Related Experiment Video
Updated: Oct 7, 2026

Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling
Published on: August 1, 2016
Reduced cardiac myofibrillar Mg-ATPase activity without changes in myosin isozymes in patients with end-stage heart
A A Alousi1, A M Grant, J R Etzler
1Sterling Research Group, Rensselaer, NY.
Insights
Reduced myofibrillar ATPase activity in end-stage heart failure does not stem from myosin isozyme redistribution. This study found no significant changes in myosin isoenzyme patterns in diseased hearts, suggesting other mechanisms are at play.
Area of Science:
- Cardiology
- Biochemistry
- Molecular Biology
Background:
- End-stage heart failure is characterized by reduced cardiac function.
- Myofibrillar ATPase activity is crucial for heart muscle contraction.
- Altered myosin isozyme distribution has been proposed as a cause for reduced ATPase activity.
Purpose of the Study:
- To investigate if reduced myofibrillar ATPase activities in end-stage heart failure are linked to myosin isozyme redistribution.
- To compare ATPase activities and myosin isozyme patterns in normal and failing human hearts.
Main Methods:
- Isolation of cardiac myofibrils from human hearts (normal and end-stage failure).
- Measurement of myofibrillar Ca2(+)-dependent Mg-ATPase and myosin Ca2(+)- and K+EDTA-ATPase activities.
- Analysis of myosin isozyme distribution using polyacrylamide gel electrophoresis.
Main Results:
- Significant reduction in myofibrillar Ca2(+)-dependent Mg-ATPase observed in all studied heart failure models.
- No changes in myofibril sensitivity to Ca2+ were noted.
- Myosin Ca2(+)-ATPase was lower only in coronary artery disease hearts; K-EDTA ATPase showed no differences.
- Polyacrylamide gel electrophoresis revealed no apparent differences in myosin isoenzyme patterns between normal and diseased hearts.
Conclusions:
- Reduced myofibrillar ATPase activity in end-stage heart failure is not associated with myosin isozyme redistribution.
- The mechanisms underlying decreased ATPase activity in heart failure require further investigation.
- Further research is needed to clarify the ATPase nature of observed myosin bands.
Abstract:
In this study we tested the hypothesis that reduced myofibrillar ATPase activities in end-stage heart failure are associated with a redistribution of myosin isozymes. Cardiac myofibrils were isolated from left ventricular free wall from normal human hearts and hearts at end-stage heart failure caused by coronary artery diseases, cardiomyopathy or immunological rejection. The hearts had been excised in preparation for a heart transplant. Myofibrillar Ca2(+)-dependent Mg-ATPase and myosin Ca2(+)- and K+EDTA-ATPase activities were compared. Possible changes in myosin isozyme distribution in the diseased heart were investigated using polyacrylamide gel electrophoresis of native myosin in the presence of pyrophosphate. Significant reduction in myofibrillar Ca2(+)-dependent Mg-ATPase with no changes in the sensitivity of the myofibrils to Ca2+ was observed in heart with coronary artery diseases (25.2 to 27.1% at pCa 5.83 to pCa 5.05), cardiomyopathy (21.1 to 25.5% at pCa 5.41 to pCa 5.05), and in the immunologically rejected heart (18.4 to 22.8% at pCa 5.41 to pCa 5.05). Significantly lower myosin Ca2(+)-ATPase was observed with coronary artery diseases only and myosin K-EDTA activities did not differ in diseased and normal hearts. Polyacrylamide gel electrophoresis of native myosin from the normal and three models of end-stage heart failure revealed two distinct bands in the human left ventricle and one diffuse band in the human right atria. No apparent differences in myosin isoenzyme pattern were observed between the normal and diseased hearts. Further evaluation is needed to clarify the ATPase nature of the two bands.
Related Concept Videos
Pathophysiology of Heart Failure
Imbalances in Cardiac Output
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...
Heart Failure II: Pathophysiology
Heart Failure V: Medical Management
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cardiomyopathy V: Interprofessional Care

