Kunihisa Miwa

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Kunihisa Miwa, MD, PhD, is a clinician and researcher in Internal Medicine, especially cardiology and cardiovascular physiology. He is the Director of Miwa Naika Clinic, Toyama, Japan.

Dr. Miwa is one of the authors of the 2011 case definition, International Consensus Criteria.[1]

Education[edit]

  • 1983, PhD, Kyoto University, Japan[2]
  • 1975, MD, Kyoto University, Japan[3]

Studies[edit]

  • 2016, Variability of postural orthostatic tachycardia in patients with myalgic encephalomyelitis and orthostatic intolerance
    Abstract-Central nervous system dysfunction with myalgic encephalomyelitis (ME) has been suggested as the main cause of chronic fatigue syndrome. Fluctuation of the symptom severity and hierarchy is a characteristic feature in ME patients. The characteristics of the sympathetic activation may differ between the “good days” and “bad days” in them. Twenty-four ME patients with orthostatic intolerance underwent a conventional 10-min active standing test and echocardiography both on a “good day” and a “bad day”, defined according to the severity of their symptoms. The mean heart rate at rest was significantly higher on the “bad days” than on the “good days”. During the standing test on a “bad day”, 5 patients (21 %) failed to maintain an upright posture for 10 min, whereas on a “good day” all the 24 patients maintained it. Postural orthostatic tachycardia (POT) (increase in heart rate ≥30 beats/min) or severe POT (heart rate ≥120 beats/min) was observed on the “bad days” in 10 patients (43 %) who did not suffer from the severe tachycardia on the “good days”, suggesting the exaggerated sympathetic nervous activation. In contrast, POT did not occur or severe POT was attenuated on the “bad days” in 5 patients (21 %) who developed POT or severe POT on the “good days”, suggesting the impaired sympathetic activation. Echocardiography revealed significantly lower mean values of both the left ventricular end-diastolic diameter and stroke volume index on the “bad days” compared with the “good days”. In conclusion, in ME patients with orthostatic intolerance, the exaggerated activation of the sympathetic nervous system while standing appears to switch to the impaired sympathetic activation after the system is loaded with the additional accentuated stimuli associated with the preload reduction.[4]
  • 2015, Cardiac dysfunction and orthostatic intolerance in patients with myalgic encephalomyelitis and a small left ventricle
    Abstract-The etiology of chronic fatigue syndrome (CFS) is unknown. Myalgic encephalomyelitis (ME) has been recently postulated to be the cause of CFS. Orthostatic intolerance (OI) has been known as an important symptom in predicting quality of life in CFS patients. Cardiac function may be impaired in patients with ME. The presence or absence of OI was determined both symptomatically and by using a 10-min stand-up test in 40 ME patients. Left ventricular (LV) dimensions and function were determined echocardiographically in the ME patients compared to 40 control subjects. OI was noted in 35 (97%) of the 36 ME patients who could stand up quickly. The mean values for the cardiothoracic ratio, systemic systolic and diastolic pressures, LV end-diastolic diameter (EDD), LV end-systolic diameter, stroke volume index, cardiac index and LV mass index were all significantly smaller in the ME group than in the controls. Both a small LVEDD (<40 mm, 45 vs. 3%) and a low cardiac index (<2 l/ min/mm2, 53 vs. 8%) were significantly more common in the ME group than in the controls. Both heart rate and LV ejection fraction were similar between the groups. In conclusion, a small LV size with a low cardiac output was common in ME patients, in whom OI was extremely common. Cardiac dysfunction with a small heart appears to be related to the symptoms of ME.[5]
  • 2014, Renin-aldosterone paradox in patients with myalgic encephalomyelitis and orthostatic intolerance
    Abstract-The etiology of chronic fatigue syndrome (CFS) is unknown. Recent studies have confirmed that almost 90% of CFS patients experience symptoms related to orthostatic intolerance (OI), which primarily predicts functional capacity in CFS. Many symptoms of OI appear to be related to reduced cerebral blood flow. Also a small heart with low cardiac output has been reported to be common in CFS patients. Recently, central nervous dysfunction due to myalgic encephalomyelitis (ME) has been postulated to be the cause of CFS.[6]
  • 2009, Cardiovascular dysfunction with low cardiac output due to a small heart in patients with chronic fatigue syndrome (FULL TEXT)
    Abstract-Objective: Little attention has been paid to possible cardiovascular involvement in patients with chronic fatigue syndrome (CFS), although many of their symptoms and signs suggest cardiovascular dysfunction. Possible cardiovascular symptoms and cardiac function were investigated in CFS patients. Methods: Cardiovascular symptoms were intensively investigated and cardiac function was evaluated echocardiographically. Patients: Fifty-three patients (23 men and 30 women, mean age: 31±7 years) with CFS under 50 years were studied. Results: Slender build (body mass index <20 kg/m2) was common (47%). Possible cardiovascular symptoms including shortness of breath (32%), dyspnea on effort (28%), rapid heartbeat (38%), chest pain (43%), fainting (43%), orthostatic dizziness (45%) and coldness of feet (42%), were all frequent complaints. Hypotension (28%) was occasionally noted. Electrocardiograms frequently revealed right axis deviation (21%) and severe sinus arrhythmia (34%) suggesting accentuated parasympathetic nervous activity. Small heart shadow (cardiothoracic ratio ≤42%) was noted on the chest roentgenogram in 32 patients (60%). Echocardiographic examination demonstrated low cardiac indexes (<2 L/min/m2) with low stroke volume indexes (<30 mL/m2) due to a small left ventricular chamber in 19 (36%, p<0.05 vs. 8% in 36 controls). None had reduced left ventricular ejection fraction. Conclusion: Cardiovascular symptoms are common in CFS patients. Cardiac dysfunction with low cardiac output due to small left ventricular chamber may contribute to the development of chronic fatigue as a constitutional factor in a considerable number of CFS patients.[7]
  • 2009, Cardiac function fluctuates during exacerbation and remission in young adults with chronic fatigue syndrome and "small heart" (FULL TEXT)
    Abstract-BACKGROUND: "Small heart syndrome", previously referred to as so-called "neurocirculatory asthenia" associated with a small heart shadow on the chest roentgenogram, is characterized by weakness or fatigue even after mild exertion, palpitation, dyspnea, and fainting, many of which resemble symptoms in patients with chronic fatigue syndrome (CFS). METHODS AND RESULTS: The study population comprised 42 patients with CFS younger than 40 years of age. Cardiothoracic ratio was determined on the chest roentgenogram and echocardiographic examination was performed to evaluate both the cardiac chamber size and function. "Small heart" (cardiothoracic ratio < or = 42%) on the chest X-ray photograph was noted in 26 (62%) of the study CFS patients. Echocardiographic examination demonstrated significantly smaller mean values of both the left ventricular (LV) end-diastolic and end-systolic dimensions, stroke volume indexes and cardiac indexes in CFS patients with "small heart" than in those without it and also in 20 control subjects. Thus, CFS patients with "small heart" had an actually small LV chamber and poor cardiac performance. During a long follow-up period of 10 CFS patients with "small heart", all echocardiographic parameters mentioned above improved and cardiothoracic ratios increased significantly during the remission phase as compared with exacerbation phase. CONCLUSIONS: "Small heart" on the chest X-ray photograph was prevalently noted in CFS patients. Echocardiographic examination revealed that CFS patients with "small heart" had an actually small LV chamber and poor cardiac performance. Cardiac functional changes evaluated by repeated examinations appeared to be directly associated with the severity of their symptoms. Small heart syndrome with impaired cardiac function may contribute to the development of CFS through low cardiac output as a constitutional factor.[8]
  • 2008, Small heart syndrome in patients with chronic fatigue syndrome
    Abstract-BACKGROUND: Small heart syndrome has previously been reported as neurocirculatory asthenia, associated with a small heart shadow on a chest roentgenogram. This is characterized as weakness or fatigue even after ordinary exertion, palpitation, dyspnea, and fainting, resembling patients with chronic fatigue syndrome (CFS). HYPOTHESIS: Small heart syndrome may be prevalent in patients with CFS. METHODS: The study population consisted of 56 patients (<50 y of age) with CFS, and 38 control subjects. Chest roentgenographic, echocardiographic, and physical examinations were performed. RESULTS: Small heart syndrome (cardiothoracic ratio <or= 42%) was significantly more prevalent in the CFS group (61%) than in the control group (24%) (p < 0.01). In CFS patients with a small heart (n = 34), narrow chest (88%), orthostatic dizziness (44%), foot coldness (41%), pretibial pitting edema (32%), r-kidney palpability (47%), and mitral valve prolapse (29%), were all significantly more prevalent than in the control group, and also in the CFS patients without small heart syndrome. Echocardiographic examination demonstrated significantly smaller values of both the left ventricular (LV) end-diastolic dimensions and end-systolic, and stroke volume and cardiac indexes in CFS with a small heart, as compared with control subjects with a normal heart size (42% < cardiothoracic ratio < 50%). CONCLUSIONS: A considerable number of CFS patients have a small heart. Small heart syndrome may contribute to the development of CFS as a constitutional factor predisposing to fatigue, and may be included in the genesis of CFS.[9]

Online presence[edit]

References[edit]

  1. Carruthers, BM; van de Sande, MI; De Meirleir, KL; Klimas, NG; Broderick, G; Mitchell, T; Staines, D; Powles, A C P; Speight, N; Vallings, R; Bateman, L; Baumgarten-Austrheim, B; Bell, DS; Carlo-Stella, N; Chia, J; Darragh, A; Jo, D; Lewis, D; Light, A; Marshall-Gradisnik, S; Mena, I; Mikovits, JA; Miwa, K; Murovska, M; Pall, ML; Stevens, S (2011), "Myalgic encephalomyelitis: International Consensus Criteria.", Journal of Internal Medicine, 270 (4): 327-38, PMID 21777306, doi:10.1111/j.1365-2796.2011.02428.x 
  2. http://prabook.com/web/person-view.html?profileId=618950
  3. http://prabook.com/web/person-view.html?profileId=618950
  4. Miwa, K. Heart Vessels (2016) 31: 1522. doi:10.1007/s00380-015-0744-3
  5. Miwa, K. Heart Vessels (2015) 30: 484. doi:10.1007/s00380-014-0510-y
  6. Miwa K, Fujita M. (2014) Renin-aldosterone paradox in patients with myalgic encephalomyelitis and orthostatic intolerance. International Journal of Cardiology, 172(2):514-5. doi: 10.1016/j.ijcard.2014.01.043. Epub 2014 Jan 23. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/24485613
  7. Miwa, Kunihisa; Fujita, Masatoshi (2009), "Cardiovascular Dysfunction with Low Cardiac Output Due to a Small Heart in Patients with Chronic Fatigue Syndrome", Internal Medicine, 48 (21): 1849-1854, PMID 19881233, doi:10.2169/internalmedicine.48.2347 
  8. Miwa, Kunihisa et al.(2009). Cardiac function fluctuates during exacerbation and remission in young adults with chronic fatigue syndrome and "small heart." Journal of Cardiology, Volume 54, Issue 1, 29 - 35. PMID:19632517 DOI: 10.1016/j.jjcc.2009.02.008
  9. Miwa K, Fujita M. (2008) Small heart syndrome in patients with chronic fatigue syndrome. Clinical Cardiology, 31(7):328-33. doi: 10.1002/clc.20227.http://www.ncbi.nlm.nih.gov/pubmed/18636530


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