| Project/Area Number |
16K19398
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Cardiovascular medicine
|
|---|
| Research Institution | Nagoya University |
|---|
Principal Investigator |
Ryota Morimoto 名古屋大学, 医学部附属病院, 病院助教 (00755499)
|
|---|
| Project Period (FY) |
2016-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
|---|
| Keywords | 肥大型心筋症 / アンモニアPET / 微小循環不全 / １３N アンモニアPET / 13N-アンモニアPET / 血管新生関連因子 / 収縮頻度連関 |
|---|
| Outline of Final Research Achievements |
Hypertrophic cardiomyopathy (HCM) is characterized by gradual thickening of the cardiac muscle and impairing myocardial blood flow (MBF). We assessed MBF undergoing NH3-PET and in order to perform transmural layer analysis, the reconstructed images were transferred to a workstation using PMOD software. We enrolled 17 control patients and 16 HCM patients. Even though there was no significant difference between control patients and HCM patients in subendocardial MBF at rest, hyperemic subendocardial MBF in HCM was significantly lower than normal patients (1.159±0.144 vs 1.422±0.202, p=0.0002). Furthermore, HOCM was significantly lower than apical HCM patients (1.32±0.18 vs 1.92±0.49). These results might relate the major cause of sudden cardiac death due to latent myocardial damage in HOCM patients.
|
| Academic Significance and Societal Importance of the Research Achievements |
循環不全とさまざまなパラメーターの直接的な関連が明らかとなれば、心筋症進展機序の解明に向けて新たな概念を提唱しうる可能性があり、予後予測や拡張障害に対する心不全治療として微小循環をターゲットにする新たな創薬について検討することが可能となり、臨床応用意義 は大きく、学術的波及効果も期待できる。
|
