| Project/Area Number |
06670709
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Mie University |
|---|
Principal Investigator |
YAMAKADO Tetsu Mie University, Department : University Hospital, Position : Assistant Professor, 医学部・附属病院, 講師 (40122121)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
IMANAKA Kyoko (YOSHIDA Ky) Mie University, Department : Faculty of Medicine, Position : Assistant Professor, 医学部, 助手 (00242967)
|
|---|
| Project Period (FY) |
1994 – 1995
|
| Project Status |
Completed (Fiscal Year 1995)
|
| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
|
|---|
| Keywords | Cardiac hypertrophy / Myocardial ischemia / Angiogenesis / 肥大心 |
|---|
| Research Abstract |
The purpose of this study was to investigate coronary angiogenesis and myocardial ischemia in left ventricular hypertrophy. First, we assessed left ventricular global and regional dynamics in response to pacing tachycardia in patients with hypertrophic cardiomyopathy. We investigated left ventricular global and regional systolic and diastolic function in 17 patients with hypertrophic cardiomyopathy and 7 control normal subjects by analyzing left ventricular angiograms and simultaneously obtained high fidelity left ventricular pressures before and after rapid cardiac pacing (150 beats/min). There were no significant changes in left ventricular function after pacing in normal subjects. In hypertrophic cardiomyopathy, the ejection fractions remained unchanged. However, left ventricular end-diastolic pressures rose (+12 mmHg, p<0.01), and the time constants of isovolumic pressure decay were significantly increased (T_<l/z> ; +4.2 msec, P<0.01, T_<l/e> ; +5.8 msec, p<0.01). The early diastolic peak filling rates were unchanged. The left ventricular global diastolic pressure-volume relationships and regional diastolic pressure-area relationships of each area of regional myocardium shifted upward in all patients. These diastolic abnormalities were not accompanied by regional asynchrony or asynergy. Most patients with hypertrophic cardiomyopathy have a reduced reactive capacity to chronotropic stress, which is hemodynamically characterized by evenly distributed diastolic dysfunction. Second, we developed a perinephritic hypertensin model in dogs. We are now analyzing relationship between left ventricular hemodynamics and coronary angiogenesis in this model.
|
