What is the clinical evidence from this study?

Study design: Case Report. Population: HER2-positive breast cancer with cancer-therapy-related cardiac dysfunction and hypotension (n=2). Intervention: Midodrine. Primary outcome: Blood pressure stabilization and left ventricular ejection fraction (LVEF) recovery.

What question did this study set out to answer?

This report explores the use of midodrine to manage hypotension in HER2-positive breast cancer patients experiencing cardiac dysfunction.

May 31, 2026Cardio-Oncology1 citationsOpen Access

Midodrine to facilitate cardioprotective therapy in hypotensive HER2-positive breast cancer patients with cancer-therapy–related cardiac dysfunction—multicenter case experience

Q: What does this research mean for the field?

Midodrine administration enables the initiation of guideline-directed cardioprotective therapy and subsequent left ventricular recovery in hypotensive patients with HER2 therapy-related cardiomyopathy. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.ESTABLISHES_NEW_DIRECTION.

EKEfstratios KoutroumpakisThe University of Texas MD Anderson Cancer Center CICezar IliescuThe University of Texas MD Anderson Cancer Center ADAnita DeswalThe University of Texas MD Anderson Cancer Center

Key Result

Midodrine stabilized blood pressure in two hypotensive patients with HER2-therapy-related cardiomyopathy, enabling guideline-directed cardioprotective therapy and subsequent recovery of LVEF.

Key Points

This report explores the use of midodrine to manage hypotension in HER2-positive breast cancer patients experiencing cardiac dysfunction.
Multicenter case experience detailing two hypotensive breast cancer patients during HER2-targeted therapy.
Initiation and titration of midodrine were performed to stabilize blood pressure.
Facilitated cardioprotective therapy with beta-blockers or sodium–glucose cotransporter-2 inhibitors.
Both patients stabilized their blood pressure and were able to tolerate guideline-directed medical therapy.
Recovery of left ventricular systolic function was observed after midodrine use.
Continuation of HER2-directed therapy occurred without worsening heart failure or significant adverse effects.

Study Design

Type

Case Report (n=2)

Multicenter

Yes

Structured PICO

Does midodrine facilitate the use of guideline-directed medical therapy and improve left ventricular recovery in hypotensive patients with HER2 therapy-related cardiac dysfunction?

Population

n=2 hypotensive breast cancer patients who developed cancer-therapy-related cardiac dysfunction (CTRCD) during HER2-targeted therapy and were unable to tolerate guideline-directed medical therapy due to symptomatic hypotension.

Intervention

Initiation and titration of midodrine to facilitate cardioprotective therapy (beta-blockers and/or sodium-glucose cotransporter-2 inhibitors).

Outcome

Stabilization of blood pressure, facilitation of cardioprotective therapy, and recovery of left ventricular systolic function.

Midodrine may be a feasible strategy to augment blood pressure and enable the use of cardioprotective therapies in hypotensive patients with cancer therapy-related cardiac dysfunction.

Limitations

Small sample size precludes conclusions about efficacy or safety
Concomitant use of cardioprotective agents makes it impossible to attribute LVEF recovery to any single intervention
Absence of comprehensive cardiac biomarkers (GLS, troponin, natriuretic peptides)
The two cases represent different institutions with different clinical approaches, limiting direct comparability

Abstract

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. 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. 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.

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