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Published on: June 14, 2016
Basic determinants of myocardial hypertrophy: a review of molecular mechanisms
1Department of Medicine, Medical University of South Carolina, Charleston 29425, USA.
Insights
Cardiac hypertrophy, an increase in heart muscle mass, can fail to compensate for increased hemodynamic load. This leads to heart failure due to abnormal contractile performance, emphasizing the need to view cardiac hypertrophy as a growth process.
Area of Science:
- Cardiology
- Physiology
- Molecular Biology
Background:
- The heart's primary response to increased hemodynamic load is cardiac hypertrophy.
- Compensated cardiac hypertrophy can maintain organ-level function despite increased workload.
Purpose of the Study:
- To understand the mechanisms underlying the failure of cardiac hypertrophy to prevent congestive heart failure.
- To identify cardiac hypertrophy as a growth process critical for developing interventions.
Main Methods:
- The study reviews existing literature on cardiac hypertrophy and hemodynamic load.
- It analyzes the phenotypic changes in myocardium during hypertrophy.
- It correlates these changes with contractile performance and heart failure outcomes.
Main Results:
- Cardiac hypertrophy can be abrogated by progressive contractile dysfunction per unit of myocardium.
- Phenotypic changes during hypertrophy are dependent on the type of hemodynamic load.
- These changes lead to imperfect compensation and eventual congestive heart failure.
Conclusions:
- Cardiac hypertrophy must be understood as a growth process to develop early interventions.
- Preventing congestive heart failure requires addressing the specific phenotypic changes in hypertrophied myocardium.
- Understanding the load-dependent nature of these changes is crucial for therapeutic strategies.
Abstract:
The essential cardiac response to a fixed increase in hemodynamic load is an increase in cardiac mass. If the load increase is neither too severe initially nor indefinitely progressive, cardiac stress is renormalized, and compensated hypertrophy ensues. But hypertrophic compensation is often abrogated by progressively abnormal contractile performance per unit mass of myocardium, even when function at the organ level is maintained by the mass increase itself. That is, even when hypertrophy is appropriate to the load imposed, and in a manner analogous to dystrophic growth of skeletal muscle, specific phenotypic changes occurring during this growth response render compensation imperfect such that congestive heart failure ensues. This fact, and the fact that the presence of deleterious phenotypic changes in hypertrophied myocardium is critically dependent on the type of hemodynamic load imposed, mandates that cardiac hypertrophy be understood on the most basic level as a growth process if early, definitive interventions to prevent congestive heart failure following pathological hemodynamic overloads are to be realized.
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