Myocardial sympathetic innervation, function, and oxidative metabolism in non-infarcted myocardium in patients with prior myocardial infarction.

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 C-hydroxyephedrine (HED) positron emission tomography (PET). Oxidative metabolism was quantified using C-acetate PET. Left ventricular systolic function was measured by echocardiography with speckle tracking technique. Results: The 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 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 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. [ABSTRACT FROM AUTHOR]