Breaking News:New Study Offers Strong Evidence of Elevated Heart Failure Risk in Adults with Prediabetes, Hypertension and Subclinical Heart Injury or Stress– What Just Happened

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A new study from researchers led by Johns Hopkins Medicine reports substantial new evidence that elevated blood biomarkers of subclinical heart injury or stress — heart muscle damage without symptoms of a heart attack — are linked to an increased risk of heart failure (HF) in adults with coexisting high blood pressure (hypertension) and prediabetes.

The findings, the researchers say, highlight an at-risk group of individuals who could be identified via routine blood work for preventive care before heart failure occurs.

The collaborative National Institutes of Health (NIH)-funded study was published in JAMA Cardiology Jan. 14 and highlights how common, asymptomatic health complications can drive heart failure risk.

Prediabetes, an intermediate stage in which a person has blood sugar levels that are considered higher than normal but not elevated enough to be considered diabetic, affects an estimated 115.2 million U.S. adults as of January 2026, and is broadly linked to an increased risk of heart, kidney and nerve damage.

“We already know there’s a link between prediabetes and heart failure,” says study senior author Justin Basile Echouffo Tcheugui, M.D., Ph.D., associate professor of medicine at the Johns Hopkins University School of Medicine. “But we wanted to see if additional factors, such as subclinical heart injury or stress, could elevate the risk of developing heart failure beyond prediabetes alone.”

For the study, Echouffo Tcheugui’s team analyzed data from adults who were previously enrolled in the NIH Systolic Blood Pressure Intervention Trial (SPRINT) — a 2010 clinical trial that investigated how reducing blood pressure in adults with hypertension affects the heart, kidneys and brain.

The researchers compared clinical data, including heart injury or stress biomarkers, collected from 8,234 SPRINT participants (62.9% male and 37.1% female) ages 50 and older (mean age 68 years) who did not have a formal diabetes diagnosis. Two analyses were performed: one that compared heart health outcomes to baseline biomarker levels and one that looked at biomarker changes 12 months into the study. 

For their analyses, prediabetes was defined as fasting blood glucose of 100 to 125 milligrams per deciliter; subclinical heart injury as a high-sensitivity cardiac troponin I (hs-cTnI) level equal to or greater than 6 nanograms per liter in men or 4 nanograms per liter in women; and subclinical heart stress as a N-terminal pro-B-type natriuretic peptide (NT-proBNP) level equal to or greater than 125 picograms per milliliter.

Then, using statistical models, they calculated hazard ratios — a measurement of how often a specific event would occur in one group in comparison to another over time — for people without prediabetes based on the presence or absence of heart injury or stress.

A hazard ratio of 1 would suggest there was no difference in heart failure risk between individuals with or without prediabetes, while a ratio greater than 1 would indicate an increased risk of heart failure. Similarly, a hazard ratio less than 1 would indicate one group had a decreased risk of heart failure versus the other.

Comparing baseline biomarkers, the researchers found 3,271 (39.7%) study participants had prediabetes, 2,942 (35.7%) had subclinical heart injury and 3,593 (43.6%) had subclinical heart stress at the study’s onset. Over a median follow-up of 3.2 years, participants with baseline prediabetes and either heart injury or stress were overall 10 times more likely to experience HF. In comparison, those without prediabetes who had heart injury or stress only experienced a moderate HF risk increase (3.28 and 3.78, respectively).

Comparing the outcomes of patients over time, the researchers found those who had both prediabetes and a 25% or greater increase in hs-cTnI or NT-proBNP levels at their 12-month follow-up were 3.05 times and 2.39 times more likely to develop heart failure. In contrast, individuals without diabetes were 2.60 times and 1.66 times more likely to experience HF, respectively, if hs-cTnI or NT-proBNP increased over time. Surprisingly, prediabetes alone was not linked to an increase or decrease in HF risk. 

Across both analyses, the stark difference in HF risk is believed to suggest that underlying metabolic abnormalities present in people with prediabetes may exacerbate specific types of cardiovascular disease.

Echouffo Tcheugui says the study findings highlight how clinicians can easily identify prediabetic patients who are at elevated risk of heart failure using blood tests and provide appropriate medical interventions before a cardiac event occurs.

“Using heart failure biomarkers, we can identify and treat these patients who have a much higher risk of cardiovascular disease, but this also means we can look at biomarkers for other cardiovascular events,” says Echouffo Tcheugui. “The prediabetes state is often overlooked in patients, but by defining vulnerable subpopulations, we can take preventive actions to care for patients before emergencies occur.”

The study was supported by the National Institutes of Health (K23HL153774, R01HL159994, K24HL166681 and UL1TR003167).

Ballantyne receives grants and research support from Abbott Diagnostics, Akcea, Amgen, Arrowhead, Eli Lilly, Ionis, Merck, New Amsterdam, Novartis, Novo Nordisk and Roche Diagnostics. During the study, Ballantyne also received grants and personal and consulting fees from 89Bio, Abbott Diagnostics, Amgen, Arrowhead, AstraZeneca, Denka Seiken, Esperion, Genentech, HeartFlow, Ionis, Eli Lilly, Merck, New Amsterdam, Novartis, Novo Nordisk and Roche Diagnostics. Berry reports receiving grants from Abbott and Roche during the study and personal fees from the Cooper Institute outside the submitted work. The other authors declare no competing interests. 

Arnaud D. Kaze is the study’s first author, and researchers who contributed to the manuscript, in alphabetical order, are Christie M. Ballantyne, Jarrett D. Berry, Jordana B. Cohen, Stephen P. Juraschek, Chiadi E. Ndumele and Siddharth Singh.

DOI: 10.1001/jamacardio.2025.4927