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Pathogenesis of ventricular hypertrophy
Insights
Heart growth shifts from cell division (hyperplasia) to cell enlargement (hypertrophy) after birth. This transition, crucial for cardiac development and response to stress, involves complex molecular mechanisms.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Cellular Physiology
Background:
- Vertebrate heart growth involves myocardial cell hyperplasia during embryonic/fetal stages.
- Postnatally, heart growth relies on myocardial cell hypertrophy and nonmuscle cell hyperplasia, increasing cell volume 30-40 fold.
- The shift from hyperplastic to hypertrophic growth is linked to binucleated cell formation but the mechanism is unclear.
Purpose of the Study:
- To elucidate the mechanisms of cardiac growth and adaptation to stress.
- To understand the transition from hyperplastic to hypertrophic myocardial growth.
- To identify stimuli and structural remodeling involved in cardiac hypertrophy.
Main Methods:
- The study describes developmental changes in myocardial cell growth patterns.
- It analyzes the heart's response to increased workload at different life stages.
- It reviews known stimuli for cardiac hypertrophy.
Main Results:
- Postnatal heart growth is characterized by myocardial cell hypertrophy and nonmuscle cell hyperplasia.
- Increased workload in early life promotes hyperplasia, while in older animals it induces hypertrophy.
- Cardiac hypertrophy involves cellular enlargement, structural remodeling, and is stimulated by pressure/volume overload and neurohumoral factors.
Conclusions:
- Cardiac growth strategies differ significantly between fetal/neonatal and older animals.
- Understanding these growth patterns is key to comprehending heart adaptation to physiological and pathological stress.
- Further research is needed to clarify the molecular basis of the hyperplastic-to-hypertrophic transition.
Abstract:
Growth of the vertebrate heart during embryonic and fetal life is characterized by hyperplasia of myocardial cells. Shortly after birth, myocardial cells lose the capability of dividing, and further growth of the heart is due to myocardial cell hypertrophy and nonmuscle cell hyperplasia. This process results in a 30- to 40-fold increase in volume of individual myocardial cells during normal postnatal growth and maturation. The transition from hyperplastic to hypertrophic growth is related to formation of binucleated myocardial cells as a result of karyokinesis without cytokinesis. The molecular mechanism of this transition is uncertain. The response of the heart to increased metabolic demands or an increased work load depends on the age of the animal at the time when the stress is imposed. Increased myocardial work loads in fetal or early neonatal life lead to cardiac enlargement by causing an increased rate of hyperplasia of myocardial cells or continuation of hyperplasia beyond the normal period of hyperplastic growth. In contrast, imposition of increased loads on the hearts of older animals results in cardiac hypertrophy due to enlargement of myocardial cells and hyperplasia of nonmuscular components. In addition to cellular enlargement, structural remodeling of the myocardial cells and of the chambers of the heart occurs during the development of hypertrophy. Important stimuli of cardiac hypertrophy include increased systolic force or tension generated by the myocardial fibers (pressure overload), increased end-diastolic wall stress (volume overload) and neurohumoral factors such as increased circulating catecholamines or discharge of cardiac sympathetic nerves, or both, activation of the renin-angiotensin system and increased levels of thyroxine and growth hormone.(ABSTRACT TRUNCATED AT 250 WORDS)