WordNet

a plane figure with rounded sides curving inward at the top and intersecting at the bottom; conventionally used on playing cards and valentines; "he drew a heart and called it a valentine"
the courage to carry on; "he kept fighting on pure spunk"; "you havent got the heart for baseball" (同)mettle, nerve, spunk
an inclination or tendency of a certain kind; "he had a change of heart" (同)spirit
a playing card in the major suit that has one or more red hearts on it; "he led the queen of hearts"; "hearts were trumps"
the locus of feelings and intuitions; "in your heart you know it is true"; "her story would melt your bosom" (同)bosom
the hollow muscular organ located behind the sternum and between the lungs; its rhythmic contractions move the blood through the body; "he stood still, his heart thumping wildly" (同)pump, ticker
a firm rather dry variety meat (usually beef or veal); "a five-pound beef heart will serve six"
able to perceive sound
an opportunity to state your case and be heard; "they condemned him without a hearing"; "he saw that he had lost his audience" (同)audience
(law) a proceeding (usually by a court) where evidence is taken for the purpose of determining an issue of fact and reaching a decision based on that evidence
the ability to hear; the auditory faculty; "his hearing was impaired" (同)audition, auditory sense, sense of hearing, auditory modality
a session (of a committee or grand jury) in which witnesses are called and testimony is taken; "the investigative committee will hold hearings in Chicago"
receive a communication from someone; "We heard nothing from our son for five years"
examine or hear (evidence or a case) by judicial process; "The jury had heard all the evidence"; "The case will be tried in California" (同)try
perceive (sound) via the auditory sense
an impairment of health or a condition of abnormal functioning
caused by or altered by or manifesting disease or pathology; "diseased tonsils"; "a morbid growth"; "pathologic tissue"; "pathological bodily processes" (同)morbid, pathologic, pathological

PrepTutorEJDIC

〈C〉『心臓』;胸 / 〈C〉(感情の中心をなす)『心』,気持ち / 〈U〉愛情,同情 / 〈U〉『勇気』,元気,熱意 / 《the ~》『中心』,内部,(物事の)本質,核心 / 〈C〉ハート形の物;(カードの)ハートの札
〈U〉『聴力』,聴覚〈U〉〈C〉(…を)『聞くこと』,(…の)聞き取り《+『of』+『名』》・〈C〉聞いてもらう機会,聞いてやること・聴取・聴聞会〈C〉(法廷などでの)尋問,審問,;(刑罰の減免を求める)釈明,意見陳述 / 〈U〉聞こえる距離(範囲)
〈音〉‘が'『聞こえる』,‘を'聞く(進行形にできない) / 〈人の言うこと〉‘に'『耳を傾ける』,‘を'注意深く聞く(listen);(裁判官などが)…の申し立てを聞く / 〈うわさ・ニュースなど〉‘を'『耳にしている』,聞いている / 『耳が聞こえる』 / 《しばしば命令形で》耳を傾ける,注意を向ける / 『うわさ』(『消息』)『を聞く』
(体の)『病気』,疾患 / (精神・道徳などの)病気,病弊
女性の話術芸人 =diseur
病気にかかった / 病的な,不健全な(morbid)

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/05/31 04:52:10」(JST)

wiki en

Valvular heart disease is any disease process involving one or more of the valves of the heart (the aortic and mitral valves on the left and the pulmonary and tricuspid valves on the right). Valve problems may be congenital (inborn) or acquired (due to another cause later in life). Treatment may be with medication but often (depending on the severity) involves valve repair or replacement (insertion of an artificial heart valve). Specific situations include those where additional demands are made on the circulation, such as in pregnancy.^[1]

Types [edit]

Valve involved	Stenotic disease	Insufficiency/regurgitation disease
Aortic valve	Aortic valve stenosis	Aortic insufficiency/regurgitation
Mitral valve	Mitral valve stenosis	Mitral insufficiency/regurgitation
Tricuspid valve	Tricuspid valve stenosis	Tricuspid insufficiency/regurgitation
Pulmonary valve	Pulmonary valve stenosis	Pulmonary insufficiency/regurgitation

Aortic and mitral valve disorders [edit]

Pulmonary and tricuspid valve disorders [edit]

Pulmonary and tricuspid valve diseases are right-side heart diseases. Pulmonary valve diseases are the least common heart valve disease in adults.^[2]

The most common types of pulmonary valve diseases are:

pulmonary valve stenosis
pulmonary valve insufficiency
- pulmonary valve incompetence
- pulmonary valve regurgitation

The International Statistical Classification of Diseases classifies non rheumatic pulmonary valve diseases as I37.

Both tricuspid and pulmonary valve diseases are less common than aortic or mitral valve diseases due to the lower pressure those valves experience.^[2]

Dysplasia [edit]

Heart valve dysplasia is an error in the development of any of the heart valves, and a common cause of congenital heart defects in humans as well as animals; tetralogy of Fallot is a congenital heart defect with four abnormalities, one of which is stenosis of the pulmonary valve. Ebstein's anomaly is an abnormality of the tricuspid valve.^[1]

Rheumatic disorders [edit]

Valvular heart disease resulting from rheumatic fever is referred to as "rheumatic heart disease". While developed countries once had a significant burden of rheumatic fever and rheumatic heart disease, medical advances and improved social conditions have dramatically reduced their incidence. Many developing countries, as well as indigenous populations within developed countries, still carry a significant burden of rheumatic fever and rheumatic heart disease and there has been a resurgence in efforts to eradicate the diseases in these populations. Inflammation of the heart valves due to any cause is called endocarditis; this is usually due to bacterial infection but may also be due to cancer (marantic endocarditis), certain autoimmune conditions (Libman-Sacks endocarditis) and hypereosinophilic syndrome (Loeffler endocarditis). Certain medications have been associated with valvular heart disease, most prominently ergotamine derivatives pergolide and cabergoline.^[3]

In pregnancy [edit]

The evaluation of individuals with valvular heart disease who are or wish to become pregnant is a difficult issue. Issues that have to be addressed include the risks during pregnancy to the mother and the developing fetus. Normal physiological changes during pregnancy require, on average, a 50% increase in circulating blood volume that is accompanied by an increase in cardiac output that usually peaks between the midportion of the second and third trimesters.^[4] The increased cardiac output is due to an increase in the stroke volume, and a small increase in heart rate, averaging 10 to 20 beats per minute.^[4] Additionally uterine circulation and endogenous hormones cause systemic vascular resistance to decrease and a disproportionately lowering of diastolic blood pressure causes a wide pulse pressure.^[4] Inferior vena caval obstruction from a gravid uterus in the supine position can result in an abrupt decrease in cardiac preload, which leads to hypotension with weakness and lightheadedness.^[4] During labor and delivery cardiac output increases more in part due to the associated anxiety and pain, as well as due to uterine contractions which will cause an increases in systolic and diastolic blood pressure.^[4]

Valvular heart lesions associated with high maternal and fetal risk during pregnancy^[4] 1. Severe aortic stenosis with or without symptoms 2. Aortic regurgitation with NYHA functional class III-IV symptoms 3. Mitral stenosis with NYHA functional class II-IV symptoms 4. Mitral regurgitation with NYHA functional class III-IV symptoms 5. Aortic and/or mitral valve disease resulting in severe pulmonary hypertension (pulmonary pressure greater than 75% of systemic pressures) 6. Aortic and/or mitral valve disease with severe LV dysfunction (EF less than 0.40) 7. Mechanical prosthetic valve requiring anticoagulation 8. Marfan syndrome with or without aortic regurgitation ^[4]

In individuals who require an artificial heart valve, consideration must be made for deterioration of the valve over time (for bioprosthetic valves) versus the risks of anticoagulation during pregnancy.

Comparison [edit]

The following table includes the main types of valvular stenosis and regurgitation. Major types of valvular heart disease not included in the table include mitral valve prolapse, rheumatic heart disease and endocarditis.

Valvular disease	Mitral stenosis	Aortic stenosis	Aortic regurgitation	Mitral regurgitation	Tricuspid regurgitation
Prevalence	Most common valvular heart disease in pregnancy^[5]	Approximately 2% of people over the age of 65, 3% of people over age 75, and 4% percent of people over age 85^[6]		2% of the population, equally in males and females.^[7]
Main causes and risk factors	Almost always caused by rheumatic heart disease^[8]	Calcification of tricuspid aortic valve with age^[8] (>50%^[9]) Calcification of bicuspid aortic valve^[8] (30-40%^[9]) Rheumatic fever^[8] (<10%^[9]) Hypertension, diabetes mellitus, hyperlipoproteinemia and uremia may speed up the process.^[9]	Acute Infective endocarditis^[8]^[9] Trauma^[8] Chronic Primary valvular: rheumatic fever, bicuspid aortic valve, Marfan's syndrome, Ehlers–Danlos syndrome, ankylosing spondylitis, systemic lupus erythematosus^[8] Disease of the aortic root: syphilitic aortitis, osteogenesis imperfecta, aortic dissection, Behçet's disease, reactive arthritis, systemic hypertension^[8]	Acute Endocarditis, mainly S. aureus^[8] Papillary muscle rupture or dysfunction,^[8] including mitral valve prolapse^[9] Chronic Rheumatic fever^[8] Marfan's syndrome^[8] Cardiomyopathy^[8]	Usually secondary to right ventricular dilation^[8] left ventricular failure is, in turn, the most common cause^[8] Right ventricular infarction^[8] Inferior myocardial infarction^[8] Cor pulmonale^[8] Other causes: Tricuspid endocarditis, rheumatic fever, Ebstein's anomaly, carcinoid syndrome and myxomatous degeneration^[8]
Hemo dynamics / Patho- physiology	Progressive obstruction of the mitral ostium causes increased pressure in the left atrium and the pulmonary circulation.^[9] Congestion may cause thromboembolism, and atrial hypertension may cause atrial fibrillation.^[9]	Obstruction through the aortic ostium causes increased pressure in the left ventricle and impaired flow through the aorta	Insufficiency of the aortic valve causes backflow of blood into the left ventricle during diastole.	Insufficiency of the mitral valve causes backflow of blood into the left atrium during systole.	Insufficiency of the tricuspid valve causes backflow of blood into the right atrium during systole.
Symptoms	Heart failure symptoms, such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea^[8] Palpitations^[8] Chest pain^[8] Hemoptysis^[8] Thromboembolism^[8] Ascites and edema (if right-sided heart failure develops)^[8] Symptoms increase with exercise and pregnancy^[8]	Heart failure symptoms, such as dyspnea on exertion (most frequent symptom^[9]), orthopnea and paroxysmal nocturnal dyspnea^[8] Angina pectoris^[8] Syncope, usually exertional^[8]	Heart failure symptoms, such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea^[8] Palpitations^[8] Angina pectoris^[8] In acute cases: cyanosis and circulatory shock^[8]	Heart failure symptoms, such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea^[8] Palpitations^[8] Pulmonary edema^[8]	Symptoms of right-sided heart failure, such as ascites, hepatomegaly, edema and jugular venous distension^[8]
Medical signs	Opening snap followed by a low-pitched diastolic rumble with presystolic accentuation.^[8]^[9] The opening snap follows closer to the S₂ heart tone with worsening stenosis.^[8] The murmur is heard best with the bell of the stethoscope^[8] lying on the left side^[9] and its duration increases with worsening disease.^[8] Loud S₁ - may be the most prominent sign^[8] Advanced disease may present with signs of right-sided heart failure such as parasternal heave, jugular venous distension, hepatomegaly, ascites and/or pulmonary hypertension (presenting with a loud P₂.^[8] Signs increase with exercise and pregnancy^[8]	Systolic murmur of a harsh crescendo-decrescendo type, heard in 2nd right intercostal space,^[9] radiating to the carotid arteries^[8] Pulsus parvus et tardus, that is, diminished and delayed carotid pulse^[8]^[9] Fourth heart sound^[8] Decreased A₂ sound^[9] Sustained apex beat^[8] Precordial thrill^[8]	Increased pulse pressure by increased systolic and decreased diastolic blood pressure,^[8] but may not be significant if acute^[9] Diastolic decrescendo murmur best heard at left sternal border^[8] Water hammer pulse^[8] Austin Flint murmur^[8] Apex beat displaced down and to the left^[8] Third heart sound may be present^[8]	Holosystolic murmur at the apex, radiating to the back or clavicular area^[8] Commonly atrial fibrillation^[8] Third heart sound^[8] Laterally displaced apex beat,^[8] often with heave^[9] Loud, palpable P₂,^[8] heard best when lying on the left side^[9] In acute cases, the murmur and tachycardia may be only distinctive signs.^[9]	Pulsatile liver Prominent V waves and rapid y descents in jugular venous pressure^[8] Inspiratory third heart sound at left lower sternal border (LLSB)^[8] Blowing holosystolic murmur at LLSB, intensifying with inspiration, and decreasing with expiration and Valsalva maneuver^[8] Parasternal heave along LLSB^[8] Atrial fibrillation is usually present^[8]
Diagnosis	Chest X-ray showing left atrial enlargement^[8] Echocardiography is the most important test to confirm the diagnosis. It shows left atrial enlargement, thick and calcified mitral valve with narrow and "fish-mouth"-shaped orifice and signs of right ventricular failure in advanced disease^[8]	Chest X-ray showing calcific aortic valve, and in longstanding disease, enlarged left ventricle^[8]^[9] and atrium^[8] ECG showing left ventricular hypertrophy and left atrial abnormality^[8] Echocardiography is diagnostic in most cases, showing left ventricular hyperthrophy, thickened and immobile aortic valve and dilated aortic root,^[8] but may appear normal if acute^[9] Cardiac chamber catheterization provides a definitive diagnosis, indicating severe stenosis in valve area of <0.8 cm² (normally 3 to 4 cm²). It is useful in symptomatic patients before surgery.^[8]	Chest X-ray showing left ventricular hypertrophy and dilated aorta^[8] ECG indicating left ventricular hypertrophy^[8] Echocardiogram showing dilated left aortic root and reversal of blood flow in the aorta. In longstanding disease there may be left ventricular dilatation. In acute aortic regurgitation, there may be early closure of the mitral valve.^[8] Cardiac chamber catetherization assists in assessing the severity of regurgitation and any left ventricular dysfunction^[8]	Chest X-ray showing dilated left ventricle^[8] Echocardiography to detect mitral reverse flow, dilated left atrium and ventricle and decreased left ventricular function^[8]	Echocardiography identifying tricuspid prolapse or flail^[8] ECG showing enlargement of right ventricle and atrium^[8]
Treatment	No therapy is required for asymptomatic patients. Diuretics for any pulmonary congestion or edema.^[8] If stenosis is severe, surgery is recommended.^[8] Any atrial fibrillation is treated accordingly.^[8] Medically, with diuretics, prophylaxis of infective endocarditis and chronic anticoagulant administration with warfarin (especially when there's atrial fibrillation)^[8] Surgically, by mitral valvuloplasty with a percutaneously inserted balloon, unless significant mitral regurgitation or too much calcification.^[9] Indicated in ostium area < 1-1.2 cm².^[9] Other options include valvulotomy or mitral valve replacement by open surgery^[8]	No treatment in asymptomatic patients.^[8] If symptomatic, treated with aortic valve replacement surgery.^[8] Medical therapy and percutaneous balloon valvuloplasty have relatively poor effect.^[8] - Any angina is treated with short-acting nitrovasodilators, beta-blockers and/or calcium blockers^[9] - Any hypertension is treated aggressively, but caution must be taken in administering beta-blockers^[9] - Any heart failure is treated with digoxin, diuretics, nitrovasodilators and, if not contraindicated, cautious inpatient administration of ACE inhibitors^[9]	If stable and asymptomatic - conservative treatment such as low sodium diet,^[8] diuretics,^[8] vasodilators^[8] (e.g. (hydralazin^[9] or prazosin^[9]), digoxin,^[8] ACE inhibitors^[8]/angiotensin II receptor antagonists,^[9] calcium blockers^[9] and avoiding very strenuous activity^[8]^[9] Aortic valve replacement in symptomatic patients (NYHA II^[9]-IV) or progressive left ventricular dilation^[9] or systolic ventricular diameter >55 mm^[9] on echocardiogrphy. Immediately if acute.^[8] Also, endocarditis prophylaxis is indicated before dental, gastrointestinal or genitourinary procedures.^[8]	Medically Afterload reduction with vasodilators^[8]^[9] Any hypertension is treated aggressively,^[9] e.g. by diuretics and low sodium diet^[8] digoxin^[8]^[9] Antiarrhythmics^[8]^[9] Chronic anticoagulation in concomitant mitral valve prolapse^[9] or atrial fibrillation^[8] In acute cases - IABP as temporary solution until surgery^[8] Surgery by either mitral valve repair or mitral valve replacement,^[8] indicated if very symptomatic (NYHA III), ventricular dilation or decreasing ejection fraction^[9]	Treatment of underlying cause^[8] Surgery^[8] Tricuspid valvular repair^[8] Valvuloplasty^[8] Valve replacement (rarely performed)^[8]
Follow-up		In moderate cases, echocardiography every 1–2 years, possibly complemented with cardiac stress test.^[9] Immediate revisit if new related symptoms appear.^[9] In severe cases, echocardiography every 3–6 months.^[9] Immediate revisit or inpatient care if new related symptoms appear.^[9]	In mild to moderate cases, echocardiography and cardiac stress test every 1–2 years^[9] In severe moderate/severe cases, echocardiography with cardiac stress test and/or isotope perfusion imaging every 3–6 months.^[9]	In mild to moderate cases, echocardiography and cardiac stress test every 1–3 years.^[9] In severe cases, echocardiography every 3–6 months.^[9]

References [edit]

^ ^a ^b Bonow RO, Carabello BA, Kanu C, et al. (2006). "ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons". Circulation 114 (5): e84–231. doi:10.1161/CIRCULATIONAHA.106.176857. PMID 16880336.
^ ^a ^b Ragavendra R. Baliga, Kim A. Eagle, William F Armstrong, David S Bach, Eric R Bates, Practical Cardiology, Lippincott Williams & Wilkins, 2008, page 452.
^ Schade R, Andersohn F, Suissa S, Haverkamp W, Garbe E (2007). "Dopamine agonists and the risk of cardiac-valve regurgitation". N. Engl. J. Med. 356 (1): 29–38. doi:10.1056/NEJMoa062222. PMID 17202453.
^ ^a ^b ^c ^d ^e ^f ^g Bonow, RO; Carabello, BA; Chatterjee, K; De Leon Jr, AC; Faxon, DP; Freed, MD; Gaasch, WH; Lytle, BW et al. (2008). "2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons". Journal of the American College of Cardiology 52 (13): e1–142. doi:10.1016/j.jacc.2008.05.007. PMID 18848134. |displayauthors= suggested (help)
^ Gelson, E.; Gatzoulis, M.; Johnson, M. (2007). "Valvular heart disease". BMJ (Clinical research ed.) 335 (7628): 1042–1045. doi:10.1136/bmj.39365.655833.AE. PMC 2078629. PMID 18007005. edit
^ Stewart BF, Siscovick D, Lind BK, Gardin JM, Gottdiener JS, Smith VE. Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study. J Am Coll Cardiol. 1997; 29: 630-634.
^ The Cleveland Clinic Center for Continuing Education > Mitral Valve Disease: Stenosis and Regurgitation Authors: Ronan J. Curtin and Brian P. Griffin. Retrieved September 2010
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r ^s ^t ^u ^v ^w ^x ^y ^z ^aa ^ab ^ac ^ad ^ae ^af ^ag ^ah ^ai ^aj ^ak ^al ^am ^an ^ao ^ap ^aq ^ar ^as ^at ^au ^av ^aw ^ax ^ay ^az ^ba ^bb ^bc ^bd ^be ^bf ^bg ^bh ^bi ^bj ^bk ^bl ^bm ^bn ^bo ^bp ^bq ^br ^bs ^bt ^bu ^bv ^bw ^bx ^by ^bz ^ca ^cb ^cc ^cd ^ce ^cf ^cg ^ch ^ci ^cj ^ck ^cl ^cm ^cn ^co ^cp ^cq ^cr ^cs ^ct ^cu ^cv ^cw ^cx ^cy ^cz ^da ^db ^dc ^dd Chapter 1: Diseases of the Cardiovascular system > Section: Valvular Heart Disease in: Elizabeth D Agabegi; Agabegi, Steven S. (2008). Step-Up to Medicine (Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7153-6.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r ^s ^t ^u ^v ^w ^x ^y ^z ^aa ^ab ^ac ^ad ^ae ^af ^ag ^ah ^ai ^aj ^ak ^al ^am ^an ^ao ^ap ^aq ^ar ^as ^at ^au VOC=VITIUM ORGANICUM CORDIS, a compendium of the Department of Cardiology at Uppsala Academic Hospital. By Per Kvidal September 1999, with revision by Erik Björklund May 2008

External links [edit]

Rheumatic Heart Disease Network

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 高齢者の弁膜症 valvular heart disease in elderly adults
2. 薬剤誘発性の弁膜症 valvular heart disease induced by drugs
3. 末期腎不全患者における弁膜症 valvular heart disease in patients with end stage renal disease
4. 弁膜症および妊娠 pregnancy and valve disease
5. リウマチ性心疾患の自然史、スクリーニング、およびマネージメント natural history screening and management of rheumatic heart disease

English Journal

Fn14 promotes differentiation of human mesenchymal stem cells into heart valvular interstitial cells by phenotypic characterization.

Huang W, Xiao DZ, Wang Y, Shan ZX, Liu XY, Lin QX, Yang M, Zhuang J, Li Y, Yu XY.Author information Medical Research Center of Guangdong General Hospital, Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China.AbstractDespite the fact that tissue engineered heart valves (TEHV) hold great promise for heart valve disease treatment, one of the challenges is to find suitable seeding cells. Bone marrow derived mesenchymal stem cells (MSCs) were considered to be one of the best seed cell sources. In this study we propose a novel approach to promote stem cell differentiation into the seed cells of TEHV, valvular interstitial cells (VICs). Newly induced MSCs (iMSCs) were created from a co-culture niche in which healthy human donor derived MSCs were co-cultured with cardiac fibroblasts (H9C2 cell line). Then iMSCs were transfected with either a mock vector (iMSCs(mock) ) as controls or with a vector that overexpresses thefibroblast inducible factor 14 (Fn14) gene (iMSCs(Fn14) ). Immunofluorescence staining was performed to assay VIC differentiation. Western blot analysis was performed to analyze the involved signaling pathway. The results demonstrate that the expression of α-smooth muscle actin (SMA) was significantly higher in iMSCs(Fn14) as compared with iMSC(mock) , and MSC, and also had higher co-alignment of α-actinin and stress fiber (F-actin) in bundles. Additionally, increased biosynthesis of extracellular matrix (ECM) proteins including collagen I, collagen III, and fibronection were observed in iMSCs(Fn14) in comparison with iMSCs(mock) . These data observed in iMSCs(Fn14) were in accordance with VIC phenotype from normal heart valves. In addition, the PI3K/Akt signaling pathway was activated in iMSCs(Fn14) which allowed higher Akt phosphorylation (p-Akt) levels and SMA levels, whereas, it was attenuated by LY294002 (PI3K/Akt inhibitor). These new findings of the effect of Fn14 on VIC-like cell differentiation may provide a novel therapeutic strategy for heart valve disease treatment. J. Cell. Physiol. 229: 580-587, 2014. © 2013 Wiley Periodicals, Inc.
Journal of cellular physiology.J Cell Physiol.2014 May;229(5):580-7. doi: 10.1002/jcp.24480.
Despite the fact that tissue engineered heart valves (TEHV) hold great promise for heart valve disease treatment, one of the challenges is to find suitable seeding cells. Bone marrow derived mesenchymal stem cells (MSCs) were considered to be one of the best seed cell sources. In this study we propo
PMID 24122208

microRNA-122 down-regulation may play a role in severe myocardial fibrosis in human aortic stenosis through TGF-β1 up-regulation.

Beaumont J1, López B1, Hermida N1, Schroen B2, San José G1, Heymans S2, Valencia F3, Gómez-Doblas JJ3, De Teresa E3, Díez J, González A1.Author information 1*Division of Cardiovascular Sciences, Centre for Applied Medical Research, University of Navarra, 31008 Pamplona, Spain.2†Center for Heart Failure Research, Cardiovascular Research Institute Maastricht, Maastricht University, 6229 ER Maastricht, The Netherlands.3‡Division of Cardiology, Virgen de la Victoria University Hospital, 29010 Málaga, Spain.AbstractmiRNAs (microRNAs) have been shown to play a role in myocardial fibrosis. The present study was designed to analyse whether alterations in miRNA expression contribute to the progression of myocardial fibrosis in AS (aortic valve stenosis) patients through up-regulation of the pro-fibrotic factor TGF-β1 (transforming growth factor-β type 1). Endomyocardial biopsies were obtained from 28 patients with severe AS, and from the necropsies of 10 control subjects. AS patients presented increased myocardial CVF (collagen volume fraction) and TGF-β1 compared with the controls, these parameters being correlated in all patients. Patients were divided into two groups by cluster analysis according to their CVF: SF (severe fibrosis; CVF >15%; n=15) and non-SF (CVF ≤15%; n=13). TGF-β1 was increased in patients with SF compared with those with non-SF. To analyse the involvement of miRNAs in SF, the miRNA expression profile of 10 patients (four with non-SF and six with SF) was analysed showing that 99 miRNAs were down-regulated and 19 up-regulated in the SF patients compared with the non-SF patients. Those miRNAs potentially targeting TGF-β1 were validated by real-time RT (reverse transcription)-PCR in the whole test population, corroborating that miR-122 and miR-18b were down-regulated in patients with SF compared with those with non-SF and the control subjects. Additionally, miR-122 was inversely correlated with the CVF, TGF-β1 and the TGF-β1-regulated PCPE-1 (procollagen C-terminal proteinase enhancer-1) in all patients. Experiments in human fibroblasts demonstrated that miR-122 targets and inhibits TGF-β1. In conclusion, for the first time we show that myocardial down-regulation of miR-122 might be involved in myocardial fibrosis in AS patients, probably through TGF-β1 up-regulation.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 Apr;126(7):497-506. doi: 10.1042/CS20130538.
miRNAs (microRNAs) have been shown to play a role in myocardial fibrosis. The present study was designed to analyse whether alterations in miRNA expression contribute to the progression of myocardial fibrosis in AS (aortic valve stenosis) patients through up-regulation of the pro-fibrotic factor TGF
PMID 24168656

Usefulness of novel hematologic inflammatory parameters to predict prosthetic mitral valve thrombosis.

Gürsoy OM1, Karakoyun S2, Kalçık M2, Gökdeniz T2, Yesin M2, Gündüz S2, Astarcıoğlu MA2, Ozkan M3.Author information 1Department of Cardiology, Koşuyolu Kartal Heart Training and Research Hospital, Istanbul, Turkey. Electronic address: dr.semra@hotmail.com.2Department of Cardiology, Koşuyolu Kartal Heart Training and Research Hospital, Istanbul, Turkey.3Department of Cardiology, Kafkas University Faculty of Medicine, Kars, Turkey.AbstractProsthetic valve thrombosis (PVT) is a life-threatening complication. Neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR) have been studied as inflammatory biomarkers in atherosclerosis, but data regarding valvular disease are lacking. The study population included patients with mitral PVT (n = 152) versus control subjects (n = 164) with functional mitral prosthesis. Transesophageal echocardiography was performed to diagnose PVT. NLR and PLR were calculated using complete blood count. C-reactive protein (CRP) levels were also analyzed. Neutrophil and platelet levels did not differ between the groups (4.9 ± 2.0 vs 4.7 ± 1.5, p = 0.84 and 254.8 ± 89.7 vs 241.5 ± 62.8 p = 0.36, respectively), but lymphocyte levels were significantly lower in patients with PVT than the controls (1.8 ± 0.7 vs 2.2 ± 0.6, p <0.001). NLR, PLR, and CRP levels were significantly higher in patients with PVT than in controls (3.2 ± 2.1 vs 2.2 ± 0.8, p <0.001; 163 ± 77.5 vs 114.9 ± 37.3, p <0.001; and 1.97 ± 3.02 vs 1.02 ± 1.22, p = 0.01, respectively). A positive correlation was observed between NLR and PLR (r = 528, p <0.001). NLR level of >2.23, measured on admission, yielded an area under the curve value of 0.659 (95% confidence interval 0.582 to 0.736, sensitivity 66%, specificity 60%, p <0.001) and PLR level of >117.78 yielded an area under the curve value of 0.707 (95% confidence interval 0.636 to 0.777, sensitivity 70%, specificity 58%, p <0.001). Multivariate analysis showed that increased PLR and inadequate anticoagulation were independent predictors of thrombosis in patients with PVT. In conclusion, patients with PVT had increased NLR, PLR, and CRP levels compared with subjects with normofunctional prosthesis, and increased PLR was an independent predictor of mitral PVT.
The American journal of cardiology.Am J Cardiol.2014 Mar 1;113(5):860-4. doi: 10.1016/j.amjcard.2013.11.029. Epub 2013 Dec 12.
Prosthetic valve thrombosis (PVT) is a life-threatening complication. Neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR) have been studied as inflammatory biomarkers in atherosclerosis, but data regarding valvular disease are lacking. The study population included patients with mi
PMID 24411287

Japanese Journal

Valvular Heart Disease : Tricuspid Annular Dynamics Before and After Tricuspid Annuloplasty : Three-Dimensional Transesophageal Echocardiography

Nishi Hiroyuki,Toda Koichi,Miyagawa Shigeru [他]
Circulation journal : official journal of the Japanese Circulation Society 79(4), 873-879, 2015-04
NAID 40020412504

Valvular Heart Disease : Major Non-Cardiac Surgery Is a Risk Factor for Rapid Hemodynamic Progression of Non-Rheumatic Aortic Stenosis

Mizuno Reiko,Yamagami Shin-taro,Higashi Tsukimi [他]
Circulation journal : official journal of the Japanese Circulation Society 79(4), 867-872, 2015-04
NAID 40020412475

Transcatheter Aortic Valve-in-Valve Implantation for Patients With Degenerative Surgical Bioprosthetic Valves

,
Circulation Journal advpub(0), 2015
Bioprosthetic tissue valves are increasingly utilized during surgical aortic valve replacement. These valves have limited durability and many fail with time, resulting in stenosis, regurgitation, or b …
NAID 130004927254

Related Pictures

★リンクテーブル★

リンク元	「心臓弁膜症」「心弁膜症」「心臓弁疾患」「valvular disease」「valvulopathy」
関連記事	「disease」「hearing」「valvular」「hear」「heart」

「心臓弁膜症」

Valvular heart disease
	Classification and external resources
ICD-10	I34-I37, I05-I08, Q22-Q23
ICD-9	394-396, 424, 746
MeSH	D006349

　　[★]

英: valvular heart disease
同: 弁膜性心疾患、弁膜症
関

	大動脈弁閉鎖不全症	大動脈弁狭窄症	僧帽弁閉鎖不全症	僧帽弁狭窄症
	AR	AS	MR	MS
左心房の変化 (慢性の経過)	拡張		拡張	肥大拡張
左心室の変化 (慢性の経過)	拡張	肥大	拡張	－
心房細動			○	○
心原性脳塞栓症				◎
心拍と病態悪化	逆流低減のため頻脈が良い		逆流低減のため頻脈が良い	左房駆出量維持のため徐脈が良い