Many thanks. I have visited my cardiologist today and he has said, that cardiac syndrome x in itself is not life threatening but it can be debilitating, which I find that it is. He has assured me that attacks happen in peaks and troughs, and once over the effects of this attack, I could be alright for a couple of months, before it rears its ugly head again. It is a very frightening and debilitating condition, robbing a sufferer of all their energy, confidence and causing anxiety not only for the sufferer but also for the family. Once again thank you for your support and information. X Sheila
A coronary artery spasm is a BRIEF, TEMPORARY tightening (contraction) of the muscles in the artery wall. This can narrow and briefly decrease or even prevent blood flow (ischemia) to part of the heart muscle cells. Unlike typical angina, which usually occurs with exertion, coronary artery spasms often occur at rest. Calcium channel blockers are the usual treatment.
It is my understanding cardiac syndrome X (a syndrome characterized by typical angina, abnormal exercise-test results, and NORMAL coronary arteries), conventional investigations have NOT found that chest pain is due to myocardial ischemia. There is a problem with the inclusion of patients with "near-normal" (ie, <50 percent) occlusion under the category of cardiac syndrome X since, in many cases, dynamic changes (ie, coronary vasoconstriction) occurring at the site of such occlusion are responsible for flow limitations that lead to angina. It is generally REQUIRED that patients with cardiac syndrome X have completely normal coronary arteriograms...Your abnormal EKG probably related to an ST interval depression on the EKG which would indicate ischemia.
In patients presenting with anginal chest pain, the effects of sublingual nitrates on exercise testing appear to be clinically useful to distinguish patients with coronary artery occlusion from patients with syndrome X. The failure of nitrates to improve exercise tolerance in patients with syndrome X suggests that a deficiency in coronary prearteriolar nitric oxide (responsible for physiological arterial dilitation) production is unlikely to play a key role in the pathophysiology of the syndrome.
In cardiac syndrome X, the presence of ischemic-like ST segment changes during chest pain, in the absence of epicardial coronary occlusion suggests that myocardial ischemia caused by CORONARY MICROVASCULAR DYSFUNCTION is responsible for angina. "This view is supported by the documentation of abnormalities in myocardial perfusion on radionuclide studies and abnormal coronary blood flow response to vasoactive stimuli".
Several abnormalities able to cause microvascular dysfunction have been reported, including increased adrenergic function, increased stress induced coronary sinus release of endothelin and increased activity of sodium–hydrogen countertransport. Yet several studies failed to show myocardial lactate production and left ventricular dysfunction1during angina and ST segment depression, thus casting some doubts on the ischemic origin of chest pain and ECG changes.
The pathogenesis of cardiac syndrome X remains uncertain. Two mechanisms that are not mutually have been proposed: myocardial ischemia that might be caused by coronary microvascular dysfunction (ie, abnormal dilatory responses and/or increased vasoconstriction); and enhanced sensitivity to intracardiac pain or the so-called "sensitive heart" syndrome . It is possible that the syndrome may result from a variable combination of CORONARY MICROVASCULAR DYSFUNCTION and increased sensitivity to painful stimuli.
It seems plausible that Sydrome X is not, or is a questionable dx, and a vessel caused ischemia can be the source of the angina, and/or blocked or partially blocked microvessels can be the underlying cause.and or the integrity of the endothelium (lining of the vessel), is deficit of nitric oxide production and the lack of nitric oxide has been identified as the prime mediator of endothelium dependent vasodilatation.