Can Cell Therapy Help a Failing Heart

Edited and approved by Stephen C. Rose, PhD, MS

Cell therapy is being investigated as a possible addition to treatment for chronic heart failure. The approach studied in DREAM-HF uses donor-derived cells that may influence inflammation and support surviving heart tissue. The trial produced encouraging findings in selected analyses, but it did not meet its primary endpoint. Understanding both results is essential when considering what this research could mean for patients. [1]

The Texas Heart Institute's DREAM-HF research, led by Emerson Perin, involved people with heart failure and reduced ejection fraction. Ejection fraction is the proportion of blood the left ventricle ejects with each contraction. A reduced value can indicate impaired pumping function. Researchers wanted to determine whether a cellular treatment could improve outcomes when added to established heart-failure care. [1]

How the cellular treatment may work

The experimental treatment used mesenchymal precursor cells derived from adult donor bone marrow. Their proposed contribution is to release signals that influence immune activity, blood vessels, and the conditions surrounding surviving heart muscle. This differs from replacing lost muscle directly with cells that become functioning cardiomyocytes, the cells responsible for contraction. The trial did not establish that donor precursor cells rebuilt the heart. [1]

Preserving existing tissue, reducing harmful inflammation, and generating new heart muscle are separate objectives. Improvement in one does not automatically establish the others. Likewise, showing that delivered cells remain alive would not demonstrate fewer hospitalizations or longer survival. A useful clinical treatment must ultimately improve outcomes that matter to patients, with an acceptable balance of benefits and risks.

Inflammation is a plausible target because its effects change during recovery. After injury, immune cells help remove damaged material and coordinate repair. Persistent inflammatory signaling can contribute to ongoing tissue stress. The therapeutic challenge is to influence harmful activity while preserving useful immune and repair functions. The timing, location, and intensity of the response are therefore important to the proposed treatment.

The description of a "single injection" requires clarification. DREAM-HF delivered cells into heart muscle through a catheter-based procedure involving access through the inner wall of the heart. It was a one-time treatment session, rather than a routine injection into an arm. Patients considering research participation need a clear explanation of the delivery procedure and its associated monitoring. [2]

The main trial result

The randomized trial assigned 565 patients to precursor-cell treatment or a sham procedure. Participants were receiving established treatment for reduced-ejection-fraction heart failure. Blinding and the sham comparison helped reduce bias related to expectations and the experience of undergoing a procedure. These features make the trial more informative than an uncontrolled report of improvement after treatment. [1]

The primary endpoint concerned recurrent episodes of decompensated heart failure and successfully resuscitated symptomatic ventricular arrhythmias. Decompensation means a worsening of heart failure that requires urgent treatment. Ventricular arrhythmias are abnormal rhythms originating in the heart's main pumping chambers. Cell therapy did not significantly improve this endpoint: the reported hazard ratio was 1.17, with a P value of 0.41. [1]

The primary endpoint is the outcome selected in advance as the principal test of treatment benefit. Missing it means the trial did not establish its main intended effect. Important secondary outcomes also failed to establish an overall mortality advantage. The evidence therefore does not support describing this treatment as a proven way to prevent heart-failure deterioration or extend patients' lives.

Other analyses nevertheless identified findings worth investigating. Heart attack or stroke was less frequent in the cell-treatment group, with a reported hazard ratio of 0.42, often expressed as a 58 percent relative reduction. These findings were exploratory. A broader composite that included cardiovascular death had a confidence interval crossing the value indicating no difference between groups. [1]

Relative risk reductions need to be interpreted alongside absolute event rates. A 58 percent relative reduction does not mean that 58 of every 100 treated patients avoid an event. The potential benefit depends on the underlying frequency of events, the population studied, and the observation period. Exploratory results also require confirmation before they can guide routine treatment decisions.

Why inflammation may identify a responsive group

Investigators observed stronger signals among participants with baseline high-sensitivity C-reactive protein, or hsCRP, of at least 2 milligrams per liter. This blood marker can reflect inflammation, but it does not identify a single cause or measure precisely what is happening inside the heart. Analyses of pumping function also suggested greater improvement among patients with inflammation. [1]

A subsequent publication examined patients with ischemic heart failure and inflammation. Ischemic heart failure is associated with inadequate blood supply, commonly following coronary artery disease or a heart attack. That analysis reported substantial reductions in selected cardiovascular event composites after precursor-cell treatment. It raised the possibility that patients with this combination of features might be more likely to benefit. [3]

However, the publication reanalyzed DREAM-HF data. It was not a separate randomized trial independently reproducing the results. Subgroup analysis can identify promising directions, but repeated comparisons increase the possibility of findings that do not recur in another population. A favorable subgroup result should therefore be treated as a hypothesis requiring further testing, particularly when the original primary endpoint was negative.

The next step is a prospectively designed trial with predefined eligibility criteria and outcomes. It should test whether inflammation reliably identifies patients who benefit, and whether any improvement extends to clinically meaningful outcomes. Such a study could confirm the subgroup signal or show that it was less dependable than expected. Either result would improve the evidence available for patient care.

How you may be able to benefit

For patients living with heart failure, the immediate priority is to review and optimize established treatment. Guidelines support complementary medication classes for reduced-ejection-fraction heart failure, including appropriate renin-angiotensin system treatment, evidence-based beta blockers, mineralocorticoid receptor antagonists, and SGLT2 inhibitors. These treatments address different pathways involved in disease progression and should be considered according to the individual's clinical circumstances. [4]

Blood pressure, kidney function, potassium, symptoms, and other illnesses influence eligibility and tolerability. A useful discussion with the treating clinician is whether each relevant treatment category has been considered and whether doses or monitoring need adjustment. Experimental cell therapy should be evaluated as a research option alongside this care, without delaying treatments whose benefits are already established.

The inflammation findings do not identify a diet that makes cell therapy effective, a supplement that reproduces its action, or a reason to pursue the lowest possible hsCRP value. An elevated marker needs interpretation in context. Guideline-based care includes activity appropriate to clinical stability, attention to congestion, and an individualized approach to nutrition and other cardiovascular risks. [4]

For eligible patients with coronary disease, structured cardiac rehabilitation provides supervised exercise, education, and support for risk-factor management. An updated review found benefits including fewer heart attacks and hospital admissions. Rehabilitation offers a practical way to support recovery and daily function while researchers investigate new approaches. It should be tailored to the person's condition, capacity, and clinical assessment. [5]

Patients considering a cell-therapy trial should ask about the specific product, study population, delivery procedure, comparison group, follow-up, and outcomes being measured. A general offer of "stem cells for the heart" does not provide this information. DREAM-HF studied a particular cellular product under a defined protocol; its results cannot be applied automatically to unrelated cells or commercial procedures.

Implications for healthy aging

Preserving cardiovascular function supports mobility, stamina, and independence in later life. DREAM-HF provides a rationale for investigating whether modifying the inflammatory environment helps a selected group of patients. It did not measure biological-age reversal, demonstrate replacement of lost heart muscle, or establish longer lifespan. Those claims would require evidence beyond the outcomes reported in this trial. [1]

The research may help refine which patients should be studied and which treatment effects deserve further investigation. Its strongest contribution is a more specific clinical question about heart failure, inflammation, and cellular signaling. For now, established heart-failure care remains the practical foundation. Further controlled trials are needed before precursor-cell therapy can be considered a dependable addition to routine treatment.

References

[1] Perin EC, Borow KM, Henry TD, et al. Randomized Trial of Targeted Transendocardial Mesenchymal Precursor Cell Therapy in Patients With Heart Failure. J Am Coll Cardiol. 2023;81(9):849-863. doi:10.1016/j.jacc.2022.11.061.

[2] ClinicalTrials.gov. DREAM-HF: Efficacy and Safety of Allogeneic Mesenchymal Precursor Cells in Patients With Chronic Heart Failure (NCT02032004). Registry record accessed October 10, 2026.

[3] Perin EC, Borow KM, Henry TD, et al. Mesenchymal precursor cells reduce mortality and major morbidity in ischaemic heart failure with inflammation: DREAM-HF. Eur J Heart Fail. 2025;27(12):3288-3296. doi:10.1002/ejhf.3522.

[4] Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(18):e895-e1032. doi:10.1161/cir.0000000000001063.

[5] Dibben G, de Vries FB, Faulkner J, et al. Exercise-based cardiac rehabilitation for coronary heart disease. Cochrane Database Syst Rev. 2026;9:CD001800. doi:10.1002/14651858.cd001800.pub5.