(b) Cardiac Abnormalities & Increased risk of heart attack

Source: ME Primer for Healthcare Professionals: based on Myalgic encephalomyelitis: International Consensus Criteria, 2012

Source: Dr. Paul Cheney, The Cheney Clinic, USA.

Reduced cardiac fillng, long IVRT, low cardiac output as a
result of mitochondria dysfunctions, infections (some cases),
toxins build up, and damage caused by high oxidative and nitrosative
stress levels over time. A very consistent finding in his medical practice.
Dr. Paul Cheney , The Cheney Clinic, USA

Source: Dr. Paul Cheney, The Cheney Clinic, USA

Cardiomyopathy arising from mitochondria dysfunction, oxidative stress and infections

• Causes of Death Among Patients With Chronic Fatigue Syndrome LEONARD A. JASON, KARINA CORRADI, SARA GRESS,
  SARAH WILLIAMS, and SUSAN TORRES-HARDING. Health Care for Women International, 27:615–626, 2006

• Peckerman A, et al. Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome. Am J Med Sci 2003 Aug;326(2):55-60.

• Peckerman A, LaManca JJ, Qureshi B, et al. 2003 Baroreceptive reflex and integrative stress responses in chronic fatigue syndrome. Psychosom Med 65:889-895.

• Hollingsworth, K. G., Hodgson, T., MacGowan, G. A., Blamire, A. M. and Newton, J. L. (2012), Impaired cardiac function in chronic fatigue syndrome measured using magnetic resonance cardiac tagging. Journal of Internal Medicine, 271: 264–270. 

• Dr. Martin Lerner's lecture on clinical findings
  


• Video lecture by Dr. Paul Cheney on cardiomyopathy findings in ME
  
  
• Markedly Impaired Cardiac Function in Chronic Fatigue Syndrome. Hollingsworth KG, Hodgson T, Macgowan GA, Blamire AM, Newton JL.: J Intern Med. 2011 Jul 27.

• Elevated nocturnal blood pressure and heart rate in adolescent chronic fatigue syndrome. Harald Hurum, Dag Sulheim, Erik Thaulow, Vegard Bruun Wyller. Acta Paediatrica. Volume 100, Issue 2, pages 289–292, February 2011 .

• Wyller VB, Due R, Saul JP, Amlie JP, Thaulow E. Usefulness of an abnormal cardiovascular response during low - grade head - up tilt - test for discriminating adolescents with chronic fatigue from healthy controls. Am J Cardiol ( 2007 ) 99 : 997 - 1001. doi: 10.1016/j.amjcard.2006.10.067.

• LaManca JJ, Peckerman A, Walker J, Kesil W, Cook S, Taylor A, et al. Cardiovascular response during head - up tilt in chronic fatigue syndrome. Clin Physiol ( 1999 ) 1 9 : 111 - 120. doi: 10.1046/j.1365 - 2281.1999.00154.

• Lerner AM, et al. Repetitively negative T waves at 24-h electrocardiographic monitors in patients with the Chronic Fatigue Syndrome. Chest 1993, Nov;104(5):1417-142

• Lerner AM, et al. Cardiac involvement in patients with chronic fatigue syndrome as documented with Holter and biopsy data in Birmingham, Michigan, 1991-1993. Infect Dis Clin Pract1997;6:327-333

• Codero DL, et al. Decreased vagal power during treadmill walking in patients with chronic fatigue syndrome. Clin Auton Res 1996 Dec;6(6):329-333

• In ME/CFS, convincing evidence of ca rdiovascular impairment can be demonstrated".
  "Research Update on ME/CFS". Behan WHM. Professor of Pathology, Glasgow. Extracts from Over - view of the Alison Hunter Memorial Foundation ME/CFS Clinical and Scientific Meeting, December 2001, Sydney, Austr alia. For the complete over - view, see http://listserv.nodak.edu/cgi - bin/wa.exe?A2=ind0207c&L=co - cure&T=0&F=&S=&P=3579

• Rowe PC, Calkins H. Neurally mediated hypotension and chronic fatigue syndrome. Am J Med 1998;105 (3A):15S-21S

• De Becker P, et al. Autonomic testing in patients with chronic fatigue syndrome. Am J of Med 1998; 105(3A):22S-26S

• Schondorf R, Freeman R. The importance of orthostatic intolerance in the chronic fatigue syndrome. Am J Med Sci 1999;317:117-123

• Hoad A, Spickett G, Elliott J, Newton J. Postural orthostatic tachycardia syndrome is an under recognized condition in chronic fatigue syndrome . QJM. 2008 Dec;101(12):961-5. Epub 2008 Sep 19.

• Bou-Holaigah I, Rowe PC, Kan J,Calkins H. The relationship between neurally mediated hypotension and the chronic fatigue syndrome. JAMA. 1995 Sept 27;274(12): 961-967

• Rowe PC, Bou-Holaigah I, Kan JS, Calkins H. Is neurally mediated hypotension an unrecognised cause of chronic fatigue? Lancet 1995;345:623-624
• Streeten DHP, Bell DS. Circulating blood volume in chronic fatigue syndrome. J CFS 1998;4(1): 3-11

• Newton JL, Sheth A, Shin J, Pairman J, Wilton K, Burt JA , Jones DE. Lower ambulatory blood pressure in chronic fatigue syndrome. Psychosom Med. 2009 Apr;71(3):361-5. Epub 2009 Mar 17.

• Hurwitz BE et al. Chronic fatigue syndrome: illness severity, sedentary lifestyle, blood volume and evidence of diminished cardiac function. Clin Sci (Lond). 2009 Oct 19;118(2):125-35

• Why myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) may kill you: disorders in the inflammatory and oxidative and nitrosative stress (IO&NS) pathways may explain cardiovascular disorders in ME/CFS.Maes M, Twisk FN.Maes Clinics, Wilrijk - Antwerp, Belgium. crc.mh@telenet.be Neuro Endocrinol Lett. 2009;30(6):677-93.

• Excerpt from The Complexities of Diagnosis By Dr. Byron Hyde, Chairman, Nightingale Research Foundation, Chapter 3 in
  Handbook of Chronic Fatigue Syndrome. Leonard A. Jason, Patricia A. Fennell, Renée R. Taylor
  ' Dr. John Richardson from Newcastle upon Tyne has followed ME patients in Durham and Northumberland counties of the United Kingdom for three to four generations. I am aware of no other physician in the world with such a historic view of ME patients. He has repeatedly demonstrated that many ME patients go on to develop structural heart injury. The injury is usually valvular or related to pericardial effusion, and although most settle down, some do not and may develop myopathy. So I started to look at the hearts of these patients.
  I have found that during the first year of acute onset ME/CFS disability, the incidence of pericardial effusion is unusually high. This seems to settle down with no apparent short-term problem, and after a year, the cases of pericardial fluid decrease considerably. However, the incidence of valvular disease in people in their 30s and 40s appears to be higher than in the normal population. When I find a significant valvular injury, I then repeat the echocardiogram yearly, and more frequently if the patient develops shortness of breath. I have observed several cases of elevated right heart pressure, significant septal defects, and increased myocardial wall thickening. Some who have had the injured valve replaced have miraculously returned to normal health. Are these incidental findings? I do not know, but Dr. Richardson has identified more than several hundred cardiopathies in his ME practice. I had two heart valve replacements in this group in the past year out of a total of 50 new patients.
  Carotid and Transcranial Doppler Few physicians investigating ME/CFS employ the visual carotid and transcranial Doppler. This is a major error. It is a relatively inexpensive and totally safe procedure that does things no other type of test can do. On rare occasions, you will find aneurysms and subclavian steal anomaly with this test. Carotid atherosclerosis – sometimes substantial – is often found in patients with lipid dysfunction. This is a treatable condition and can be part of the cause of a CNS fatigue syndrome. You may say that any internist or cardiologist can pick up carotid pathology with a stethoscope, but few do who do not have an office Doppler. The carotid scan is also essential if you wish to do a transcranial Doppler
  I examined a patient from the United States who had been diagnosed as having CFS in two major U.S. CFS clinics. She was given alternative medications and told to return in one year. She had complete obstruction of the vertebral basilar arteries and approximately 80% and 90% obstruction in either carotid. I was amazed that she was still alive. She was successfully operated on in Boston and her CFS has significantly improved.
  The transcranial Doppler is not a perfect test. Patients with small foramen magnum space are difficult to visualize. But it will demonstrate high level internal carotid and other arterial obstruction that is beyond the normal range of a stethoscope. Only rarely do I get the chance to investigate posttraumatic mitral valve area (MVA) patients who develop an acute fatigue syndrome where personality or intellectual change has given rise to the diagnosis of CFS. In two of the past four such patients, I have demonstrated small subcortical arterial blowouts that had been missed by neurologists and that were possibly the cause of their pathophysiology.
  In patients with ME/CFS, it is possible to demonstrate spasmodic disease of both major and smaller arteries with no typical evidence of migraine. This arterial pathology may be the end organ underlying cause of some ME patients' illness. Often MRls and MRAs miss such arterial physiological pathology. Why? The technology of the MRA consists of a receiving computer revolving around the brain that may only give a picture of the maximum arterial diameter. In other words, what you see on the MRA is not reality but one view of reality. With the transcranial Doppler, the operator actually watches and films the kinetic movement of the arteries within the brain and can measure the velocity of the blood flow. Not only can you see these arteries move; if they are in spasm, you can observe this as well. Like ME/CFS muscles, ME brains are sometimes in significant pathological spasm. This knowledge may lead to more effective treatments of ME/CFS disease. Arterial spasm may account for some, but not all, of the SPECT changes that are routinely seen in ME patients.
  I often find partial or complete vertebral or basilar artery obstruction. Frequently, I find left middle cerebral artery spasm or obstruction and, less frequently, frontal artery spasm in ME/CFS patients who do not report a migraine history. Left middle cerebral arterial field hypoperfusion is typical of ME. '

• Prevalence of abnormal cardiac wall motion in the cardiomyopathy associated with incomplete multiplication of Epstein-Barr virus and/or cytomegalovirus in patients with chronic fatigue syndrome. Lerner et al. In Vivo, 18:417-424 (2004)

• Hurwitz BE, Cor yell VT, Parker M, Martin P, Laperriere A, Klimas NG, et al. Chronic fatigue syndrome: illness severity, sedentary lifestyle, blood volume and evidence of diminished cardiac function. Clin Sci (Lond) ( 2009 ) 118 : 125 - 135. doi: 10.1042/CS20090055.

• Hollingswo rth KG, Hodgson T, Macgowan GA, Blamire AM, Newton JL. Impaired cardiac function in chronic fatigue syndrome measured using magnetic resonance cardiac tagging. J Intern Med ( 2012 ) 271 : 264 - 270. doi: 10.1111/j.1365 - 2796.2011.02429.x.

• Miwa K, Fujita M. Cardi ac function fluctuates during exacerbation and remission in young adults with chronic fatigue syndrome and "small heart". J Cardiol ( 2009 ) 54 : 29 - 35. doi: 10.1016/j.jjcc.2009.02.008.

• Streeten DH, Bell DS. Circulating blood volume in chronic fatigue syndrom e. J Chronic Fatigue Syndr ( 1998 ) 4 : 3 - 11. doi: 10.1300/J092v04n01_02