# Cardiac markers for risk stratification and prognosis in elderly patients with HFpEF

**Authors:** Omar Abusedera, Jana Sherif, Leena Karar, Dana Arekat

PMC · DOI: 10.3389/fmed.2026.1754295 · Frontiers in Medicine · 2026-02-18

## TL;DR

This paper reviews how specific cardiac biomarkers can help diagnose and predict outcomes in elderly patients with heart failure with preserved ejection fraction.

## Contribution

The paper highlights a multimarker strategy for better risk stratification in elderly HFpEF patients.

## Key findings

- BNP/NT-proBNP are key for diagnosing HFpEF but interpretation is complex in older adults.
- High-sensitivity troponins predict mortality and hospitalizations in HFpEF patients.
- Galectin-3 provides strong prognostic value for myocardial fibrosis in HFpEF.

## Abstract

Heart failure with preserved ejection fraction (HFpEF) is increasingly prevalent among the elderly, particularly women, and is characterized by complex pathophysiology driven by comorbidities such as hypertension, diabetes, and renal dysfunction. These overlapping mechanisms make diagnosis and prognosis challenging, highlighting the importance of circulating biomarkers that reflect key biological processes such as myocardial stretch, fibrosis, inflammation, and injury.

This mini-review explores the diagnostic and prognostic roles of major cardiac biomarkers BNP/NT-proBNP, high-sensitivity troponins, soluble suppression of tumorigenicity 2 (sST2), and Galectin-3 in elderly patients with HFpEF.

BNP and NT-proBNP remain the cornerstone biomarkers for diagnosing HFpEF, reflecting ventricular wall stress and providing strong prognostic value, although their interpretation in older adults can be influenced by renal function, age, and comorbidities. High-sensitivity troponins indicate chronic myocardial injury and have emerged as reliable predictors of mortality and recurrent hospitalizations. sST2 reflects inflammatory and fibrotic remodeling; while limited diagnostically, it shows consistent association with adverse outcomes. Galectin-3 captures ongoing myocardial fibrosis and structural remodeling, offering particularly strong prognostic information in HFpEF compared to HFrEF.

Collectively, these biomarkers represent complementary windows into the pathophysiology of HFpEF. A multimarker strategy that integrates markers of wall stress, injury, inflammation, and fibrosis may enhance diagnostic precision and risk stratification in elderly patients, guiding more personalized approaches to management.

## Linked entities

- **Proteins:** NPPB (natriuretic peptide B), CORT (cortistatin), LGALS3 (galectin 3)
- **Diseases:** heart failure (MONDO:0005252), diabetes (MONDO:0005015)

## Full-text entities

- **Genes:** PRRT2 (proline rich transmembrane protein 2) [NCBI Gene 112476] {aka BFIC2, BFIS2, DSPB3, DYT10, EKD1, FICCA}, IL33 (interleukin 33) [NCBI Gene 90865] {aka C9orf26, DVS27, IL1F11, NF-HEV, NFEHEV}, ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383] {aka BB2, CD54, P3.58}, LGALS3 (galectin 3) [NCBI Gene 3958] {aka CBP35, GAL3, GALBP, GALIG, L31, LGALS2}, TNNT2 (troponin T2, cardiac type) [NCBI Gene 7139] {aka CMD1D, CMH2, CMPD2, LVNC6, RCM3, TnTC}, NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}, ST2 (suppression of tumorigenicity 2) [NCBI Gene 6761], TRIM67 (tripartite motif containing 67) [NCBI Gene 440730] {aka TNL}
- **Diseases:** HFpEF (MESH:D054144), cardiac remodeling (MESH:D020257), dysfunction (MESH:D006331), Heart failure (MESH:D006333), renal dysfunction (MESH:D007674), right ventricular dysfunction (MESH:D018497), myocardial infarction (MESH:D009203), cardiovascular death (MESH:D002318), atrial fibrillation (MESH:D001281), cardiomyocyte hypertrophy (MESH:D006984), myocardial stiffness (MESH:C566112), hypertension (MESH:D006973), left ventricular hypertrophy (MESH:D017379), Mortality (MESH:D003643), ischaemic (MESH:D018917), anemia (MESH:D000740), pulmonary congestion (MESH:D001261), cardiomyocyte damage (MESH:D020263), hypotension (MESH:D007022), ischemia (MESH:D007511), OA (MESH:D010003), myocardial injury (MESH:D009202), stroke (MESH:D020521), diastolic dysfunction (MESH:D018487), arrhythmias (MESH:D001145), tachycardia (MESH:D013610), aortic stenosis (MESH:D001024), obesity (MESH:D009765), Chronic kidney disease (MESH:D051436), dyspnea (MESH:D004417), valve obstruction (MESH:D006349), endothelial dysfunction (MESH:D014652), diabetes (MESH:D003920), acute coronary syndromes (MESH:D054058), coronary microvascular dysfunction (MESH:D003327), myocardial stretch (MESH:D057896), Chronic inflammation (MESH:D007249), Fibrosis (MESH:D005355)
- **Chemicals:** cTn (MESH:C403585), valsartan (MESH:D000068756), calcium (MESH:D002118), hs (MESH:D006859), sacubitril (MESH:C000717211), Natriuretic peptides (MESH:D045265), PDBu (-), oxygen (MESH:D010100)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

37 references — full list in the complete paper: https://tomesphere.com/paper/PMC12956511/full.md

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Source: https://tomesphere.com/paper/PMC12956511