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Cellular basis for improved left ventricular pump function after digoxin therapy in experimental left ventricular

W S McMahon¹, H H Holzgrefe, J D Walker

¹Division of Pediatric Cardiology, Medical University of South Carolina, Charleston 29425, USA.

Journal of the American College of Cardiology

|August 1, 1996

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Digoxin treatment improved left ventricular (LV) function and myocyte performance in a canine model of LV failure. This study suggests digoxin has direct, beneficial cellular effects on contractile function and electrophysiology in heart failure.

Area of Science:

Cardiology
Pharmacology
Cellular Biology

Background:

Digoxin is a key treatment for chronic left ventricular (LV) dysfunction.
Direct effects of digoxin on myocyte function and electrophysiology in LV failure are not well understood.

Purpose of the Study:

To investigate the impact of long-term digoxin on LV and myocyte contractile performance and electrophysiology in a rapid pacing-induced LV failure model.
To explore the cellular mechanisms underlying digoxin's therapeutic effects in heart failure.

Main Methods:

Utilized a canine model with rapid pacing to induce left ventricular (LV) failure.
Administered digoxin (0.25 mg/day) during the pacing period.
Assessed LV function, isolated myocyte shortening velocity, and action potential characteristics.

Related Experiment Videos

Main Results:

Digoxin improved LV ejection fraction and myocyte shortening velocity compared to rapid pacing alone.
Digoxin normalized action potential maximal upstroke velocity and duration in myocytes.
LV end-diastolic volume remained elevated but showed improvement with digoxin.

Conclusions:

Long-term digoxin treatment enhances LV pump function and myocyte contractile performance in LV failure.
Digoxin exerts direct, beneficial effects on myocyte electrophysiology, contributing to improved cardiac function.
Provides cellular evidence for digoxin's efficacy in managing heart failure.