Relations Among Coronary Flow Reserve, Left Ventricular Mass and Diastolic Function in Patients with Chest Pain and Normal Coronary Angiograms.
10.4070/kcj.2000.30.3.287
- Author:
Hojun RHEE
;
Do Sun LIM
;
Hong Euy LIM
;
Sung Hee SHIN
;
Young Jae OH
;
Gyo Seung HWANG
;
Young Hoon KIM
;
Hong Seog SEO
;
Wan Joo SHIM
;
Dong Joo OH
;
Young Moo RO
- Publication Type:Original Article
- Keywords:
Hypertension;
Left ventricular hypertrophy;
Coronary flow reserve;
Diastolic function
- MeSH:
Adenosine;
Blood Flow Velocity;
Chest Pain*;
Coronary Artery Disease;
Deceleration;
Humans;
Hypertension;
Hypertrophy;
Hypertrophy, Left Ventricular;
Relaxation;
Risk Factors;
Thorax*
- From:Korean Circulation Journal
2000;30(3):287-294
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND PURPOSE: Left ventricular hypertrophy (LVH) is a well known cardiovascular risk factor, independent of hypertension, even in the absence of epicardial coronary artery disease. Possible mechanisms have been proposed, including increased LV mass, reduced coronary flow reserve (CFR) and diastolic filling abnormalities. However, the relations among LV hypertrophy, diastolic function, hypertension and coronary flow reserve (CFR) in patients with chest pain and normal coronary angiograms have not been well defined. SUBJECTS AND METHOD: Twenty-six patients with chest pain and normal coronary angiograms were included. LV mass, isovolumic relaxation time (IVRT), deceleration time (DT) and E/A ratio were assessed by 2-D echo-cardiography. Coronary blood flow velocity before and after intracoronary adenosine were measured using intracoronary Doppler wire (FIoWire). CFR was defined as ratio of peak flow velocity after adenosine to baseline flow velocity. Subjects were devided into 4 groups according to presence of LVH and hypertension and the parameters were compared among groups. RESULTS: FR was lower (p<0.01) in the groups with either hypertension or LVH or both than in the groups without them. The decrement in CFR was not linearly related to the degree of LVH (r=0.31, p=0.135). Although there were modest increment in IVRT and DT and decrement in E/A ratio in the groups with hypertension or LVH or both, there was no statistical significance. CONCLUSION: These findings suggest that the underlying mechanism of impaired CFR in patients with LVH or hypertension may be the consequence of primary coronary microvascular lesion rather than the process of left ventricular hypertrophy.
