Prediabetes plus myocardial dysfunction increases HF risk in people with hypertension

medwireNews: Adults with hypertension and prediabetes in combination with subclinical myocardial injury or stress have a significantly elevated risk for heart failure (HF), say investigators who suggest that integrating glycemic status and cardiac biomarkers could improve HF risk stratification and prevention in these patients.

The team analyzed data from the SPRINT cohort study carried out between 2010 and 2013, which showed that targeting a low systolic blood pressure (<120 mmHg) versus a standard blood pressure target (<140 mmHg) reduced the risk for cardiovascular events and mortality in high-risk hypertensive patients without diabetes.

The current post-hoc study included 8234 participants with hypertension but no diabetes or prior HF who had both baseline and 12-month measurements of high-sensitivity cardiac troponin I (hs-cTnI) and N-terminal pro–B-type natriuretic peptide (NT-proBNP). They had a mean age of 68 years and 62.9% were men.

Among the participants, 39.7% had prediabetes, defined as a fasting plasma glucose of 100–125 mg/dL (5.6–6.9 mmol/L), 35.7% had subclinical myocardial injury (hs-cTnI ≥6 ng/L in men and ≥4 ng/L in women), and 43.6% had subclinical myocardial stress (NT-proBNP ≥125 mg/mL).

In total, 122 participants developed HF over a median follow-up of 3.2 years, equating to an incidence rate of 4.6 per 1000 person–years.

Justin Echouffo-Tcheugui (Johns Hopkins University School of Medicine, Baltimore, Maryland, USA) and colleagues report in JAMA Cardiology that the participants with both prediabetes and subclinical myocardial injury had four times the risk for developing HF than the individuals without prediabetes and myocardial injury, after taking into account factors such as age, sex, ethnicity, blood pressure, BMI, cholesterol and lipid levels, and kidney-related risk factors (adjusted hazard ratio [aHR]=4.20).

Participants without prediabetes but with subclinical myocardial injury had a more than three times higher risk for HF than those without either risk factor (aHR=3.28).

The findings were similar for people who had subclinical myocardial stress with and without prediabetes, with significant aHRs for HF of 5.20 and 3.78, respectively, compared with individuals without prediabetes and myocardial stress. 

The study authors note that prediabetes alone was associated with “only a modest” nonsignificant increase in HF risk, but that it “serves as a clinically meaningful modifier that may amplify vulnerability to myocardial dysfunction.”

Indeed, the aHR for HF in people with prediabetes in conjunction with either subclinical myocardial injury or stress was 10.15, relative to individuals with neither risk factor, whereas it was 7.96 in people without prediabetes who had either type of myocardial dysfunction.

Moreover, in a longitudinal analysis of the cardiac biomarkers in 7449 participants over a median follow-up of 2.3 years, during which there were 78 HF events, the risk for HF was significantly increased in individuals whose levels of hs‑cTnI increased by at least 25% between baseline and 12 months, particularly for those with than without prediabetes, with significant aHRs of 3.05 and 2.60, respectively, compared with individuals without prediabetes whose hs-cTnI levels did not increase.

This was also the case for individuals with and without prediabetes who experienced 12-month increases of at least 25% in NT-proBNP levels, with significant aHRs for HF of 2.39 and 1.66, respectively, relative to their peers without prediabetes and no increase in NT-proBNP.

Echouffo-Tcheugui conclude: “From a clinical perspective, these results underscore the potential value of combining metabolic and cardiac biomarker profiling to refine HF risk assessment for adults with hypertension,” adding that “[s]uch an approach could enable earlier preventive interventions and guide precision-based risk stratification in hypertension management.”

 medwireNews is an independent medical news service provided by Springer Healthcare Ltd. © 2026 Springer Healthcare Ltd, part of Springer Nature

JAMA Cardiol 2026; doi:10.1001/jamacardio.2025.4927