Corin as novel biomarker for myocardial infarction

Feistritzer, Hans‐Josef; Metzler, Bernhard

doi:10.21037/atm.2016.08.17

Cited by 4 publications

(3 citation statements)

References 14 publications

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“…However, there are discrepancies among clinical reports of circulating corin levels post-MI [ 11 – 14 ]. This may be due to differences among the studies in sample collection times from patients after hospital admission, as well additional variation among patients in the duration time of onset of ischemia and medical care [ 29 ]. Corin levels were measured in plasma [ 11 , 14 , 15 ] and serum [ 12 , 13 ] in different studies.…”

Section: Discussionmentioning

confidence: 99%

Increases in plasma corin levels following experimental myocardial infarction reflect the severity of ischemic injury

et al. 2018

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Following acute myocardial infarction, clinical studies show alterations in the blood levels of corin, a cardiac-selective activator of the natriuretic peptides pro-atrial natriuretic peptide (pro-ANP) and pro-B-type natriuretic peptide (pro-BNP). However, the temporal changes in circulating and cardiac corin levels and their relationships to the severity of myocardial infarction have not been studied. The main objective of this study was to examine the relationship between cardiac and circulating corin levels and their association with cardiac systolic function and infarct size during the early phase of acute myocardial infarction (<72 h) in a translationally relevant induced coronary ligation mouse model. This acute phase timeline was chosen to correlate with the clinical practice within which blood samples are collected from myocardial infarction patients. Heart and plasma samples were examined at 3, 24, and 72 hours post acute myocardial infarction. Plasma corin levels were examined by enzyme-linked immunosorbent assay, transcripts of cardiac corin, pro-ANP and pro-BNP by quantitative real-time polymerase chain reaction, cardiac corin expression by immunohistology, infarct size by histology and heart function by echocardiography. Plasma corin levels were significantly increased at 3 (P<0.05), 24 (P<0.001), and 72 hours (P<0.01) post-acute myocardial infarction. In contrast, cardiac corin transcript levels dropped by 5% (P>0.05), 69% (P<0.001) and 65% (P<0.001) and immunoreactive cardiac corin protein levels dropped by 30% (P<0.05), 76% (P<0.001) and 75% (P<0.001), while cardiac pro-ANP and pro-BNP transcript levels showed an opposite pattern. Plasma corin levels were negatively correlated with immunoreactive cardiac corin (P<0.01), ejection fraction (P<0.05) and fractional shortening (P<0.05), but positively correlated with infarct size (P<0.01). In conclusion, acute myocardial infarction induces rapid increases in plasma corin and decreases in cardiac corin levels. In the early phase of acute myocardial infarction, plasma corin levels are inversely correlated with heart function and may reflect the severity of myocardial damage.

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Section: Discussionmentioning

confidence: 99%

Increases in plasma corin levels following experimental myocardial infarction reflect the severity of ischemic injury

et al. 2018

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“…Additionally, corin is also found in the blood system in its circulating forms. Previous studies demonstrated the decreased concentration of soluble circulating corin in patients with HF and acute myocardial infarction, compared to healthy individuals (183)(184)(185)(186)(187)(188)(189)(190)(191). Noteworthy, clinical studies demonstrated that decompensated heart failure, assessed by edema and elevated plasma ANP/BNP levels, is associated with reduced corin levels and decreased cleavage of proANP/proBNP peptides (179,(192)(193)(194)(195).…”

Section: Natriuretic Peptides Blunted Response In Heart Failurementioning

confidence: 99%

Edema formation in congestive heart failure and the underlying mechanisms

Abassi

Khoury

Karram

et al. 2022

Front. Cardiovasc. Med.

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Congestive heart failure (HF) is a complex disease state characterized by impaired ventricular function and insufficient peripheral blood supply. The resultant reduced blood flow characterizing HF promotes activation of neurohormonal systems which leads to fluid retention, often exhibited as pulmonary congestion, peripheral edema, dyspnea, and fatigue. Despite intensive research, the exact mechanisms underlying edema formation in HF are poorly characterized. However, the unique relationship between the heart and the kidneys plays a central role in this phenomenon. Specifically, the interplay between the heart and the kidneys in HF involves multiple interdependent mechanisms, including hemodynamic alterations resulting in insufficient peripheral and renal perfusion which can lead to renal tubule hypoxia. Furthermore, HF is characterized by activation of neurohormonal factors including renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system (SNS), endothelin-1 (ET-1), and anti-diuretic hormone (ADH) due to reduced cardiac output (CO) and renal perfusion. Persistent activation of these systems results in deleterious effects on both the kidneys and the heart, including sodium and water retention, vasoconstriction, increased central venous pressure (CVP), which is associated with renal venous hypertension/congestion along with increased intra-abdominal pressure (IAP). The latter was shown to reduce renal blood flow (RBF), leading to a decline in the glomerular filtration rate (GFR). Besides the activation of the above-mentioned vasoconstrictor/anti-natriuretic neurohormonal systems, HF is associated with exceptionally elevated levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). However, the supremacy of the deleterious neurohormonal systems over the beneficial natriuretic peptides (NP) in HF is evident by persistent sodium and water retention and cardiac remodeling. Many mechanisms have been suggested to explain this phenomenon which seems to be multifactorial and play a major role in the development of renal hyporesponsiveness to NPs and cardiac remodeling. This review focuses on the mechanisms underlying the development of edema in HF with reduced ejection fraction and refers to the therapeutic maneuvers applied today to overcome abnormal salt/water balance characterizing HF.

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“…Corin is a type II transmembrane serine protease synthesized by cardiomyocytes (11). The enzyme regulates blood volume, blood pressure, and cardiac function through the synthesis of natriuretic peptides (12). Previous studies have revealed that corin plays a key role in the transformation of pro-atrial natriuretic peptides (proANP) and pro-brain natriuretic peptides (proBNP) to active peptides (13).…”

Section: Introductionmentioning

confidence: 99%

Low serum corin levels predict end-organ damage in patients with hypertensive crisis

Yavuz

Söğüt

Çolak

et al. 2021

The Anatolian Journal of Cardiology

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Objective: The study aimed to investigate the predictive power of serum corin levels for distinguishing between hypertensive urgency (HU) and hypertensive emergency (HE) in patients with hypertensive crisis (HC) admitted to the emergency department. Methods: A total of 120 consecutive consenting adult patients diagnosed with HC and 55 age-and sex-matched healthy controls were enrolled. Blood pressure measurements [(systolic, diastolic, and mean arterial pressure (MAP)] and the evidence of end-organ damage at the first admission were recorded. Patients with HC were classified as patients with HE or HU according to the presence or absence of acute end-organ damage. Serum corin levels were compared between the 2 groups. Results: The mean serum corin level was significantly lower in the HC group than in the control group; it was also lower in the HE group than in the HU group (p<0.001 for all). In the HE group, clinical features associated with end-organ damage included ST-elevation myocardial infarction (n=28, 46.7%), hemorrhagic stroke (n=11, 18.3%), ischemic stroke (n=11, 18.3%), and non-ST-elevation myocardial infarction (n=10, 16.7%). The receiving operator characteristic (ROC) analysis identified a serum corin cutoff value of 45 pg/mL for distinguishing patients with HE from patients with HU with 98.3% sensitivity and 95% specificity. Conclusion: Our findings suggest that serum corin levels play an important role in regulating blood pressure and are involved in the pathogenesis of HC. Low serum corin levels may predict end-organ damage and serve as a guide for diagnostic decision making in patients with HC.

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Corin as novel biomarker for myocardial infarction

Cited by 4 publications

References 14 publications

Increases in plasma corin levels following experimental myocardial infarction reflect the severity of ischemic injury

Increases in plasma corin levels following experimental myocardial infarction reflect the severity of ischemic injury

Edema formation in congestive heart failure and the underlying mechanisms

Low serum corin levels predict end-organ damage in patients with hypertensive crisis

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