TY - JOUR
T1 - Myocardial sympathetic innervation, function, and oxidative metabolism in non-infarcted myocardium in patients with prior myocardial infarction
AU - Aoki, Hirofumi
AU - Matsunari, Ichiro
AU - Nomura, Yusuke
AU - Fujita, Wataru
AU - Komatsu, Ryoko
AU - Miyazaki, Yoshiharu
AU - Nekolla, Stephan G.
AU - Kajinami, Kouji
N1 - Funding Information:
Acknowledgments This work was supported by Ishikawa prefectural government.
PY - 2013/7
Y1 - 2013/7
N2 - 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 11C-hydroxyephedrine (HED) positron emission tomography (PET). Oxidative metabolism was quantified using 11C-acetate PET. Left ventricular systolic function was measured by echocardiography with speckle tracking technique. Results: The 11C-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 11C-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 11C-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.
AB - 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 11C-hydroxyephedrine (HED) positron emission tomography (PET). Oxidative metabolism was quantified using 11C-acetate PET. Left ventricular systolic function was measured by echocardiography with speckle tracking technique. Results: The 11C-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 11C-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 11C-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.
KW - Myocardial infarction
KW - Oxidative metabolism
KW - Positron emission tomography
KW - Speckle tracking echocardiography
KW - Sympathetic innervation
UR - http://www.scopus.com/inward/record.url?scp=84880814804&partnerID=8YFLogxK
U2 - 10.1007/s12149-013-0716-6
DO - 10.1007/s12149-013-0716-6
M3 - Article
C2 - 23494212
AN - SCOPUS:84880814804
SN - 0914-7187
VL - 27
SP - 523
EP - 531
JO - Annals of Nuclear Medicine
JF - Annals of Nuclear Medicine
IS - 6
ER -