We demonstrated that MTG content was significantly higher in the LGE (−) group than in the LGE (+) group. In addition, MTG content was associated with LV ejection fraction, LV end-diastolic volume, LV end-systolic volume, and LV mass. In multivariate analysis, LV ejection fraction had an independent association with MTG content. There are no reports of MRS performed on sites with delayed contrast images.
The LGE (−) group had a higher MTG content than the LGE (+) group. MTG has been reported to be associated with aging and metabolic disorders that increase free fatty acids, such as obesity, diabetes mellitus and fatty liver [9, 23–25]. The triglyceride pool was reactively enlarged under a high concentration of fatty acid in the myocardium to absorb the excess fatty acid and avoid cardiotoxicity . In our data, although there is no significant difference between the two groups, the LGE (+) group had higher BMI, more patients with diabetes mellitus and a higher level of transaminases suggesting fatty liver. These factors suggesting metabolic abnormalities inherently increase MTG in the LGE (+) group. On the other hand, the LGE (−) group tended to be older, and MTG is increased by aging. However, even considering there factors, these may be a metabolic abnormality specific to HCM that is responsible for the higher MTG in the LGE (−) group.
Thickened septum is thought to contain abnormal myocardium. Visual loss of midline cricothyroid muscle structure has been reported in the ventricular septum of subjects with HCM, especially in cases of asymmetric septal thickening. Therefore, the septum of subjects with HCM with ASH is thought to contain a complex arrangement of abnormal myocardium . Although LGE is thought to be consistent with myocardial fibrosis, the LGE in the ventricular septum is thought to be an increase in interstitium due to the complex arrangement. In our method, MTG is calculated by dividing the signal of the fat component by the signal of the water component. If there is more extracellular fluid, MTG will inevitably decrease. Another possibility is that because LGE reflects fibrosis of the myocardium, MTG will inevitably decrease in fibrotic myocardium if the fibroblast is already in an energy-depleted state.
Another possibility is that the metabolism of cardiomyocytes is different in abnormal myocardium compared with normal myocardium. A decrease in intracellular creatine has been reported to be observed in HCM from the beginning of the disease . Because adenosine diphosphate (ADP) is originally transformed into adenosine triphosphate (ATP) using creatine as a catalyst, a decrease in creatine causes an increase in intracellular ADP and an increase in Ca2+ concentration . High ADP levels reported to impair relaxation of hearts via ADP-mediated defects in sarcomere function in an animal study , and ADP increased myofilament Ca2+ sensitivity in HCM patients . Increased binding of Ca2+ to the myofilaments by way of increased Ca2+ sensitivity will reduce Krebs cycle activity. Consequently, impaired sarcomere energetics may thus provoke mitochondrial dysfunction, which may increase MTG by reducing the efficiency of fatty acid oxidation. These findings suggest that MTG tends to accumulate from the early stage of the disease and may decrease as the disease progress.
MTG significantly related to morphologic parameters, such as LV ejection fraction, LV end-diastolic volume, LV end-systolic volume, and LV mass. Several studies have reported a positive correlation between MTG and LV mass in patients with diabetes mellitus, and obesity, and increased LV mass was accompanied by both increased LV concentricity and a subtle decrease in regional systolic performance. In addition, there are similar reports that increased MTG content leads to disturbance of LV systolic and diastolic functions [9, 11, 24]. In contrast, we have previously shown that MTG is negatively correlated with LV ejection fraction, LV end-diastolic volume, LV end-systolic volume, and LV mass in athletes and healthy subjects . These differences suggest that the implications of MTG differ between cardiomyopathy and normal myocardium. Especially in HCM, sarcomere energetics is impaired due to genetic predisposition as described above, and myocardial metabolism is thought to be very different. Further research focusing on myocardial metabolism is required.