scholarly journals Assessment of left ventricular dysfunction by thallium-201 lung uptake during exercise in coronary artery disease.

1983 ◽  
Vol 47 (4) ◽  
pp. 381-390 ◽  
Author(s):  
KATSUMI MINAMIJI ◽  
KAZUMI MAEDA ◽  
YOSHIHARU NAKASHIMA ◽  
TEISHI KAJIYA ◽  
YOSHIAKI OHMORI ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Thallium 201 ◽  
Lung Uptake ◽  
Artery Disease

scholarly journals Impact of Renin-Angiotensin-Aldosterone System Gene Polymorphisms on Left Ventricular Dysfunction in Coronary Artery Disease Patients

2012 ◽  
Vol 32 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Avshesh Mishra ◽  
Anshika Srivastava ◽  
T. Mittal ◽  
N. Garg ◽  
B. Mittal
Keyword(s):  
Coronary Artery Disease ◽  
Cardiac Output ◽  
Coronary Artery ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
P Value ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Artery Disease

Background: Left ventricular dysfunction (LVD), followed by fall in cardiac output is one of the major complications in some coronary artery disease (CAD) patients. The decreased cardiac output over time leads to activation of the renin-angiotensin-aldosterone system which results in vasoconstriction by influencing salt-water homeostasis. Therefore, the purpose of the present study was to explore the association of single nucleotide polymorphisms (SNPs) in angiotensin I converting enzyme;ACE(rs4340), angiotensin II type1 receptor; AT1 (rs5186) and aldosterone synthase;CYP11B2(rs1799998) with LVD.Methods and results: The present study was carried out in two cohorts. The primary cohort included 308 consecutive patients with angiographically confirmed CAD and 234 healthy controls. Among CAD, 94 with compromised left ventricle ejection fraction (LVEF ≤ 45) were categorized as LVD. The ACE I/D, AT1 A1166C andCYP11B2T-344C polymorphisms were determined by PCR. Our results showed that ACE I/D was significantly associated with CAD but not with LVD. However, AT1 1166C variant was significantly associated with LVD (LVEF ≤ 45) (p value=0.013; OR=3.69), butCYP11B2(rs1799998) was not associated with either CAD or LVD. To validate our results, we performed a replication study in additional 200 cases with similar clinical characteristics and results again confirmed consistent findings (p value=0.020; OR=5.20).Conclusion: AT1 A1166C plays important role in conferring susceptibility of LVD.

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