Concentric versus eccentric remodeling
1Department of Medicine, Baylor College of Medicine Medical, Houston, and Houston Veterans Affairs Medical Center, Houston, Texas, USA.
Insights
Cardiac hypertrophy compensates for heart overload through protein synthesis or reduced degradation. Non-mechanical factors influence the extent of this cardiac response, impacting heart muscle mass.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Cardiac hypertrophy is a heart response to pressure or volume overload.
- It's traditionally viewed as a feedback loop normalizing cardiac function.
- However, the degree of hypertrophy doesn't always match the overload severity.
Purpose of the Study:
- To investigate non-mechanical mechanisms modulating cardiac hypertrophy.
- To understand how mechanical signals translate into myocardial mass increase.
- To differentiate protein synthesis and degradation roles in pressure vs. volume overload.
Main Methods:
- The study focuses on the balance between myocardial protein synthesis and degradation rates.
- It analyzes the differential impact of pressure overload versus volume overload.
- The research infers mechanisms based on observed hypertrophy levels and known physiological processes.
Main Results:
- In pressure overload, cardiac hypertrophy occurs due to increased protein synthesis.
- In volume overload, hypertrophy results from decreased protein degradation.
- Non-mechanical factors play a crucial role in regulating the hypertrophic response.
Conclusions:
- Cardiac hypertrophy's extent is modulated by non-mechanical pathways.
- Protein synthesis drives hypertrophy in pressure overload.
- Reduced protein degradation drives hypertrophy in volume overload.
Abstract:
Cardiac hypertrophy has long been recognized as one of the heart's mechanisms for compensating a pressure or volume overload. This compensation has often been viewed as a feedback loop in which the concentric hypertrophy, which develops in pressure overload, normalizes wall stress while the eccentric hypertrophy, which develops in volume overload, allows for an increase in total stroke volume to compensate that which is lost from regulation. While the concentric hypertrophy of pressure overload often is compensatory, many examples are noted where either too little hypertrophy occurs to normalize stress or in other cases, in which hypertrophy exceeds the amount needed for normalization. These observations invoke nonmechanical mechanisms which modulate the degree to which the mechanical signal of pressure overload is translated into an increase in myocardial mass. Hypertrophy develops when the rate of myocardial protein synthesis exceeds that of protein degradation. It now appears that in pressure overload this imbalance is created as synthesis rate increases while in volume overload hypertrophy appears to accrue because degradation rate decreases.
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