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Excitation-contraction coupling in heart failure
1Laboratory of Cardiovascular Science, National Institute on Aging, Baltimore.
Insights
Cardiomyopathy alters myocardial calcium handling, a key part of the excitation-contraction cycle in the heart. These changes, similar to those in aged or hypertensive animals, can lead to heart failure by causing systolic or diastolic insufficiency.
Area of Science:
- Cardiology
- Physiology
- Molecular Biology
Background:
- Myocardial calcium (Ca2+) handling is central to the cardiac excitation-contraction (EC) cycle.
- Alterations in EC coupling are implicated in the pathophysiology of human heart failure.
Purpose of the Study:
- To investigate the role of altered myocardial Ca2+ handling in human cardiomyopathy.
- To understand how adaptive changes in EC mechanisms contribute to heart failure.
Main Methods:
- This study focuses on the physiological mechanisms of cardiac function.
- Analysis of cellular and molecular changes in myocardial tissue.
Main Results:
- Excitation-contraction coupling, specifically myocardial Ca2+ handling, is significantly altered in human cardiomyopathy.
- Adaptive changes in EC mechanisms seen in animal models of aging and hypertension are also observed in the failing human heart.
Conclusions:
- Altered myocardial Ca2+ handling is a critical feature of human cardiomyopathy.
- The progression of heart failure may be linked to maladaptive changes in EC coupling leading to impaired systolic or diastolic function.
Abstract:
A central feature of the excitation-contraction cycle-myocardial Ca2+ handling--is altered in humans with cardiomyopathy. Many adaptive changes in excitation-contraction mechanisms observed in aged or hypertensive animals also supervene in the failing human heart. Heart failure may thus emerge when such changes lead to systolic or diastolic insufficiency.