Cardio-oncology (London, England) · 2026
Midodrine to facilitate cardioprotective therapy in hypotensive HER2-positive breast cancer patients with cancer-therapy-related cardiac dysfunction-multicenter case experience.
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Koutroumpakis Efstratios, Iliescu Cezar, Deswal Anita, Porter Charles
Аннотация
BACKGROUND: HER2-targeted therapies significantly improve outcomes in HER2-positive breast cancer but are associated with cancer therapy-related cardiac dysfunction (CTRCD), which may necessitate interruption of oncologic treatment. Hypotension, which is not uncommon in patients with cancer, may limit the use of guideline-directed medical therapy (GDMT) required for left ventricular (LV) recovery, and no approved strategy exists to safely augment blood pressure in this setting.
CASE PRESENTATION: We report two cases of hypotensive breast cancer patients who developed CTRCD during HER2-targeted therapy and were unable to tolerate GDMT due to symptomatic hypotension. In both cases, initiation and titration of midodrine enabled stabilization of blood pressure, facilitation of cardioprotective therapy with beta-blockers and/or sodium-glucose cotransporter-2 inhibitors, and subsequent recovery of LV systolic function. This strategy allowed continuation or reinitiation of life-prolonging HER2-directed therapy without worsening heart failure or significant adverse effects.
DISCUSSION AND CONCLUSIONS: Midodrine may serve as a practical hemodynamic adjunct to enable guideline-directed cardioprotective therapy in selected hypotensive patients with HER2 therapy-related cardiomyopathy. These cases illustrate the feasibility of blood pressure augmentation as a strategy to facilitate cardiac recovery while preserving access to essential oncologic therapy. They do not establish efficacy or safety, and prospective studies with systematic assessment and predefined endpoints are warranted to define patient selection and long-term outcomes.
CASE PRESENTATION: We report two cases of hypotensive breast cancer patients who developed CTRCD during HER2-targeted therapy and were unable to tolerate GDMT due to symptomatic hypotension. In both cases, initiation and titration of midodrine enabled stabilization of blood pressure, facilitation of cardioprotective therapy with beta-blockers and/or sodium-glucose cotransporter-2 inhibitors, and subsequent recovery of LV systolic function. This strategy allowed continuation or reinitiation of life-prolonging HER2-directed therapy without worsening heart failure or significant adverse effects.
DISCUSSION AND CONCLUSIONS: Midodrine may serve as a practical hemodynamic adjunct to enable guideline-directed cardioprotective therapy in selected hypotensive patients with HER2 therapy-related cardiomyopathy. These cases illustrate the feasibility of blood pressure augmentation as a strategy to facilitate cardiac recovery while preserving access to essential oncologic therapy. They do not establish efficacy or safety, and prospective studies with systematic assessment and predefined endpoints are warranted to define patient selection and long-term outcomes.