[Non-transmural anterior wall infarct: changes in myocardial energy metabolism in remaining vital myocardium].
To characterize energy metabolism in vivo after nontransmural anterior myocardial infarction, patients (group A, n = 19) with a stenosis of left anterior descending artery (LAD) and anterior wall hypokinesia by levocardiography were examined by phosphorus magnetic resonance spectroscopy (MRS). Spectra were compared to those of healthy volunteers (n = 15). The volume of interest was placed into the anterior myocardial wall by magnetic resonance imaging. Phosphorus spectra were recorded under optimal antiischemic medication. To separate the influence of coronary stenosis from that of the ischemic insult, additional patients (group B, n = 4) with LAD-stenosis but without left ventricular dysfunction were examined. The effect of antiischemic medication on the phosphorus spectra was evaluated in patient group C (n = 4), who had the same clinical features as group A. In these patients, MRS was first performed without antiischemic medication (washout period > one day) and then repeated during intravenous application of glyceroltrinitrate (GTN). Mean PCr/ATP-ratio was significantly lower in group A patients (1.24 +/- 0.18) than in healthy volunteers (1.74 +/- 0.23; p < 0.01 unpaired t-test). Patients with normal left ventricular function (group B) showed PCr/ATP-ratios (1.64 +/- 0.22) similar to those of normal controls (p = 0.23). After GTN infusion PCr/ATP-ratio of group C rose from 1.12 +/- 0.08 to 1.32 +/- 0.13 (p < 0.01 paired t-test). Thus, hypokinetic myocardium after nontransmural infarction is characterized by a larger decrease of the cellular energy buffer PCr compared to the myocardial ATP-content. These findings may reflect degenerative changes of myocytes due to disturbed microperfusion in viable areas of the infarct or remodeling processes of viable myocytes in the infarct region. Both mechanisms may lead to adaptive changes of cellular enzyme concentrations resulting in a reduced PCr content of the myocytes.
Moka
D
D
Klinik und Poliklinik für Nuklearmedizin, Universität zu Köln.
Sechtem
U
U
Theissen
P
P
Voth
E
E
Schicha
H
H
D000255:Adenosine Triphosphate / Q000378:metabolism; D000328:Adult; D000368:Aged; D003327:Coronary Disease / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D003937:Diagnosis, Differential; D004562:Electrocardiography / Q000295:instrumentation*; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000295:instrumentation*; D009682:Magnetic Resonance Spectroscopy / Q000295:instrumentation*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D009203:Myocardial Infarction / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D005996:Nitroglycerin / Q000627:therapeutic use; D010725:Phosphocreatine / Q000378:metabolism; D012815:Signal Processing, Computer-Assisted / Q000295:instrumentation*; D014665:Vasodilator Agents / Q000627:therapeutic use
D014665:Vasodilator Agents; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D005996:Nitroglycerin