Myocardial adaptive changes and damage in ischemic heart disease.
Changes in two of the elements of myocardial subcellular organelles relating to cardiac energetics, ventricular myosin isozymes and mitochondrial DNA mutations, were examined using left ventricular tissue samples obtained at autopsy from patients with ischemic heart disease. Myosin isozymes were examined in tissues from nine patients with ischemic heart disease and 12 control patients with cancer but no heart disease. Extracted myosin was separated by pyrophosphate gel electrophoresis. The relative concentration of each component was determined by densitometry. Mitochondrial DNA mutations were evaluated in tissues from ten patients with myocardial infarction and 11 control patients with cancer but no heart disease. DNA was extracted and mitochondrial DNA mutations were detected by the polymerase chain reaction. Two bands were revealed by pyrophosphate gel electrophoresis. These contained VM-A, which exhibited faster electrophoretic mobility and was present in lower concentrations, and VM-B, which had a lower mobility and a higher concentration, respectively. SDS polyacrylamide gel electrophoresis showed that these two components contained the heavy chain and light chains 1 and 2 of myosin. VM-A concentrations tended to be higher in patients with ischemic heart disease than in controls. A 7.4-kb deletion was detected between the D-loop and the ATPase 6 genes of mitochondrial DNA from the myocardium of 6 out of 10 patients with myocardial infarction. The relative amounts of the two myosin isozymes could be altered by ischemic heart disease, although the functional significance of these components is unclear. The changes in the two myosin isozymes might be an adaptive change to disordered energy metabolism, but this change was small. The myocardial mitochondrial DNA deletions in patients with myocardial infarction were thought to result from ischemic damage.
Takeda
N
N
Department of Internal Medicine, Aoto Hospital, Jikei University School of Medicine, Tokyo, Japan.
Ota
Y
Y
Tanaka
Y
Y
Shikata
C
C
Hayashi
Y
Y
Nemoto
S
S
Tanamura
A
A
Iwai
T
T
Nakamura
I
I
D004272:DNA, Mitochondrial / Q000235:genetics*; D006352:Heart Ventricles / Q000201:enzymology / Q000473:pathology; D006801:Humans; D007527:Isoenzymes / Q000032:analysis*; D009154:Mutation; D017202:Myocardial Ischemia / Q000201:enzymology / Q000235:genetics; D009218:Myosins / Q000032:analysis*
D004272:DNA, Mitochondrial; D007527:Isoenzymes; D009218:Myosins