What question did this study set out to answer?

Investigate the role and mechanisms of the mineralocorticoid receptor downstream target NGAL in cardiac damage and remodeling after myocardial infarction.

October 23, 2017HypertensionOpen Access

Aldosterone Target NGAL (Neutrophil Gelatinase–Associated Lipocalin) Is Involved in Cardiac Remodeling After Myocardial Infarction Through NFκB Pathway

Q: What is the clinical evidence from this study?

Study design: Cohort. Population: Myocardial infarction (n=119). Intervention: Higher baseline and increasing serum NGAL levels vs. Lower NGAL levels. Primary outcome: 6-month left ventricular ejection fraction recovery.

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Key result

In 119 post-MI patients, higher baseline NGAL and greater increases in serum NGAL were significantly associated with lower 6-month left ventricular ejection fraction recovery.

Why the study?

Does NGAL mediate cardiac remodeling and fibrosis after myocardial infarction?

Key Points

Investigate the role and mechanisms of the mineralocorticoid receptor downstream target NGAL in cardiac damage and remodeling after myocardial infarction.
Evaluated baseline and follow-up serum NGAL in 119 post-MI patients assessed for 6-month left ventricular ejection fraction recovery using cardiac MRI.
Subjected wild-type and NGAL knockout mice to myocardial infarction, with a subset of wild-type mice treated with the nonsteroidal MR antagonist finerenone (1 mg/kg per day) for up to 3 months.
Examined cultured human cardiac fibroblasts stimulated with aldosterone (10⁻⁸ mol/L) or NGAL (500 ng/mL) alongside finerenone (10⁻⁶ mol/L), NGAL knockdown, or the NFκB inhibitor BAY11-7082.
Higher baseline serum NGAL and greater increases during follow-up significantly correlated with impaired 6-month left ventricular ejection fraction recovery in post-MI patients.
NGAL knockout mice with MI exhibited significantly reduced left ventricular interstitial fibrosis and inflammation, accompanied by improved contractility, compliance, stroke volume, and cardiac output at 3 months post-MI compared with wild-type mice.
Aldosterone- and NGAL-induced type I collagen synthesis in human cardiac fibroblasts was completely abrogated by finerenone, NGAL knockdown, or NFκB inhibition via BAY11-7082.

Study Design

Type

Cohort (n=119)

Structured PICO

Does NGAL mediate cardiac remodeling and fibrosis after myocardial infarction?

Population

119 post-myocardial infarction patients followed for 6 months to assess left ventricular ejection fraction recovery.

Exposure

Finerenone (1 mg/kg per day in mice, 10^-6 mol/L in cells), NGAL knockout, aldosterone (10^-8 mol/L), NGAL (500 ng/mL), NFκB inhibitor BAY11-7082.

Comparator

Wild-type mice with MI; untreated cells.

Outcome

Left ventricular ejection fraction recovery at 6 months (patients); LV interstitial fibrosis, inflammation, contractility, compliance, stroke volume, and cardiac output at 3 months (mice); collagen type I production (cells).surrogate

NGAL is a key downstream mediator of mineralocorticoid receptor-induced cardiac damage and fibrosis post-MI, presenting a potential therapeutic target.

Discussion

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Implication

NGAL elevation may aid post-MI risk stratification; leaves open its causal role in remodeling and value as therapeutic target.

Cite This Study

Martínez‐Martínez et al. (2017) conducted a cohort in Myocardial infarction (n=119). Higher baseline and increasing serum NGAL levels vs. Lower NGAL levels was evaluated on 6-month left ventricular ejection fraction recovery. In 119 post-MI patients, higher baseline NGAL and greater increases in serum NGAL were significantly associated with lower 6-month left ventricular ejection fraction recovery.

synapsesocial.com/papers/6a9dffbac448d60cdc367ec4 https://doi.org/10.1161/hypertensionaha.117.09791

Topics

STEMI management

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Aldosterone Target NGAL (Neutrophil Gelatinase–Associated Lipocalin) Is Involved in Cardiac Remodeling After Myocardial Infarction Through NFκB Pathway

Key Points

Study Design

Structured PICO

Discussion

Implication

Cite This Study

Topics

Aldosterone Target NGAL (Neutrophil Gelatinase–Associated Lipocalin) Is Involved in Cardiac Remodeling After Myocardial Infarction Through NFκB Pathway

Key Points

Study Design

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Topics

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