title: Myocardial sympathetic innervation, function, and oxidative metabolism in non-infarcted myocardium in patients with prior myocardial infarction.
abstract: OBJECTIVE
  The purpose of this study was to investigate the relationship between sympathetic innervation, contractile function, and the oxidative metabolism of the non-infarcted myocardium in patients with prior myocardial infarction.
  
  
  METHODS
  In 19 patients (14 men, 5 women, 65 ± 9 years) after prior myocardial infarction, sympathetic innervation was assessed by (11)C-hydroxyephedrine (HED) positron emission tomography (PET). Oxidative metabolism was quantified using (11)C-acetate PET. Left ventricular systolic function was measured by echocardiography with speckle tracking technique.
  
  
  RESULTS
  The (11)C-HED retention was positively correlated with left ventricular ejection fraction (LVEF) (r = 0.566, P < 0.05), and negatively with peak longitudinal strain in systole in the non-infarcted myocardium (r = -0.561, P < 0.05). Kmono, as an index of oxidative metabolism, was significantly correlated with rate pressure product (r = 0.649, P < 0.01), but not with (11)C-HED retention (r = 0.188, P = 0.442). Furthermore, there was no significant correlation between Kmono and LVEF (r = 0.106, P = 0.666) or peak longitudinal strain in systole (r = -0.256, P = 0.291) in the non-infarcted myocardium. When the patients were divided into two groups based on the median value of left ventricular end-systolic volume index (LVESVI) (41 mL), there were no significant differences in age, sex, and rate pressure product between the groups. However, the large LVESVI group (>41 mL) was associated with reduced (11)C-HED retention and peak longitudinal strain in systole, whereas Kmono was similar between the groups.
  
  
  CONCLUSIONS
  This study indicates that remodeled LV after myocardial infarction is associated with impaired sympathetic innervation and function even in the non-infarcted myocardial tissue. Furthermore, oxidative metabolism in the non-infarcted myocardium seems to be operated by normal regulatory mechanisms rather than pre-synaptic sympathetic neuronal function.
authors.affiliation: Department of Cardiology, Kanazawa Medical University, Uchinada, Ishikawa, Japan.
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Aoki
authors.forename: Ichiro
authors.initials: I
authors.lastname: Matsunari
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Nomura
authors.forename: Wataru
authors.initials: W
authors.lastname: Fujita
authors.forename: Ryoko
authors.initials: R
authors.lastname: Komatsu
authors.forename: Yoshiharu
authors.initials: Y
authors.lastname: Miyazaki
authors.forename: Stephan G
authors.initials: SG
authors.lastname: Nekolla
authors.forename: Kouji
authors.initials: K
authors.lastname: Kajinami
mesh_terms: D000368:Aged; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000294:innervation*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction; D049268:Positron-Emission Tomography; D013564:Sympathetic Nervous System / Q000503:physiopathology*