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====9. Testable Vascular & Cardiac Dysfunction==== This is the most obvious set of dysfunctions when looked for and is probably the cause behind a significant number of the above complaints. All moderate to severe M.E. patients have one or more and at times multiple of the following vascular dysfunctions. As noted, the primary vascular change is seen in abnormal SPECT brain scans and clinically most evident in patients with: :'''a) POTS''': severe [[postural orthostatic tachycardia syndrome]]. ::'''Note''': This group can be confused with [[diabetes]] insipidus due to the fact that they may have polydipsia from their attempt to increase their circulating blood volume by consuming large amounts of fluids. This group can be verified by the absence of pituitary adenoma or pathology and the fact that they can sleep through the night without waking to drink fluids. <sup>''(Streeten, David)''</sup> ::Despite the great steps forward in the understanding of this relatively common pathophysiology seen routinely in M.E. patients, a pathology which is really related to either an autonomic injury to the CNS, injury to the vascular receptors or both, very little of the present treatment protocol is of much use. The situation is so bad that few major centres have any well-funded expertise in either autonomic or vascular receptor injury. Many of the M.E. patients that are dismissed by physicians as suffering from lack of activity have significant proprioceptive injuries in these areas. Nor can we always rely on the few [[autonomic]] laboratories and their [[tilt table]] testing abilities. Many of the tilt table examination reports return as normal, many as grossly abnormal. Yet all the physician has to do is have each M.E. patient stand for 8-12 minutes to realize that a large number of these normal tilt table patients simply cannot maintain a normal blood pressure and normal heart rate. Compare this to non-M.E. patients and one immediately can tell the difference. A large number of M.E. patients have significant autonomic difficulties. :'''b) Cardiac Irregularity''': on minor positional changes or after minor physical activity, including inability of the heart to increase or decrease in speed and pump volume in response to increase or decrease in physical activity. <sup>''(Hyde, B., Chapter on Cardiac Aspects): (Montague, T.,)''</sup> [[Cardiac irregularity]] is closely related to the above discussion. In many M.E. patients there is an unusual daytime tachycardia, particularly since these patients are often very sedentary. In doing a 24-hour Holter monitor this may be missed since the 24 hour average is usually given. One should always ask for wake time and sleep time heart rates. :'''c) [[Raynaud's syndrome|Raynaud's phenomenon]]''': vasoconstriction of small arteries or arterioles of extremities, with change in colour of the skin, [[pallor]] and cyanosis. It is associated with coldness and pain of extremities. This is in part, the cause for temperature and pain dysfunctions seen in M.E. This phenomenon is found in many other conditions than M.E. Some of the associations are post-traumatic, neurogenic conditions, occlusive arterial diseases, toxic chemical associations and a wide range of [[rheumatoid]] conditions. Many of these conditions have associations with M.E. <sup>''(See Magallni, S. for more detail.)''</sup> :'''d) Circulating Blood Volume Decrease''': This is a nuclear medicine test in which the circulating red blood cell levels in some M.E. patients can fall to below 50%, preventing adequate oxygenation to the brain, [[gut]] and [[muscle]]s. These patients do not generally have aenemia and are not blood deficient. This is undoubtedly a subcortical dysregulation. It is associated with serum and total blood volume measurements. This is a concept that many physicians have difficulty understanding. I have heard physicians repeatedly tell the patient they are not aenemic and therefore dismiss this important finding. ::'''Note''': So where does the blood go? Body servomechanisms are genetically designed so that blood flow and oxygen to the heart are always protected. Thus, when the body of the M.E. patient is stressed, the blood flow to organs not necessary for short-term survival, such as the brain, the gut and skeletal muscles, can be temporarily decreased. This of course gives rise to many of the M.E. symptoms. :'''e) Bowel Dysfunction''': vascular dysfunction may be the most significant causal basis of the multiple bowel dysfunctions occurring in M.E. <sup>''(See d. above.)''</sup> :'''f) Ehlers-Danlos Syndromes Group''': This is a group of illnesses with a genetic predisposition to M.E. or M.E.- like illness. In fact it probably represents a spectrum of illnesses that start with (i) hyper-reflexia syndrome, moving through any of the (ii) various [[Ehlers-Danlos syndrome]]s and climaxing in (iii) Marfan Syndrome where there tends to be early death if the aortic and cardiac changes are not repaired. Ehlers-Danlos syndromes can go undetected until what appears to be a switch is turned on, usually in late teens to early thirties. The “switch” may be viral or possibly age or hormonal related. Raynaud’s phenomenon is usually associated. ::'''Diagnosis''': briefly, patients over the age of 16 who can (i) touch their nose with their tongue, (ii) touch their forearm with the thumb of the same extremity (joint laxity), (iii) touch the floor readily with the full palm should be considered suspect for further examination. There are several fascination variations of Ehlers-Danlos. They are generally considered to be a group of genetic illnesses but in my examination of M.E. patients most often are not manifested until well past puberty and in adulthood. Additional generalized features of this spectrum of illnesses include (v) India rubber or hyperelastic skin, (vi) easy bruisability (vascular fragility), (vii) Arachnodactyly (long spiderlike fingers). Many of the patients with a more severe form tend to be tall, slender with a dolichocephalic skull, high palate and long narrow feet with hammertoes verging on Marfan syndrome. <sup>''(See Magalini, S. I., Magalini S. C. for both E-D Syndrome and Marfan 1 and Marfanoid hypermobility.)''</sup> :'''g) Persantine Effect in M.E. Patients''': Persantine is a chemical manufactured by Boehringer Ingelheim. It is employed to perform chemical cardiac stress testing when a patient cannot exercise sufficiently to stress the heart. It is a particularly safe medication but when employed with many M.E. patients it can cause severe muscle pain over the extremities and entire musculature. Normally this can be reversed by injection of an antidote but this does not always work rapidly in M.E. patients. Severe pain and fatigue can be intolerable and persist for minutes to days in some M.E. patients following Persantine use. Persantine works by dilating both peripheral and cardiac blood vessels and causing the heart rate to increase as in a POTS patient. Obviously one major pain and fatigue factor in M.E. patients is caused by abnormal dilatation of peripheral blood vessels. The resulting pain may be related to reflex vasospasm as in severe Raynaud’s phenomenon that I note elsewhere is one of the causes of M.E. pain. To my knowledge, no testing of M.E. patients with Persantine has ever been published by Boehringer Ingelheim or others. It is one of the reasons I believe that pain syndromes in M.E. patients are due to a pathological vascular physiology. :'''h) M.E. Associated Clotting Defects''': M.E. represents both a vasculitis and a central and peripheral change in vascular physiology. All such vascular illnesses should be potentially treatable. We do not yet know how to adequately treat the (i) genetic forms of vasculitis & vascular patho-physiology mentioned here, nor (ii) the probable viral triggered genetic vascular pathologies also mentioned. Nor do we know how to treat those (iii) centrally caused injuries causing the circulating blood volume defects that are demonstratedwhen we do the “nuclear medicine circulating blood volume tests. It is important to do this test on all patients. POTS is poorly treatable and more often success in treatment presently escapes physicians’ ability. Eventually, I have no doubt that these will be treatable causes of M.E. type disease. However there is a significant group of M.E. patients who are ill due to a treatable form of vasculitis and can be treated if the physician takes the time to diagnose the subgroup. These patients are the clotting defect patients. Some of these clotting defects are genetic and some appear to be genetic with an age or viral switching mechanism, as I have mentioned elsewhere with Ehlers Danlos Syndromes; although they may develop in childhood, they are more frequently noted well after puberty and before the age of 40. Many of these patients can be diagnosed by the following tests: (1) Serum viscosity test, (2) Antiphospholipid Ab., (3) Protein C defects, (4) Protein S defects, (5) Factor V Leiden defect, to name the most common that we have uncovered. However, there are others for which we also test. These conditions are all potentially treatable and when treated adequately may allow the patient to return to school or work. Although any physician can order these tests, a haematologist should review all M.E. patients for these and other possible clotting anomalies. Most clotting defects are treatable and treatment has resulted in recovery in some cases. Remember M.E. is essentially a problem of microcirculation and any improvement in this area can have dramatically positive effects. It is well worthwhile for all physicians reading this definition who have an interest in M.E. to examine the Internet for Hughes Syndrome. Curiously, Hughes Syndrome was first outlined in St. Thomas’ Hospital London, the home of the Nightingale School of Nursing. Hughes Syndrome, a vascular syndrome also called Sticky Blood Syndrome, closely parallels the definition of M.E. :'''i) Anti-smooth muscle Antibodies''': This is an antibody to the muscle tissue in the arterial bed. It is elevated in about 5% of M.E. patients but whether this is different in non-M.E. patients is unknown but unlikely. It rarely is over 1:40. :'''j) Cardiac Dysfunction''': There are a large number of [[cardiac dysfunctions]] that can regularly appear in an M.E. patient. Certain are obvious and discussed under Ehlers-Danlos Syndrome and Marfan syndrome. I also discussed cardiac dysfunction in Chapter 42, The Clinical and Scientific Basis of M.E./CFS. Since that chapter was written a large number of other cardiac pathologies and pathophysiologies have been noted by various researchers and clinicians, particularly by Dr. [[Paul Cheney]]. Without a clear understanding of these significant problem areas it is simply indefensible and potentially dangerous to place an unsuspecting patient in a graduated exercise program. This is particularly true if the patient is not being tested in a cardiac unit. Although in our clinic we have performed what we believe to be a complete cardiac assessment on all patients seen, what the Ottawa Cardiac Institute and I believed was a complete assessment may be wanting. Over the next year we will reassess these patients with a more detailed cardiac examination and report on it in these diagnostic criteria.
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