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Updated: Aug 20, 2026
Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Calcium handling in post-infarction arrhythmias - evidence from large animals
Tristan Hellstrand1, Godfrey L Smith1,2, Mathis Korseberg Stokke1
1Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
Insights
Altered sarcoplasmic reticulum calcium handling contributes to ventricular arrhythmias post-myocardial infarction (MI) in humans and large animals. Further research is needed to clarify mechanisms and develop new therapies.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Ventricular arrhythmias post-myocardial infarction (MI) are a significant clinical challenge.
- Rodent models suggest sarcoplasmic reticulum (SR) calcium handling is crucial, but rodent cardiac electrophysiology differs from humans.
- Insights from large animal and human studies are needed to understand human pathophysiology.
Purpose of the Study:
- To summarize existing literature on the role of SR calcium handling in ventricular tachyarrhythmias after the acute phase of MI.
- To focus on evidence from large animal and human studies.
Main Methods:
- Systematic literature search for original articles on calcium handling after MI in large animals and humans.
- Summarized key findings and assessed risk of bias.
Main Results:
- Twenty-five studies involving cellular calcium handling in large animals or human tissue post-MI were included.
- Ambiguous findings on calcium transient amplitude and kinetics.
- Consistent evidence of increased calcium sparks, calcium waves, delayed afterdepolarizations, and reduced t-tubule density.
- Some studies reported increased calcium alternans propensity.
Conclusions:
- Altered SR calcium handling is implicated in ventricular arrhythmias following MI in large animals and humans.
- Current evidence is limited, necessitating further investigation.
- More studies in relevant models are required for mechanistic understanding and therapeutic development.
Abstract:
Understanding the causes of ventricular arrhythmias after myocardial infarction (MI) remains a major challenge to academic and clinical medicine. Key concepts in the pathophysiology underlying such events are based on studies in rodents, in whom altered sarcoplasmic reticulum (SR) calcium handling is key even in chronic stages after MI. Since cardiac electrophysiology in rodents has important differences from humans, an overview of insights directly from large animals and humans is needed. Our objective was to provide a summary of existing literature on the role of SR calcium handling in ventricular tachyarrhythmias after the acute phase of MI in large animals and humans. We conducted a systematic search of original articles on calcium handling after MI in large animals and humans, summarized key findings, and assessed risk of bias in the included articles. Twenty-five studies explicitly measuring cellular calcium handling after MI in large animals or human tissue were included. Overall, the studies were somewhat ambiguous regarding calcium transient amplitude and kinetics; but consistently showed increased frequency of calcium sparks, calcium waves, delayed afterdepolarizations and reduced t-tubule density; and some reported increased propensity for calcium alternans. Abundance and posttranslational modification of calcium handling proteins were less consistent. In conclusion, existing evidence from large animals and human material supports a role for altered calcium handling in ventricular arrhythmias after MI. However, the evidence is still limited. More studies in such models are needed to provide mechanistic explanations that can be used as a basis for development of new therapies.
