Small Heart With Low Cardiac Output for Orthostatic Intolerance in Patients With Chronic Fatigue Syndrome

Cardiovascular and autonomic dysfunction have been suggested to underlie the symptoms accompanying CFS (chronic fatigue syndrome). In the present issue of Clinical Science, Hurwitz and co-workers have investigated whether deficits were present in cardiac output and blood volume in a cohort of patients with CFS and if these were linked to illness severity and sedentary lifestyle. The results clearly demonstrate reduced cardiac stroke volume and cardiac output in more severely afflicted patients with CFS, which is primarily attributable to a measurable reduction in blood volume. Similar findings are observed in microgravity and bed rest deconditioning, in forms of orthostatic intolerance and, to a lesser extent, in sedentary people. The circulatory consequences of reduced cardiac output may help to account for many of the findings of the syndrome.

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770 Small heart and single coronary artery in a young patient with chronic fatigue syndrome: a case report

European Heart Journal Supplements ◽

10.1093/eurheartj/suab133.018 ◽

2021 ◽

Vol 23 (Supplement_G) ◽

Author(s):

Cristina Poleggi ◽

Silvia Perfetti ◽

Davide Restelli ◽

Alessia Perna ◽

Rocco Donato ◽

...

Keyword(s):

Cardiac Output ◽

Coronary Artery ◽

Chronic Fatigue Syndrome ◽

Stroke Volume ◽

Rare Case ◽

Chronic Fatigue ◽

Anomalous Origin ◽

Single Coronary Artery ◽

Fatigue Syndrome ◽

Small Heart

Abstract Aims Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a clinically defined condition reported mostly in adults, characterized by fatigue and unexplained aspecifical symptoms. Patients with CFS/ME frequently have reduced stroke volume with an inverse relation between cardiac output and post-exertional malaise severity. We describe a rare case of a young man affected by CFS/ME, small heart, and anomalous anatomy of left main coronary artery (LMCA). Methods and results A 19-year-old Caucasian male referred to our clinic complaining weakness, lack of concentration, and sleepiness. He suffered by CFS/ME, D hypovitaminosis, inflammatory bowel disease, and exocrine pancreas insufficiency. Blood tests revealed no pathological findings. Faecal exams documented intestinal dysbiosis and low pancreatic elastase. He was treated with oxygen-ozone rectal insufflations and probiotics. Physical examination was unremarkable. Electrocardiogram showed normal sinus rhythm. Echocardiogram revealed reduced diameters of the left ventricle (LV), normal aortic root dimensions and, in a five-chamber apical view, a binary structure that seemed to cross the aorta perpendicularly. Cardiac magnetic resonance (CMR) found reduced LV stroke volume (34 ml/m2) and end-diastolic volume (57 ml/m2) together with reduced end-diastolic wall mass (51 g/m2). Right ventricle volumes were reduced too. In addition, the exam confirmed the anomalous origin of LMCA stemming from the proximal segment of right coronary artery and following a retro-aortic course. Mechanism of CFS/ME remains unknown, although various factors have been implicated, including immune activation, chronic viral infection, and emotional disorders. A considerable number of patients affected by CFS has an anatomically small heart. Small heart syndrome, in fact, may contribute to the onset of CFS/ME. Previous studies hypothesized that clinical manifestations of CMS/ME were caused by reduced venous return, cardiac output, and heart mass, together with decreased arterial oxygen saturation. Single coronary artery is an uncommon congenital anatomic abnormality identified by a single coronary ostium giving rise to all arteries supplying the heart. Thus, we reported a rare case of a very young man affected by chronic fatigue syndrome and small heart, investigated not only with echocardiogram but also with CMR, not often used in this clinical setting. More, we found an anomalous origin of LMCA. From literature, it’s not reported any cases of a patient including these three rare conditions (CFS/ME, small heart, and single coronary artery). Conclusions This case highlights that CFS/ME together with small heart is a condition possible also in young people. More studies and reports could be necessary to better define the association between cardiac congenital anomalies and CFS/ME. 770 Figure

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COVID-19 and post-infectious myalgic encephalomyelitis/chronic fatigue syndrome: a narrative review

Therapeutic Advances in Infectious Disease ◽

10.1177/20499361211009385 ◽

2021 ◽

Vol 8 ◽

pp. 204993612110093

Author(s):

Sonia Poenaru ◽

Sara J. Abdallah ◽

Vicente Corrales-Medina ◽

Juthaporn Cowan

Keyword(s):

Chronic Fatigue Syndrome ◽

Sleep Disturbances ◽

Q Fever ◽

Orthostatic Intolerance ◽

Chronic Fatigue ◽

Myalgic Encephalomyelitis ◽

Exercise Intolerance ◽

Laboratory Findings ◽

Fatigue Syndrome ◽

Post Infectious

Coronavirus disease 2019 (COVID-19) is a viral infection which can cause a variety of respiratory, gastrointestinal, and vascular symptoms. The acute illness phase generally lasts no more than 2–3 weeks. However, there is increasing evidence that a proportion of COVID-19 patients experience a prolonged convalescence and continue to have symptoms lasting several months after the initial infection. A variety of chronic symptoms have been reported including fatigue, dyspnea, myalgia, exercise intolerance, sleep disturbances, difficulty concentrating, anxiety, fever, headache, malaise, and vertigo. These symptoms are similar to those seen in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a chronic multi-system illness characterized by profound fatigue, sleep disturbances, neurocognitive changes, orthostatic intolerance, and post-exertional malaise. ME/CFS symptoms are exacerbated by exercise or stress and occur in the absence of any significant clinical or laboratory findings. The pathology of ME/CFS is not known: it is thought to be multifactorial, resulting from the dysregulation of multiple systems in response to a particular trigger. Although not exclusively considered a post-infectious entity, ME/CFS has been associated with several infectious agents including Epstein–Barr Virus, Q fever, influenza, and other coronaviruses. There are important similarities between post-acute COVID-19 symptoms and ME/CFS. However, there is currently insufficient evidence to establish COVID-19 as an infectious trigger for ME/CFS. Further research is required to determine the natural history of this condition, as well as to define risk factors, prevalence, and possible interventional strategies.

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Chronic fatigue syndrome: illness severity, sedentary lifestyle, blood volume and evidence of diminished cardiac function

Clinical Science ◽

10.1042/cs20090055 ◽

2009 ◽

Vol 118 (2) ◽

pp. 125-135 ◽

Cited By ~ 45

Author(s):

Barry E. Hurwitz ◽

Virginia T. Coryell ◽

Meela Parker ◽

Pedro Martin ◽

Arthur LaPerriere ◽

...

Keyword(s):

Cardiac Output ◽

Chronic Fatigue Syndrome ◽

Blood Volume ◽

Sedentary Lifestyle ◽

Cardiac Contractility ◽

Chronic Fatigue ◽

Group Differences ◽

Control Groups ◽

Cardiac Volume ◽

Fatigue Syndrome

The study examined whether deficits in cardiac output and blood volume in a CFS (chronic fatigue syndrome) cohort were present and linked to illness severity and sedentary lifestyle. Follow-up analyses assessed whether differences in cardiac output levels between CFS and control groups were corrected by controlling for cardiac contractility and TBV (total blood volume). The 146 participants were subdivided into two CFS groups based on symptom severity data, severe (n=30) and non-severe (n=26), and two healthy non-CFS control groups based on physical activity, sedentary (n=58) and non-sedentary (n=32). Controls were matched to CFS participants using age, gender, ethnicity and body mass. Echocardiographic measures indicated that the severe CFS participants had 10.2% lower cardiac volume (i.e. stroke index and end-diastolic volume) and 25.1% lower contractility (velocity of circumferential shortening corrected by heart rate) than the control groups. Dual tag blood volume assessments indicated that the CFS groups had lower TBV, PV (plasma volume) and RBCV (red blood cell volume) than control groups. Of the CFS subjects with a TBV deficit (i.e. ≥8% below ideal levels), the mean±S.D. percentage deficit in TBV, PV and RBCV were −15.4±4.0, −13.2±5.0 and −19.1±6.3% respectively. Lower cardiac volume levels in CFS were substantially corrected by controlling for prevailing TBV deficits, but were not affected by controlling for cardiac contractility levels. Analyses indicated that the TBV deficit explained 91–94% of the group differences in cardiac volume indices. Group differences in cardiac structure were offsetting and, hence, no differences emerged for left ventricular mass index. Therefore the findings indicate that lower cardiac volume levels, displayed primarily by subjects with severe CFS, were not linked to diminished cardiac contractility levels, but were probably a consequence of a co-morbid hypovolaemic condition. Further study is needed to address the extent to which the cardiac and blood volume alterations in CFS have physiological and clinical significance.

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Orthostatic intolerance in the chronic fatigue syndrome

Journal of the Autonomic Nervous System ◽

10.1016/s0165-1838(98)00177-5 ◽

1999 ◽

Vol 75 (2-3) ◽

pp. 192-201 ◽

Cited By ~ 89

Author(s):

Ronald Schondorf ◽

Julie Benoit ◽

Theodore Wein ◽

Denis Phaneuf

Keyword(s):

Chronic Fatigue Syndrome ◽

Orthostatic Intolerance ◽

Chronic Fatigue ◽

Fatigue Syndrome

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Orthostatic intolerance and chronic fatigue syndrome: New light on an old problem

The Journal of Pediatrics ◽

10.1067/mpd.2002.124318 ◽

2002 ◽

Vol 140 (4) ◽

pp. 387-389 ◽

Cited By ~ 9

Author(s):

Peter C. Rowe

Keyword(s):

Chronic Fatigue Syndrome ◽

Orthostatic Intolerance ◽

Chronic Fatigue ◽

Fatigue Syndrome

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Small Heart Syndrome in Patients with Chronic Fatigue Syndrome

Clinical Cardiology ◽

10.1002/clc.20227 ◽

2008 ◽

Vol 31 (7) ◽

pp. 328-333 ◽

Cited By ~ 28

Author(s):

Kunihisa Miwa ◽

Masatoshi Fujita

Keyword(s):

Chronic Fatigue Syndrome ◽

Chronic Fatigue ◽

Fatigue Syndrome ◽

Small Heart

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Numeric Rating Scales Show Prolonged Post-exertional Symptoms After Orthostatic Testing of Adults With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Frontiers in Medicine ◽

10.3389/fmed.2020.602894 ◽

2021 ◽

Vol 7 ◽

Author(s):

C (Linda) M. C. van Campen ◽

Peter C. Rowe ◽

Freek W. A. Verheugt ◽

Frans C. Visser

Keyword(s):

Chronic Fatigue Syndrome ◽

Pain Perception ◽

Rating Scales ◽

Orthostatic Intolerance ◽

Chronic Fatigue ◽

Myalgic Encephalomyelitis ◽

Fatigue Syndrome ◽

Important Symptom ◽

Head Up Tilt ◽

Numeric Rating

Introduction: Muscle pain, fatigue, and concentration problems are common among individuals with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). These symptoms are commonly increased as part of the phenomenon of postexertional malaise (PEM). An increase in the severity of these symptoms is described following physical or mental exercise in ME/CFS patients. Another important symptom of ME/CFS is orthostatic intolerance, which can be detected by head-up tilt testing (HUT). The effect of HUT on PEM has not been studied extensively. For this purpose, we assessed numeric rating scales (NRS) for pain, fatigue, and concentration pre- and post-HUT. As pain is a core symptom in fibromyalgia (FM), we subgrouped ME/CFS patients by the presence or absence of FM.Methods and Results: In eligible ME/CFS patients who underwent HUT, NRS of pain, fatigue, and concentration were obtained pre-HUT, immediately after HUT, at 24 and 48 h, and at 7 days posttest. We studied 174 ME/CFS patients with FM, 104 without FM, and 30 healthy controls (HC). Values for all symptoms were unchanged for HC pre- and post-HUT. Compared with pre-HUT, the three NRS post-HUT were significantly elevated in both ME/CFS patient groups even after 7 days. NRS pain was significantly higher at all time points measured in the ME/CFS patients with FM compared with those without FM. In ME/CFS patients, the maximum fatigue and concentration scores occurred directly post-HUT, whereas pain perception reached the maximum 24 h post-HUT.Conclusion: NRS scores of pain, fatigue, and concentration were significantly increased even at 7 days post-HUT compared with pre-HUT in ME/CFS patients with and without FM, suggesting that orthostatic stress is an important determinant of PEM.

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Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.2024358118 ◽

2021 ◽

Vol 118 (34) ◽

pp. e2024358118

Author(s):

Bindu D. Paul ◽

Marian D. Lemle ◽

Anthony L. Komaroff ◽

Solomon H. Snyder

Keyword(s):

Chronic Fatigue Syndrome ◽

Bacterial Infections ◽

Orthostatic Intolerance ◽

Neurological Diseases ◽

Chronic Fatigue ◽

Myalgic Encephalomyelitis ◽

Redox Imbalance ◽

Fatigue Syndrome ◽

Unrefreshing Sleep ◽

Hypometabolic State

Although most patients recover from acute COVID-19, some experience postacute sequelae of severe acute respiratory syndrome coronavirus 2 infection (PASC). One subgroup of PASC is a syndrome called “long COVID-19,” reminiscent of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a debilitating condition, often triggered by viral and bacterial infections, leading to years-long debilitating symptoms including profound fatigue, postexertional malaise, unrefreshing sleep, cognitive deficits, and orthostatic intolerance. Some are skeptical that either ME/CFS or long COVID-19 involves underlying biological abnormalities. However, in this review, we summarize the evidence that people with acute COVID-19 and with ME/CFS have biological abnormalities including redox imbalance, systemic inflammation and neuroinflammation, an impaired ability to generate adenosine triphosphate, and a general hypometabolic state. These phenomena have not yet been well studied in people with long COVID-19, and each of them has been reported in other diseases as well, particularly neurological diseases. We also examine the bidirectional relationship between redox imbalance, inflammation, energy metabolic deficits, and a hypometabolic state. We speculate as to what may be causing these abnormalities. Thus, understanding the molecular underpinnings of both PASC and ME/CFS may lead to the development of novel therapeutics.

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