Diabetes drugs improve survival for patients with ‘broken hearts’
The early use of sodium-glucose cotransporter-2 (SGLT2) inhibitors can help patients with Takotsubo syndrome (TTS) live longer, according to new real-world data published in The American Journal of Cardiology.[1]
TTS, often called “broken heart syndrome,” often resolves without the use of any medical therapies. However, the study’s authors explained, recent studies have suggested TTS could be associated with long-term cardiac risks that remain even after the patient’s heart returns to normal.
SGLT inhibitors, meanwhile, are primarily known as type 2 diabetes medications, but they have also been linked to certain cardiac benefits.
“SGLT2 inhibitors have demonstrated consistent cardioprotective effects across the heart failure spectrum regardless of ejection fraction, yet evidence specifically in TTS remains sparse,” wrote first author Amro Taha, MD, a researcher with the West Virginia University School of Medicine, and colleagues.
Taha et al. tracked data from more nearly 55,000 patients with TTS who underwent treatment from 2015 to 2025. Patients were propensity matched into two groups of 1,803 patients—one group that received SGLT2 inhibitor therapy within 14 days and another group that did not.
Overall, the SGLT2 inhibitor patients were associated with a significantly lower all-cause mortality rate (8.1% vs. 13.6%). There were no significant differences in terms of heart failure hospitalizations, cardiogenic shock, cardiac arrest or major adverse cardiovascular events.
The authors did note that SGLT2 inhibitors could still be linked to certain benefits related to heart failure symptoms, even after no difference was seen in heart failure hospitalization rates.
“This null finding should be interpreted cautiously rather than as evidence of no benefit,” they wrote. “Event counts were modest, endpoint-specific at-risk denominators varied, death may have acted as a competing event, and EHR-based ascertainment of heart failure hospitalization is susceptible to misclassification. Accordingly, our data do not establish a mechanistic dissociation between mortality and heart failure outcomes; rather, they suggest that any association with nonfatal cardiovascular events remains uncertain in this design.”
Taha and colleagues also called for additional research into the treatment of TTS.
“Our data is hypothesis-generating and supports the need for randomized trials to evaluate the role of SGLT2 inhibitors and other cardioprotective therapies in patients with TTS,” the group concluded.
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