scholarly journals Longitudinal myocardial function is more compromised in cardiac Syndrome x compared to insignificant CAD: Role of stress echocardiography and calcium scoring

2021 ◽  
Author(s):  
Ibadete Bytyçi ◽  
Tarek M Bengrid ◽  
Michael Y Henein
Keyword(s):  
Stress Echocardiography ◽  
Myocardial Function ◽  
Syndrome X ◽  
Calcium Scoring ◽  
Cardiac Syndrome X ◽  
Cardiac Syndrome

scholarly journals TCTAP A-103 Cardiac Syndrome X – The Role of Endothelial Dysfunction

2016 ◽  
Vol 67 (16) ◽  
pp. S49-S50
Author(s):  
Ashwin Lysander ◽  
Sujai Nikhil Ramakrishnan ◽  
Raghava Chowdary ◽  
Ashish Kansal ◽  
Sri Vidhya
Keyword(s):  
Endothelial Dysfunction ◽  
Syndrome X ◽  
Cardiac Syndrome X ◽  
Cardiac Syndrome

scholarly journals Cardiac syndrome X. the possible role of Na+-Li+-countertransport activity and other pathophysiological mechanisms in pathogenesis

2013 ◽  
Vol 94 (3) ◽  
pp. 355-361
Author(s):  
V N Oslopov ◽  
Y V Oslopova ◽  
D V Borisov
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Vascular Dysfunction ◽  
Syndrome X ◽  
Cardiac Syndrome X ◽  
Pathophysiological Mechanisms ◽  
Cardiac Syndrome ◽  
Number Of Patients

There are numerous pathophysiological mechanisms unequally responsible for the cardiac syndrome X development. The most important is endothelium and smooth muscle cells dysfunction that can intensify vasoconstriction and depress both endothelium-dependant and endothelium-independent vasodilatation, finally leading to coronary micro vascular dysfunction as the basis of the cardiac syndrome X pathogenesis. Together with other possible mechanisms of pathogenesis, studying the importance of increased cell membrane Na+-Li+-countertransport activity seems promising. If was found that a significant number of patients with cardiac syndrome X have increased Na+-Li+-countertransport activity, which is an in vitro marker of Na+-H+-antiporter. Therefore, it is important to measure Na+-Li+-countertransport speed in patients with coronary heart disease, because its high levels increases the chance for cardiac syndrome X, which is a coronary heart disease with no anatomic signs of coronary arteries involvement.

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