Atrial and ventricular isomyosin composition in patients with different forms of cardiac hypertrophy.
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.
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D001706:Biopsy; D006332:Cardiomegaly / Q000378:metabolism*; D009202:Cardiomyopathies / Q000378:metabolism*; D006325:Heart Atria / Q000378:metabolism; D006352:Heart Ventricles / Q000378:metabolism; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D009218:Myosins / Q000378:metabolism*
D007527:Isoenzymes; D000251:Adenosine Triphosphatases; D009218:Myosins