocyte surface ERBB3 and TNF-α mRNA expression were inversely correlated in subjects with HF but not in human subjects without HF. GGF2 activation of ERBB signaling ex vivo inhibited LPS-induced TNF-α production, specifically in the CD14
MeSH term(s)	ErbB Receptors/biosynthesis ; ErbB Receptors/drug effects ; ErbB Receptors/genetics ; Female ; Humans ; In Vitro Techniques ; Inflammation/physiopathology ; Macrophage Activation ; Male ; Middle Aged ; Monocytes ; Neuregulin-1/metabolism ; Neuregulin-1/therapeutic use ; Phosphatidylinositol 3-Kinases/metabolism ; Receptor, ErbB-2/biosynthesis ; Receptor, ErbB-2/genetics ; Receptor, ErbB-3/biosynthesis ; Receptor, ErbB-3/genetics ; Recombinant Proteins/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/biosynthesis
Chemical Substances	NRG1 protein, human ; Neuregulin-1 ; Recombinant Proteins ; Tumor Necrosis Factor-alpha ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; EGFR protein, human (EC 2.7.10.1) ; ERBB2 protein, human (EC 2.7.10.1) ; ERBB3 protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; Receptor, ErbB-3 (EC 2.7.10.1)
Language	English
Publishing date	2017-02-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00486.2016
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Article: Blunted hemodynamic response and reduced oxygen delivery with exercise in anemic heart failure patients with systolic dysfunction.

Listerman, Jennifer / Geisberg, Carrie / Nading, Mary A / Goring, Joann / Huang, Robert / Butler, Javed

Congestive heart failure (Greenwich, Conn.)

2007 Volume 13, Issue 2, Page(s) 71–77

Abstract: Anemic heart failure patients with systolic dysfunction are known to have reduced exercise capacity. Whether this is related to poor hemodynamic adaptation to anemia is not known. Peak exercise oxygen consumption (VO2) and hemodynamics at rest and peak ... ...

Abstract	Anemic heart failure patients with systolic dysfunction are known to have reduced exercise capacity. Whether this is related to poor hemodynamic adaptation to anemia is not known. Peak exercise oxygen consumption (VO2) and hemodynamics at rest and peak exercise were assessed among 209 patients and compared among those who were (n=90) and were not (n=119) anemic. Peak VO2 was significantly lower among anemic patients (11.7+/-3.3 mL/min/kg vs 13.4+/-3.1 mL/min/kg; P=.01). At rest, right atrial pressure was higher (10+/-5 mm Hg vs 8+/-4 mm Hg; P=.02) and venous oxygen saturation lower (62%+/-8% vs 58%+/-10%; P<.01) among anemic patients. At peak exercise, anemic patients had a higher wedge pressure (27+/-9 mm Hg vs 24+/-10 mm Hg; P=.04). No significant differences in stroke volume, cardiac index, systemic vascular resistance, or oxygen saturation were noted between the 2 groups. In conclusion, the relative hemodynamic response to exercise among anemic heart failure patients appears blunted and may contribute to worse exercise tolerance.
MeSH term(s)	Adult ; Aged ; Anemia/complications ; Anemia/physiopathology ; Blood Gas Analysis ; Blood Pressure/physiology ; Cardiac Output/physiology ; Case-Control Studies ; Exercise/physiology ; Female ; Heart Failure/complications ; Heart Failure/physiopathology ; Humans ; Male ; Middle Aged ; Oxygen Consumption/physiology
Language	English
Publishing date	2007-03-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	1239105-0
ISSN	1751-7133 ; 1527-5299 ; 1079-7998
ISSN (online)	1751-7133
ISSN	1527-5299 ; 1079-7998
DOI	10.1111/j.1527-5299.2007.05948.x
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Article ; Online: A Phase I, Single Ascending Dose Study of Cimaglermin Alfa (Neuregulin 1β3) in Patients With Systolic Dysfunction and Heart Failure.

Lenihan, Daniel J / Anderson, Sarah A / Lenneman, Carrie Geisberg / Brittain, Evan / Muldowney, James A S / Mendes, Lisa / Zhao, Ping Z / Iaci, Jennifer / Frohwein, Stephen / Zolty, Ronald / Eisen, Andrew / Sawyer, Douglas B / Caggiano, Anthony O

JACC. Basic to translational science

2016 Volume 1, Issue 7, Page(s) 576–586

Abstract: A first-in-human, phase 1, double blind, placebo-controlled, single ascending dose study examined the safety, tolerability, and exploratory efficacy of intravenous infusion of a recombinant growth factor, cimaglermin alfa, in patients with heart failure ... ...

Abstract	A first-in-human, phase 1, double blind, placebo-controlled, single ascending dose study examined the safety, tolerability, and exploratory efficacy of intravenous infusion of a recombinant growth factor, cimaglermin alfa, in patients with heart failure and left ventricular systolic dysfunction (LVSD). In these patients on optimal guideline-directed medical therapy, cimaglermin treatment was generally tolerated except for transient nausea and headache and a dose-limiting toxicity was noted at the highest planned dose. There was a dose-dependent improvement in left ventricular ejection fraction lasting 90 days following infusion. Thus, cimaglermin is a potential therapy to enhance cardiac function in LVSD and warrants further investigation.
Language	English
Publishing date	2016-12-26
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2016.09.005
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Article ; Online: Circulating neuregulin during the transition from stage A to stage B/C heart failure in a breast cancer cohort.

Geisberg, Carrie A / Abdallah, Wissam M / da Silva, Monica / Silverstein, Cheri / Smith, Holly M / Abramson, Vandana / Mayer, Ingrid / Means-Powell, Julie / Freehardt, Darla / White, Brenda / Lenihan, Daniel / Sawyer, Douglas B

Journal of cardiac failure

2012 Volume 19, Issue 1, Page(s) 10–15

Abstract: Background: Breast cancer (BC) treatments can cause heart failure (HF) in a subset of patients. ACC/AHA guidelines classify patients receiving cardiotoxic medications as stage A, a high-risk population for the development of HF. Circulating neuregulin ( ... ...

Abstract	Background: Breast cancer (BC) treatments can cause heart failure (HF) in a subset of patients. ACC/AHA guidelines classify patients receiving cardiotoxic medications as stage A, a high-risk population for the development of HF. Circulating neuregulin (NRG) correlates with outcomes in stage C and D HF. We examined the levels of NRG in a BC cohort receiving cardiotoxic chemotherapy and its relationship with adverse cardiac effects during the transition from stage A to stage B or C HF. Methods and results: In an ongoing prospective study, a planned interim analysis of 78 BC women receiving either anthracycline (AC) or trastuzumab (Tsz) was performed. Biometric data, cardiac risk factors, and NRG levels, were collected before chemotherapy and after completion of AC therapy and/or 3 months into Tsz therapy. Cardiac function was measured by left ventricular ejection fraction (LVEF) by echocardiography at the above time points and longitudinally as standard of care. The interim cohort was predominately white with stage II BC and a median age of 50 years. A reduction of >10 absolute percentage points in LVEF was observed in 21.4% of the cohort, representing a transition from stage A to stage B or C HF. A statistically significant drop in plasma NRG was observed in women treated with AC and/or Tsz (P < .001). Additionally, baseline NRG correlated with the maximal change in LVEF. Conclusions: More than 20% of women experienced cardiac dysfunction, detected by decline in LVEF, and were reclassified as stage B or C HF. Plasma NRG levels were reduced after exposure to cardiotoxic chemotherapy, suggesting a loss in a cardioprotective growth factor. Higher baseline NRG levels were observed in those with the greatest decline in LVEF, supporting the continued investigation of NRG as a potential prognostic marker in early-stage HF.
MeSH term(s)	Adult ; Aged ; Anthracyclines/adverse effects ; Anthracyclines/therapeutic use ; Antibodies, Monoclonal, Humanized/adverse effects ; Antibodies, Monoclonal, Humanized/therapeutic use ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/adverse effects ; Biomarkers/blood ; Breast Neoplasms/drug therapy ; Breast Neoplasms/mortality ; Breast Neoplasms/pathology ; Cohort Studies ; Disease-Free Survival ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Female ; Heart Failure/blood ; Heart Failure/chemically induced ; Heart Failure/mortality ; Heart Failure/pathology ; Humans ; Middle Aged ; Neoplasm Invasiveness/pathology ; Neoplasm Staging ; Neuregulins/blood ; Neuregulins/metabolism ; Predictive Value of Tests ; Prognosis ; Prospective Studies ; Risk Assessment ; Severity of Illness Index ; Statistics, Nonparametric ; Stroke Volume/drug effects ; Survival Rate ; Trastuzumab
Chemical Substances	Anthracyclines ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents ; Biomarkers ; Neuregulins ; Trastuzumab (P188ANX8CK)
Language	English
Publishing date	2012-12-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1281194-4
ISSN	1532-8414 ; 1071-9164
ISSN (online)	1532-8414
ISSN	1071-9164
DOI	10.1016/j.cardfail.2012.11.006
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Article ; Online: Circulating neuregulin-1β levels vary according to the angiographic severity of coronary artery disease and ischemia.

Geisberg, Carrie Anna / Wang, Guisong / Safa, Radwan N / Smith, Holly M / Anderson, Brent / Peng, Xu-Yang / Veerkamp, Brian / Zhao, David X / Blakemore, Dana / Yu, Chang / Sawyer, Douglas B

Coronary artery disease

2011 Volume 22, Issue 8, Page(s) 577–582

Abstract: Background: Coronary artery disease (CAD) is the leading killer in the United States. Patients with severe CAD and ischemia have worse prognosis. Therefore expansion of biomarker research, to identify at-risk individuals and explain the complex biology ... ...

Abstract	Background: Coronary artery disease (CAD) is the leading killer in the United States. Patients with severe CAD and ischemia have worse prognosis. Therefore expansion of biomarker research, to identify at-risk individuals and explain the complex biology between cardiovascular growth factors and atherosclerosis is needed. Neuregulin-1β (NRG-1β) is a myocardial stress activated growth and survival factor released from endocardial and endothelial cells. NRG-1β is essential for cardiovascular development and a regulator of angiogenesis. We postulated that plasma and serum levels of NRG-1β would vary in relation to CAD severity and the presence of stress-induced ischemia. Methods: We measured serum and plasma levels of NRG-1β and vascular endothelial growth factor (VEGF) in 60 patients undergoing cardiac catheterization. CAD severity was calculated from angiographic results using a modified Duke jeopardy score. Results: Serum NRG-1β (sNRG-1β), plasma NRG-1β (pNRG-1β), serum VEGF, and plasma VEGF were detectable in the majority of patients. The pNRG-1β levels were approximately two-fold higher than sNRG-1β. Both sNRG-1β and pNRG-1β correlated inversely with CAD severity. pNRG-1β levels were statistically higher in patients with stress-induced ischemia denoted by a positive myocardial perfusion imaging study that correlated with angiographic findings (P=0.02). Conclusion: Both sNRG-1β and pNRG-1β correlated inversely with angiographic severity of CAD. pNRG-1β levels were two-fold higher than serum and were higher in patients with stress-induced ischemia. Therefore we conclude that plasma is the optimal source for the further exploration of the biological significance of NRG-1β as a biomarker of CAD severity and ischemia.
MeSH term(s)	Adult ; Aged ; Biomarkers/blood ; Chi-Square Distribution ; Coronary Angiography ; Coronary Artery Disease/blood ; Coronary Artery Disease/diagnostic imaging ; Female ; Humans ; Male ; Middle Aged ; Myocardial Ischemia/blood ; Myocardial Ischemia/diagnostic imaging ; Neuregulin-1/blood ; Predictive Value of Tests ; Retrospective Studies ; Severity of Illness Index ; Tennessee ; Vascular Endothelial Growth Factor A/blood
Chemical Substances	Biomarkers ; Neuregulin-1 ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; neuregulin beta
Language	English
Publishing date	2011-10-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1047268-x
ISSN	1473-5830 ; 0954-6928
ISSN (online)	1473-5830
ISSN	0954-6928
DOI	10.1097/MCA.0b013e32834d3346
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