A drug developed for diabetes treatment may significantly reduce the risk of heart failure among people with specific genetic traits linked to cardiomyopathy, according to new research in Nature Medicine.

Scientists from Harvard Medical School, Mass General Brigham, and MIT analyzed data from more than 12,000 adults with type 2 diabetes who participated in the DECLARE-TIMI 58 trial.

Participants had elevated cardiovascular risk, and about 121 carried inherited gene variants that could increase their likelihood of developing cardiomyopathy, a disease that weakens the heart muscle over time.

The study focused on the SGLT2 inhibitor dapagliflozin, a medication commonly prescribed for type 2 diabetes management.

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Researchers found that the drug lowered rates of hospitalization for heart failure, particularly among those with the cardiomyopathy-linked genetic variants.

While benefits were observed across all participants, the reduction in hospitalizations was about eight times greater in those carrying the genetic variants compared with non-carriers. The team followed participants for a median of 4.2 years.

Among variant carriers with no prior history of heart failure, 12.8% of those taking a placebo eventually developed the condition.

In contrast, none of the participants with the same genetic risk who took dapagliflozin experienced heart failure events during the study period.

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Dr. Shinwan Kany, a visiting scientist at the Cardiovascular Research Center within Mass General Brigham Heart and Vascular Institute and the Broad Institute, said the findings could change how cardiologists approach prevention.

He noted that “historically, identifying a genetic variant for cardiomyopathy mostly meant telling a patient they were at high risk and not having a specific preventive therapy to offer,” adding that the new data suggest “we do have tools to lower risk in these individuals.”

Despite the promising results, scientists cautioned that the analysis drew from a subset of a larger trial and included a relatively small number of carriers.

They emphasized that further studies are needed to confirm the findings and determine broader applicability.

Dr. Andrew Freeman, a cardiologist at National Jewish Health who was not involved in the study, described the research as “important and provocative.” He said the results point toward an emerging era of “precise and genetically informed” strategies for preventing heart failure.

Freeman also observed that participants without prior heart failure who took dapagliflozin were less likely to develop the condition, suggesting SGLT2 inhibitors might offer special benefit for people with known genetic risks.

However, he urged that these results be seen as "an exciting hypothesis-generating finding, not yet a practice-changing mandate."

SGLT2 inhibitors are already considered essential in cardiology and nephrology, used to manage type 2 diabetes, chronic kidney disease, and heart failure. Freeman explained that these medications are known to lower rates of heart failure hospitalization across broad patient populations.

What this research adds, he said, is evidence that genetic testing could eventually help pinpoint patients who might gain the greatest benefit from treatment before symptoms occur.

Genetic testing for cardiomyopathy is currently used for diagnostic purposes, family screening, and risk assessment.

If confirmed through future clinical trials, the findings could pave the way for more targeted early interventions using genetic screening to identify individuals at the highest risk. Freeman noted that heart failure risk can begin long before symptoms appear, making preventive cardiology a potential focus for early care.

He advised that decisions about medication use be made in consultation with a clinician, particularly for those with a personal or family history of cardiovascular disease.