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I found this article and think it may be of interest to some especially us EDSers:

Left Ventricular Systolic Dysfunction

Left ventricular systolic dysfunction is primarily a difficulty of the left ventricle to empty or eject the blood from its chamber. It is defined in terms of left ventricular ejection fraction (
), which is a good clinical indicator of ventricular systolic function.

Left ventricular systolic dysfunction is a progressive process, which begins with injury to the myocardium. In the body’s efforts to compensate for this wall injury, the left ventricle wall thickens from increased impairment of myocardial contractility. The ventricle then eventually hypertrophies and dilates. This process changes the normal left ventricle geometrical shape from oval to spherical, which in turn decreases the mechanical performance as well as increases blood flow back through the mitral valve (mitral valve regurgitation). This change in shape occurs in a process called remodeling.

Ventricular remodeling is thought to proceed the development of heart failure symptoms by months to years. It is now believed that the body’s compensation to these cardiac abnormalities activates endogenous neurohormonal systems (e.g., angiotensin II, norepinephrine, aldosterone, endothelin, vasopressin, and cytokines), because heart failure patients have increased circulating and tissue levels of these neurohormones. Current disease management for heart failure centers on pharmacologic and non-pharmacologic treatments, which reduce or prevent cardiac remodelling.

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I have asked so many doctors about doing an angiotension II test on me. I was recently told by an endo. doc that they have no way of checking it. That test can only be done in a clinical setting that is conducting research.

I have thought that possibly the high angiotension II levels could have been coming from the heart and not the function pathways related to the kidney. Since I have low renin and aldosterone levels ---according to kidney docs the high angiotension II levels (if they are in me) could not be coming from that pathway. Since the heart can produce it's own angiotension II ---I wonder if that is why some POTS people have high levels and if that is the pathway that it comes from.

Thanks Anna for posting this. It really might explain some things. I also have left ventricular dysfunction.


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Would the ejection faction percentage give an indication of this remodeling.

Or how do you know if this is happening?

I know my % went down from about 70%-55%. Still looking for a reason for chest pain but also i have sinus rhythm tachy's that last for seconds but produce hours of chest pain?

Is this a new finding?

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