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Atrial and ventricular isomyosin composition in patients with different forms of cardiac hypertrophy
1Dept. of Pharmacology, University of Zürich, Switzerland.
Insights
Cardiac hypertrophy involves changes in myosin heavy and light chains, with atrial myosin light chain-1 (ALC-1) increasing in ventricles under certain conditions. This suggests ALC-1 may influence myofibril contractile properties and wall stress.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Biochemistry
Background:
- Cardiac hypertrophy, characterized by increased heart muscle mass, presents diverse hemodynamic and angiographic profiles.
- Morphologically, hypertrophic states are similar regarding muscle fiber diameter and non-muscle tissue content.
- Contractile dysfunction, ranging from impairment to hypercontractility, accompanies these hypertrophic states.
Purpose of the Study:
- To investigate changes in myosin heavy chain (HC) and myosin light chain (LC) isoform expression in various human cardiac hypertrophic states.
- To determine if atrial myosin light chain-1 (ALC-1) expression in ventricular tissue correlates with specific conditions or hemodynamic parameters.
- To explore the independent regulation of myosin HC and LC isoform expression in response to cardiac workload.
Main Methods:
- Analysis of peptide patterns of myosin heavy chain (HC) types VM-3 (slow ventricular) and fast atrial type.
- Quantification of myosin light chain-2 (VLC-2) and atrial type ALC-1 in ventricular tissue across different cardiac conditions.
- Correlation analysis between ALC-1 content and peak circumferential wall stress.
Main Results:
- Ventricular myosin HC type VM-3 peptide patterns remain unchanged in chronic workload increase.
- Fast atrial type HC expression changes, and atrial type ALC-1 is found in ventricular tissue in certain hypertrophies (e.g., dilated cardiomyopathy, pressure/volume overload).
- ALC-1 ventricular content significantly correlates with peak circumferential wall stress, but not in hypertrophic cardiomyopathy or coronary heart disease without infarction.
Conclusions:
- Myosin HC and LC isoform expression are independently regulated in response to altered cardiac physiological or pathological conditions.
- The presence and level of atrial type ALC-1 in ventricular tissue may be linked to specific hypertrophic states and wall stress.
- ALC-1 involvement in myofibril contractile properties is suggested by its correlation with ventricular wall stress.
Abstract:
In man, various forms of compensatory and idiopathic hypertrophic states can be differentiated by haemodynamic and angiographic parameters. They are morphologically indistinguishable with regard to muscle fibre diameter and non-muscle tissue content. They are, however, accompanied by contractile dysfunction of various degrees or even by hypercontractility. In hearts subjected to chronic increase in workload the peptide pattern of the slow ventricular myosin heavy chain (HC) type VM-3 does not change, while that of the fast atrial type HC does. In atria also the ventricular type of myosin light chain-2 (VLC-2) is occurring. In certain forms of hypertrophy we found the atrial type ALC-1 occurring in the ventricular tissue, in individual cases amounting to 30% of total LC-1, on average, 12% in dilated cardiomyopathy, 6% in pressure and 3% in volume overload and 2% in cases with reduced myocardial mass due to infarction. No such increase of ALC-1 was found in hypertrophic cardiomyopathy or in coronary heart disease without infarction. The isoform expression of myosin HC and LC is thus governed independently of one another in response to altered physiological or pathological conditions. A significant correlation of the ALC-1 content in ventricles could be established with the peak circumferential wall stress. This may imply the involvement of the LC-1 in the contractile properties of the myofibrils.