Brain Natriuretic Peptide (BNP) as a Biomarker of Myocardial Ischemia-Reperfusion Injury in Cardiac Transplantation

McIlroy, David R.; Wallace, Sophie; Roubos, Nicholas

doi:10.1053/j.jvca.2010.05.008

Cited by 8 publications

(6 citation statements)

References 29 publications

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“…Present study significantly adds to current knowledge on this topic, and, to the best of our knowledge, this is the largest series so far that evaluated the prognostic implications of cTnI release after heart transplant [ 29 – 33 ]. Moreover, it is the first to focus broadly on both morbidity and mortality as well as on the determinants of early troponin release.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, most of published reports focused on the correlation of later troponin release with rejection and subsequent survival [ 30 , 32 – 33 ]. Other studies tried to correlate the pattern of release of these biomarkers with newly introduced markers of ischemic-reperfusion injury in small prospective series [ 29 ]. In the present study, myocardial enzyme leakage clearly emerged as an epiphenomenon of more complicated clinical course.…”

Section: Discussionmentioning

confidence: 99%

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Perioperative Myocardial Injury after Adult Heart Transplant: Determinants and Prognostic Value

et al. 2015

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Background and Aim of the StudyImplications of Cardiac troponin (cTnI) release after cardiac transplantation are still unclear. This study disclosed risk factors and prognostic implication of cTnI early levels in a single centre cohort operated on between January 1999 and December 2010.MethodsData on 362 consecutive recipients (mean age: 47.8±13.7, 20.2% female, 18.2% diabetics, 22.1% with previous cardiac operations, 27.6% hospitalized, 84.9±29.4 ml/min preoperative glomerular filtration rate) were analyzed using multivariable logistic regression modeling. Target outcomes were determinants of troponin release, early graft failure (EGF), acute kidney injury (AKI) and operative death.ResultsMean cTnI release measured 24 hours after transplant was 10.9±11.6 μg/L. Overall hospital mortality was 10.8%, EGF 10.5%, and AKI was 12.2%. cTnI release>10 μg/L proved an independent predictor of EGF (OR 2.2; 95% CI, 1.06–4.6) and AKI (OR 1.031; 95% CI, 1.001-1.064). EGF, in turn, proved a determinant of hospital mortality. Risk factors for cTnI>10 μg/L release were: status 2B (OR 0.35; 95% CI, 0.18-0.69, protective), duration of the ischemic period (OR 1.006; 95% CI, 1.001-1.011), previous cardiac operation (OR 2.9; 95% CI, 1.67-5.0), and left ventricular hypertrophy (OR 3.3; 95% CI, 1.9-5.6).ConclusionsMyocardial enzyme leakage clearly emerged as an epiphenomenon of more complicated clinical course. The complex interplay between surgical procedure features, graft characteristics and recipient end-organ function highlights cTnI release as a risk marker of graft failure and acute kidney injury. The search for optimal myocardial preservation is still an issue.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Perioperative Myocardial Injury after Adult Heart Transplant: Determinants and Prognostic Value

et al. 2015

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“…BNP or NT-proBNP is another easily measureable serum biomarker that is a sensitive indicator of myocardial dysfunction. As with troponin, several authors have reported a significant correlation between elevated serum BNP (or NTproBNP) in the donor and donor heart dysfunction; however, there has been an inconsistent relationship between donor BNP and post-transplant graft function [35][36][37][38].…”

Section: Biomarkers Of Primary Graft Dysfunctionmentioning

confidence: 99%

Primary Graft Dysfunction After Heart Transplantation

et al. 2014

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Primary graft dysfunction (PGD) is a lifethreatening complication of heart transplantation that presents as left, right, or biventricular dysfunction occurring within the first 24 hours of transplant surgery for which there is no identifiable secondary cause. Myocardial injury caused by acute catecholamine toxicity and the release of multiple proinflammatory mediators in the donor, followed by ischaemiareperfusion injury sustained during retrieval, have been considered the predominant pathogenetic processes leading to PGD. Donor, recipient, and procedural factors contribute to the development and severity of the clinical syndrome. The changing donor and recipient characteristics over the last two decades, particularly the increasing donor and recipient age, have led to heightened risk of PGD. PGD is graded from mild to severe depending on the extent of circulatory support that is required to maintain haemodynamic stability and vital organ function. While advances in acute mechanical support devices have improved the outlook for patients with PGD, the rate of mortality remains high for those with severe PGD, reaching 40 %. Potential approaches to preventing or minimising the severity of PGD include optimising donor management, donor heart preservation, and donor/recipient matching.

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“…It has been shown that the timely administration of C-peptide is able to ameliorate and reverse the degrading effects of neuropathy [2,3]. Just as APL1b28 [4] and natriuretic peptides [5,6] can serve as biomarkers for Alzheimer's disease and myocardial ischemia reperfusion injury respectively, it is desirable to monitor C-peptide concentration in the blood to permit timely intervention [7,8].…”

Section: Introductionmentioning

confidence: 99%

Peptide–Peptide Co-Assembly: A Design Strategy for Functional Detection of C-peptide, A Biomarker of Diabetic Neuropathy

Chan

Lim

Jee

et al. 2020

IJMS

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Diabetes-related neuropathy is a debilitating condition that may be averted if it can be detected early. One possible way this can be achieved at low cost is to utilise peptides to detect C-peptide, a biomarker of diabetic neuropathy. This depends on peptide-peptide co-assembly, which is currently in a nascent stage of intense study. Instead, we propose a bead-based triple-overlay combinatorial strategy that can preserve inter-residue information during the screening process for a suitable complementary peptide to co-assemble with C-peptide. The screening process commenced with a pentapeptide general library, which revealed histidine to be an essential residue. Further screening with seven tetrapeptide focused libraries led to a table of self-consistent peptide sequences that included tryptophan and lysine at high frequencies. Three complementary nonapeptides (9mer com-peptides), wpkkhfwgq (Trp-D), kwkkhfwgq (Lys-D), and KWKKHFWGQ (Lys-L) (as a negative control) were picked from this table for co-assembly studies with C-peptide. Attenuated total reflectance Fourier transform infrared (ATR-FTIR) and circular dichroism (CD) spectroscopies were utilized to study inter-peptide interactions and changes in secondary structures respectively. ATR-FTIR studies showed that there is indeed inter-peptide interaction between C-peptide and the tryptophan residues of the 9mer com-peptides. CD studies of unaggregated and colloidal C-peptide with the 9mer com-peptides suggest that the extent of co-assembly of C-peptide with Trp-D is greatest, followed by Lys-D and Lys-L. These results are promising and indicate that the presented strategy is viable for designing and evaluating longer complementary peptides, as well as complementary peptides for co-assembly with other polypeptides of interest and importance. We discuss the possibility of designing complementary peptides to inhibit toxic amyloidosis with this approach.

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Brain Natriuretic Peptide (BNP) as a Biomarker of Myocardial Ischemia-Reperfusion Injury in Cardiac Transplantation

Cited by 8 publications

References 29 publications

Perioperative Myocardial Injury after Adult Heart Transplant: Determinants and Prognostic Value

Perioperative Myocardial Injury after Adult Heart Transplant: Determinants and Prognostic Value

Primary Graft Dysfunction After Heart Transplantation

Peptide–Peptide Co-Assembly: A Design Strategy for Functional Detection of C-peptide, A Biomarker of Diabetic Neuropathy

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