Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (498 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The amount of blood pumped out of the heart per beat, not to be confused with cardiac output (volume/time). It is calculated as the difference between the end-diastolic volume and the end-systolic volume.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Stroke Volumes; Volumes, Stroke; Volume, Stroke; Ventricular Ejection Fraction; Ejection Fractions, Ventricular; Ejection Fraction, Ventricular; Fractions, Ventricular Ejection; Fraction, Ventricular Ejection.
Where it fits in the MeSH classification
- Broader topics
- Cardiac Output
Related concepts
- Blood
- Heart
Research landscape
PubMed indexes 61,013 records tagged with the MeSH heading “Stroke Volume” (counts retrieved 2026-10-29). 19,889 of them (32.6%) were published from 2020 onward, and the busiest period so far is 2020 onward with 19,889 records.
Reviews account for 5,691 records (9.3%) and meta-analyses for 1,286. Randomized controlled trials number 4,484 (7.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 13,275 |
| 2000-2009 | 10,391 |
| 2010-2019 | 17,458 |
| 2020 onward | 19,889 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,691 | 9.3% |
| Meta-analyses | 1,286 | 2.1% |
| Randomized controlled trials | 4,484 | 7.3% |
Method: PubMed query "Stroke Volume"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Pathophysiology of HFpEF: Insights from a Metabolic-Mitochondrial Perspective | 2025 | Review article Design not recorded in structured metadata | 15 | cc by PMID 41516161 · DOI · PMC12785657 |
| Heart failure and preserved ejection fraction: pathophysiology, clinical assessment, and management of exercise intolerance | 2026 | Review article Design not recorded in structured metadata | 10 | cc by PMID 41984824 · DOI · PMC13286652 |
| The microRNA inhibitor CDR132L in patients with reduced left ventricular ejection fraction after myocardial infarction: a randomized phase 2 trial | 2026 | Randomized controlled trial Design not recorded in structured metadata | 8 | cc by PMID 42108271 · DOI · PMC13375544 |
Pathophysiology of HFpEF: Insights from a Metabolic-Mitochondrial Perspective [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Heart failure with preserved ejection fraction (HFpEF) represents a growing clinical challenge, accounting for more than half of all cases of heart failure, for which there are currently no effective treatments.
- Closing excerpt
- Deepening the understanding of mitochondrial metabolism could enable the development of personalized treatments capable of improving outcomes for HFpEF patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (181 words)
Heart failure with preserved ejection fraction (HFpEF) represents a growing clinical challenge, accounting for more than half of all cases of heart failure, for which there are currently no effective treatments. Emerging evidence identifies mitochondrial dysfunction as a central mechanism linking metabolic comorbidities, systemic inflammation, and energy failure in HFpEF. This review provides a comprehensive overview of the metabolic-mitochondrial mechanisms underlying the pathophysiology of HFpEF. Loss of metabolic flexibility, characterized by reduced fatty acid and glucose oxidation, leads to energy inefficiency, lipid accumulation, and oxidative stress. Structural and functional mitochondrial abnormalities, including damaged cristae, altered fission-fusion dynamics, and impaired oxidative phosphorylation, contribute to diastolic dysfunction and ventricular remodeling. In parallel, chronic inflammation and redox imbalance amplify mitochondrial damage through cytokine- and ROS-mediated pathways, creating a cycle of bioenergetic failure. From a therapeutic perspective, strategies aimed at restoring mitochondrial homeostasis, such as physical training, metabolic modulation, SGLT2 inhibition, ketone supplementation, and mitochondria-targeted antioxidants, show promising preclinical results. However, clinical translation remains limited. Deepening the understanding of mitochondrial metabolism could enable the development of personalized treatments capable of improving outcomes for HFpEF patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41516161 · DOI · PMC12785657
Heart failure and preserved ejection fraction: pathophysiology, clinical assessment, and management of exercise intolerance [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Exercise intolerance is a clinical hallmark of heart failure with preserved ejection fraction (HFpEF) that confers high morbidity and predicts mortality.
- Closing excerpt
- The domain-based phenotyping approach described highlights the value of comprehensive phenotyping of both cardiac and extra-cardiac reserve capacity to advance understanding of how to deploy individualized interventions to bolster exercise tolerance in HFpEF.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (111 words)
Exercise intolerance is a clinical hallmark of heart failure with preserved ejection fraction (HFpEF) that confers high morbidity and predicts mortality. The mechanisms underlying exercise intolerance in HFpEF are diverse and often include compound deficits in multi-organ reserve capacity that culminate in marked functional limitations. This review describes aetiologies of exercise intolerance in HFpEF, tools to quantify relative physiologic deficits unmasked during exercise, and insights gained from interventional trials that have aimed to augment exercise capacity in HFpEF. The domain-based phenotyping approach described highlights the value of comprehensive phenotyping of both cardiac and extra-cardiac reserve capacity to advance understanding of how to deploy individualized interventions to bolster exercise tolerance in HFpEF.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41984824 · DOI · PMC13286652
The microRNA inhibitor CDR132L in patients with reduced left ventricular ejection fraction after myocardial infarction: a randomized phase 2 trial [3]
Abstract reading summary — source excerpts
- Opening excerpt
- MicroRNA-132 (miR-132) is a central regulator of adverse cardiac remodeling.
- Closing excerpt
- gov: NCT05350969 .
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (206 words)
MicroRNA-132 (miR-132) is a central regulator of adverse cardiac remodeling. Here we evaluated CDR132L, a synthetic antisense oligonucleotide miR-132 inhibitor, in a multinational, randomized, double-blind, placebo-controlled phase 2 trial (HF-REVERT) in patients with recent myocardial infarction (MI) and left ventricular (LV) systolic dysfunction. Within 3-14 days after MI, 294 patients were randomized to receive CDR132L 5 mg kg-1, CDR132L 10 mg kg-1 or placebo as three intravenous doses at 4-week intervals plus guideline-directed therapy. In total, 280 patients (245 men and 35 women) who received at least one dose of the study drug were included in the modified intention-to-treat population. CDR132L was well tolerated, with no hepatic, renal, hematologic or cardiac toxicity signals. The primary endpoint-the percentage change in LV end-systolic volume index at 6 months-improved in all groups but did not differ significantly between the CDR132L groups (5 mg kg-1 and 10 mg kg-1) and the placebo group. Secondary endpoints, including LV ejection fraction, global longitudinal strain and N-terminal pro B-type natriuretic peptide, were also not significantly different between the CDR132L and placebo groups. Prespecified exploratory analyses suggested potential benefits of CDR132L treatment in patients with advanced adverse remodeling at baseline, supporting further evaluation of CDR132L, including in chronic heart failure conditions. ClinicalTrials.gov: NCT05350969 .
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42108271 · DOI · PMC13375544
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article SGLT2 inhibitors in patients with heart failure with reduced ejection fraction: a meta-analysis of the EMPEROR-Reduced and DAPA-HF trials [4]
- Research article Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature [5]
- Research article Beta-blockers for heart failure with reduced, mid-range, and preserved ejection fraction: an individual patient-level analysis of double-blind randomized trials [6]
- Research article Assessment of Prognostic Value of Left Ventricular Global Longitudinal Strain for Early Prediction of Chemotherapy-Induced Cardiotoxicity: A Systematic Review and Meta-analysis [7]
- Research article Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography and for Heart Failure With Preserved Ejection Fraction Diagnosis: An Update From the American Society of Echocardiography [8]
- Research article Meta-analysis of aerobic interval training on exercise capacity and systolic function in patients with heart failure and reduced ejection fractions [9]
References
- Gatto C, Rusciano MR, Visco V, Vecchione C, Ciccarelli M. Pathophysiology of HFpEF: Insights from a Metabolic-Mitochondrial Perspective. . 2025. PMID 41516161 · DOI · PMC12785657
- Landsteiner I, Verwerft J, Belov D, Verbrugge FH, Lewis GD. Heart failure and preserved ejection fraction: pathophysiology, clinical assessment, and management of exercise intolerance. . 2026. PMID 41984824 · DOI · PMC13286652
- Bauersachs J, Solomon SD, Anker SD, Antorrena-Miranda I, de Boer RA, Filippatos G, et al.. The microRNA inhibitor CDR132L in patients with reduced left ventricular ejection fraction after myocardial infarction: a randomized phase 2 trial. . 2026. PMID 42108271 · DOI · PMC13375544
- Zannad F, Ferreira JP, Pocock SJ, Anker SD, Butler J, Filippatos G, et al.. SGLT2 inhibitors in patients with heart failure with reduced ejection fraction: a meta-analysis of the EMPEROR-Reduced and DAPA-HF trials. Lancet. 2020. PMID 32877652 · DOI
- Marik PE, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Crit Care Med. 2009. PMID 19602972 · DOI
- Cleland JGF, Bunting KV, Flather MD, Altman DG, Holmes J, Coats AJS, et al.. Beta-blockers for heart failure with reduced, mid-range, and preserved ejection fraction: an individual patient-level analysis of double-blind randomized trials. Eur Heart J. 2018. PMID 29040525 · DOI · PMC5837435
- Oikonomou EK, Kokkinidis DG, Kampaktsis PN, Amir EA, Marwick TH, Gupta D, et al.. Assessment of Prognostic Value of Left Ventricular Global Longitudinal Strain for Early Prediction of Chemotherapy-Induced Cardiotoxicity: A Systematic Review and Meta-analysis. JAMA Cardiol. 2019. PMID 31433450 · DOI · PMC6705141
- Nagueh SF, Sanborn DY, Oh JK, Anderson B, Billick K, Derumeaux G, et al.. Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography and for Heart Failure With Preserved Ejection Fraction Diagnosis: An Update From the American Society of Echocardiography. J Am Soc Echocardiogr. 2025. PMID 40617625 · DOI
- Haykowsky MJ, Timmons MP, Kruger C, McNeely M, Taylor DA, Clark AM. Meta-analysis of aerobic interval training on exercise capacity and systolic function in patients with heart failure and reduced ejection fractions. Am J Cardiol. 2013. PMID 23433767 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.