ライフサイエンスコーパス: valvular

1 No significant correlation was noted between valvular 18F-FDG uptake and change in calcium score (r=-

2 delineation of congenital heart defects and valvular abnormalities are the primary diagnostic applic

3 erentiation of mesenchymal cushion cells and valvular abnormalities via a transforming growth factor-

4 No cardiac structural or valvular abnormalities were observed after treatment wit

5 eter-based procedures for the repair of many valvular abnormalities.

6 no knockdown, including vascular and cardiac valvular abnormalities.

7 Mitral valve prolapse is a common valvular abnormality but the pathogenic cause of myxomat

8 On the basis of the definitions of the Valvular Academic Research Consortium, the rate of major

9 Consecutive outpatients with non-valvular AF were recruited and rates of thrombotic/cardi

10 Id-FTR valvular alterations (versus controls) were largest annu

11 ss the incremental role of 3DE in evaluating valvular anatomic features, volumetric quantification, p

12 varying cause of the disease, complexity of valvular anatomy, imaging, and delivery issues.

13 within the normal range were associated with valvular and annular calcification in a community-based

14 Left-sided cardiac valvular and annular calcifications are suspected as ris

15 Both conditions pose the risk of valvular and aortic complications not only for affected

16 For mechanistic purposes, we measured valvular and right ventricular (RV) remodeling in 141 Id

17 atment alone induces matrix calcification of valvular and vascular cells, we next examined whether RA

18 our patients afflicted with arteriosclerotic valvular and vascular diseases.

19 ught to characterize the interaction between valvular and vascular functions in patients with AS by u

20 ersus 2.74+/-0.4 cm(2), P<0.0001) and lowest valvular/annular coverage ratio (1.06+/-0.1 versus 1.45+

21 ss annular and RV-basal enlargement exhausts valvular/annular coverage reserve, and RV conical deform

22 iagnosed with ventricular hypertrophy due to valvular aortic stenosis, acromegaly, or growth hormone

23 Valvular dynamics showed stable valvular area in systole in FED versus considerable syst

24 by multiple factors, valvular (AVC) and non-valvular (arterial compliance) independently of flow.

25 ount the interrelation between the different valvular, arterial, and ventricular variables that may b

26 udy of adults >/=40 years of age with severe valvular AS (peak velocity >/=4 m/s, mean gradient >40 m

27 ystem Systemic Embolism in Patients With Non-Valvular Atrial Fibrillation [ROCKET AF]; NCT00403767).

28 Adult patients with non-valvular atrial fibrillation were eligible for inclusion

29 pensity-matched cohorts of patients with non-valvular atrial fibrillation with incident exposure to d

30 ystem Systemic Embolism in Patients With Non-Valvular Atrial Fibrillation) trial.

31 In patients with non-valvular atrial fibrillation, embolic stroke is thought

32 In patients with non-valvular atrial fibrillation, oral anticoagulation with

33 for stroke prophylaxis in patients with non-valvular atrial fibrillation.

34 ation for cardioversion of patients with non-valvular atrial fibrillation.

35 s undergoing electrical cardioversion of non-valvular atrial fibrillation.

36 ystem Systemic Embolism in Patients With Non-Valvular Atrial Fibrillation: NCT00403767).

37 m AVA and is determined by multiple factors, valvular (AVC) and non-valvular (arterial compliance) in

38 -targeted molecular imaging for detection of valvular biology in CAVD.

39 -to-background ratio (TBR) was calculated as valvular/blood activity.

40 The presence of any annular or valvular calcification (mitral annular calcification, ao

41 tion is challenging, owing to the absence of valvular calcification and distortion of aortic root ana

42 and repeatable approach to the evaluation of valvular calcification and inflammation in patients with

43 al PET/CT Study Examining the Role of Active Valvular Calcification and Inflammation in Patients With

44 nderstood, and the relative contributions of valvular calcification and inflammation to disease progr

45 lve and similar AS severity, women have less valvular calcification but more fibrosis compared with m

46 ntervening in the progression of annular and valvular calcification could reduce the incidence of cov

47 17 patients (39.5%) had the degree of aortic valvular calcification documented on CT or echocardiogra

48 erum mineral metabolism markers with cardiac valvular calcification have not been evaluated in a well

49 ed with a greater prevalence of vascular and valvular calcification in people with moderate CKD.

50 Valvular calcification is associated with the developmen

51 t cohorts of persons with either CT-detected valvular calcification or clinical aortic stenosis.

52 Hence, the relationship between valvular calcification process and AS severity differs i

53 The degree of annular or valvular calcification severity showed a direct relation

54 In all patients requiring second valves, valvular calcification was absent (p = 0.014).

55 (defined by aortic, thoracic, coronary, and valvular calcification); (2) adiposity (defined by peric

56 haracterized by early and extreme aortic and valvular calcification, dental anomalies (early-onset pe

57 available regarding genetic contributions to valvular calcification, which is an important precursor

58 Key features of CAVD-leaflet thickening and valvular calcification-were noted after 6 mo of WD and w

59 g older people and may contribute to cardiac valvular calcification.

60 Left-sided cardiac annular and valvular calcifications are associated with covert MRI-d

61 Both intimal and valvular calcifications are closely associated with athe

62 decreased myofibroblast activation, reduced valvular calcium burden, suppressed pro-osteogenic signa

63 nd molecular mechanisms converge to regulate valvular calcium load; this is evidenced not only in his

64 left-sided heart failure from myocardial or valvular causes, right ventricular volume and pressure o

65 ptation, including a profibrotic increase in valvular cell activation, CD45-positive cells, and matri

66 es; (b) the role of developmental processes, valvular cell behavior, and extracellular matrix remodel

67 (OxPL) are key mediators of calcification in valvular cells and are carried by Lp(a).

68 Valvular changes were linked to specific RV changes, lar

69 o inspiratory annular enlargement (decreased valvular coverage) and to inspiratory right ventricular

70 contractile activity, may be responsible for valvular cusp retraction, stiffening, and formation of c

71 me of the reported endocarditis patients had valvular damage as a predisposing condition.

72 sease may help prevent progression to severe valvular damage.

73 Congenital valvular defects are prevalent among newborns and can ca

74 peutic modality in the management of various valvular defects.

75 ond, cardiac structural problems, especially valvular degeneration, can have a dramatic impact long t

76 uction of cushion mesenchyme as required for valvular development and septation of the heart.

77 al regurgitation severity and of annular and valvular dimensions by real-time 3-dimensional-transesop

78 cular disease (11.7%, 10.8%, and 17.6%), and valvular disease (16.7%, 21.2%, and 35.8%), increased, a

79 patients with angina pectoris without known valvular disease (n = 95).

80 disease (RR, 6.1), heart failure (RR, 19.4), valvular disease (RR, 13.6), and arrhythmia (RR, 6.0; al

81 valve structures is the most common form of valvular disease and is characterized by the appearance

82 ibrillation is associated with more advanced valvular disease and noncardiac comorbidities.

83 ore likely than men to have hypertension and valvular disease as the underlying etiology.

84 cterization of the mechanism and severity of valvular disease as well as determining the hemodynamic

85 tery disease, heart failure, and significant valvular disease from the fifth visit of the ARIC study

86 seases of the myocardium, and the effects of valvular disease on myocardial function, and to advance

87 der age, diabetes mellitus, and a history of valvular disease predicted both types of HF (P</=0.0025

88 y surveillance and overutilization of TTE in valvular disease provides a model to study variation in

89 proportions of deaths from heart failure and valvular disease specifically increased with declining e

90 re AS (valve area </= 1 cm(2)) without other valvular disease underwent cardiac catheterization.

91 phy, dilation or dysfunction, or significant valvular disease), C1 (clinical HF without prior hospita

92 e of coronary artery disease, heart failure, valvular disease, and arrhythmia by 45 years of age was

93 h as coronary artery disease, heart failure, valvular disease, and arrhythmia.

94 RIC) study who were in sinus rhythm, free of valvular disease, and had acceptable quality 3-dimension

95 ic disease, hypertension, heart failure, and valvular disease, and it is a strong predictor of increa

96 han 65 years on April 1, 2002, without prior valvular disease, coronary artery disease, heart failure

97 For patients without significant valvular disease, decisions around anticoagulation thera

98 morbid conditions (congestive heart failure, valvular disease, hypertension, paralysis, neurologic di

99 gery, hypertrophic cardiomyopathy, rheumatic valvular disease, or greater than mild mitral stenosis).

100 mal or persistent AF and without significant valvular disease, uncontrolled hypertension, coronary ar

101 c dysfunction is the result of aortic and/or valvular disease.

102 on as a potential genetic basis for calcific valvular disease.

103 explain the association of aortic vessel and valvular disease.

104 nd NOTCH mutations are associated with adult valvular disease.

105 prone to developing severe aortic disease or valvular disease.

106 g former drinkers and those with significant valvular disease.

107 es, including advanced calcific arterial and valvular disease; however, the mechanisms of accelerated

108 rtic stenosis (AS) is one of the most common valvular diseases encountered in clinical practice.

109 surgery, elective versus emergent CABG, any valvular disorder) and post-operative adverse events (st

110 her physiological differences in annular and valvular dynamics exist between these phenotypes remains

111 Valvular dynamics showed stable valvular area in systole

112 rdial effusion (1C), cardiac tamponade (1B), valvular dysfunction (1C), endocarditis in native (2C) o

113 on differently from skeletal osteoblasts) to valvular dysfunction have been facilitated by the develo

114 =38), regurgitation in 50% (n=102), combined valvular dysfunction in 26% (n=54), and normal aortic va

115 ction fraction [EF] <50%) but without severe valvular dysfunction were eligible.

116 an increased risk of other CVD (dysrhythmia, valvular dysfunction, and pericarditis) (adjusted, 1.29

117 (BAV) morphologic findings and the degree of valvular dysfunction, presence of aortopathy, and compli

118 wild-type littermate controls to examine the valvular effects of deficient CNP/NPR2 signaling in vivo

119 e demonstrated is expressed predominantly by valvular endocardium during cardiac valve maturation, ex

120 e, where they influence the functions of the valvular endothelial cells that line the leaflet surface

121 Combining strain with timing of valvular events and a measurement of peak arterial press

122 Timing of LV valvular events and LV dimensions were evaluated by cine

123 V pressure concurrent with identification of valvular events by Doppler-echocardiography for the purp

124 arterial pressure and MRI-derived timing of valvular events, represent a noninvasive approach for es

125 a standard LV pressure curve, normalized to valvular events.

126 e categorized according to AV calcification, valvular FDG uptake was increased in mildly (median 1.50

127 CDH11 mediates cell-cell contacts in both valvular fibroblasts and myofibroblasts.

128 These data suggest that valvular fibroblasts are sensing the changes in matrix e

129 Recent studies also suggest that valvular fibrosis, as well as calcification, may play an

130 mic (from 68% to 17%), SH (from 14% to 76%), valvular (from 3% to 22%), and alcohol related (from 1.1

131 t, we studied the contractile properties and valvular functions of mesenteric lymphatics, developed a

132 Primary outcomes were the change in AVA and valvular gradients over time.

133 d/or blood cultures, 63 of whom had positive valvular Gram stains.

134 4%), pulmonary vascular disease (1.2%-7.1%), valvular heart disease (5.0%-9.8%), and renal failure (7

135 Younger age (P = 0.004), valvular heart disease (P = 0.046), and the tricuspid an

136 Valvular heart disease (VHD) and atrial fibrillation (AF

137 Drug-induced valvular heart disease (VHD) is a serious side effect of

138 with atrial fibrillation (AF) and coexisting valvular heart disease (VHD) is of substantial interest.

139 art valves, significant mitral stenosis, and valvular heart disease (VHD) requiring intervention were

140 tion of Q fever in patients with preexisting valvular heart disease (VHD).

141 itial association between the development of valvular heart disease and drugs stems from observations

142 Furthermore, comorbidities such as valvular heart disease and renal failure as well as an e

143 and comorbidities such as renal failure and valvular heart disease are independent predictors for AF

144 American College of Cardiology guidelines on valvular heart disease generated considerable controvers

145 c disease guideline and Section 5.1.3 of the valvular heart disease guideline.

146 k and benefit of mechanical interventions in valvular heart disease have been primarily described amo

147 2), atrial fibrillation HR 1.54 (1.36-1.73), valvular heart disease HR 1.23 (1.05-1.44), thromboembol

148 es were dilated cardiomyopathy in 119 (53%), valvular heart disease in 34 (15%), arrhythmogenic right

149 ary heart disease in 278 participants (52%), valvular heart disease in 42 (8%), hypertension in 140 (

150 the pulmonic position in 2000, treatment for valvular heart disease in the outflow position has becom

151 Aortic stenosis is the most frequent valvular heart disease in the USA, and aortic valve repl

152 Transcatheter management of valvular heart disease is an emerging area of intense in

153 Patients with valvular heart disease often have left ventricular diast

154 ts (N=114, 49%) compared with (ischemic and) valvular heart disease patients (N=26, 17%; P<0.001).

155 METHODS AND We enrolled 335 consecutive valvular heart disease subjects who underwent echocardio

156 Valvular heart disease was defined as history or baselin

157 jection fraction of less than 40%, or severe valvular heart disease were excluded.

158 ion fractions lower than 50%, or significant valvular heart disease were excluded.

159 gy/American Heart Association guidelines for valvular heart disease were released to help guide the c

160 ed age, with chronic kidney disease, or with valvular heart disease will be discussed as well as the

161 uideline for the Management of Patients With Valvular Heart Disease".

162 ry disease, 20% atrial fibrillation, and 17% valvular heart disease).

163 ute excess risks for ischemic heart disease, valvular heart disease, and cardiomyopathy.

164 ting factors, such as renal artery stenosis, valvular heart disease, and ischemia, should be strongly

165 Mitral regurgitation (MR) is the most common valvular heart disease, and mitral valve surgery is the

166 erial revascularization, rheumatic and other valvular heart disease, and symptomatic bradyarrhythmia;

167 ders & Lipids, Rhythm Disorders, Statistics, Valvular Heart Disease, and Vascular Medicine (1-63).

168 tabolic & Lipid Disorders, Rhythm Disorders, Valvular Heart Disease, and Vascular Medicine (1-84).

169 urodegenerative Disorders, Rhythm Disorders, Valvular Heart Disease, and Vascular Medicine (1-86).

170 tabolic & Lipid Disorders, Rhythm Disorders, Valvular Heart Disease, and Vascular Medicine.

171 ders & Lipids, Rhythm Disorders, Statistics, Valvular Heart Disease, and Vascular Medicine.

172 urodegenerative Disorders, Rhythm Disorders, Valvular Heart Disease, and Vascular Medicine.

173 es have much promise as biomarkers in common valvular heart disease, but the impact of their measurem

174 olesterol; history of myocardial infarction, valvular heart disease, diabetes, lung disease, and use

175 m surrounding the diagnosis and treatment of valvular heart disease, driven in part by emerging percu

176 The 4 adventures include valvular heart disease, hypertrophic cardiomyopathy, hea

177 hypertension, sex, left atrial enlargement, valvular heart disease, left ventricular ejection fracti

178 rol ratio, prevalent coronary heart disease, valvular heart disease, left ventricular hypertrophy, an

179 In patients with advanced valvular heart disease, mechanical approaches (both perc

180 Valvular heart disease, particularly aortic stenosis and

181 ry artery disease, congestive heart failure, valvular heart disease, pericardial disease, conduction

182 stive heart failure, ischemic heart disease, valvular heart disease, pulmonary hypertension, and cong

183 used on hemodynamic measurements to evaluate valvular heart disease, pulmonary hypertension, cardiomy

184 gh surgery was the mainstay of treatment for valvular heart disease, transcatheter valve therapies ha

185 ion, and research in the field of structural valvular heart disease.

186 cardiomyopathy, ischemic heart disease, and valvular heart disease.

187 is that selective 5-HT2C agonism would avoid valvular heart disease.

188 heter therapies are being developed to treat valvular heart disease.

189 Aortic stenosis is the most common form of valvular heart disease.

190 ost challenging encountered in patients with valvular heart disease.

191 and quality of echocardiographic studies for valvular heart disease.

192 re more likely to have history of stroke and valvular heart disease.

193 guidance, and post-procedural assessment of valvular heart disease.

194 ntional surgery in the treatment of acquired valvular heart disease.

195 ic dysfunction, diastolic abnormalities, and valvular heart disease.

196 clerosis, myocardial infarction, stroke, and valvular heart disease.

197 l for identifying compounds likely to induce valvular heart disease.

198 idelines for the Management of Patients With Valvular Heart Disease.

199 ociated with improved concordance in grading valvular heart disease.

200 echanism for development of the drug-induced valvular heart disease.

201 ccredited laboratories for the evaluation of valvular heart disease.

202 s (289 male, 67+/-10 years) with ischemic or valvular heart disease.

203 Aortic stenosis is the most frequent valvular heart disease.

204 nowledge for the management of patients with valvular heart disease.

205 impact the treatment of coronary artery and valvular heart disease: SYNTAX, ART, and PARTNER.

206 c stenosis is perhaps the most common of all valvular heart diseases in the developed nations of the

207 aortic stenosis is the most prevalent of all valvular heart diseases.

208 Trabeculation and valvular hyperplasia were diminished in hearts of embryo

209 erlands and excluded patients with ischemic, valvular, hypertensive, and congenital heart disease.

210 Pathologically, valvular incompetence or absence of valves are common fe

211 MMP-targeted imaging detected valvular inflammation and remodeling in a murine model o

212 vity as determined by in situ zymography and valvular inflammation by CD68 staining were maximal at 6

213 itial cells (AVIC) play an important role in valvular inflammation.

214 AS is associated with valvular inflammation.

215 e common and are associated with progressive valvular insufficiency and/or stenosis.

216 imension, frequency of aortic valve opening, valvular insufficiency, blood pressure, and CF-LVAD para

217 inant hallmark of early CAVD, but culture of valvular interstitial cells (VICs) in biomaterial enviro

218 sense matrix elasticity, we cultured primary valvular interstitial cells (VICs) isolated from porcine

219 igated effects of TNF-alpha on murine aortic valvular interstitial cells (VICs) within three-dimensio

220 elevated transvalvular pressure can activate valvular interstitial cells and latent paracrine signali

221 cles (EVs) derived from smooth muscle cells, valvular interstitial cells and macrophages as the media

222 TGF-beta1-treated valvular interstitial cells had higher pre-stress (1100

223 In response to equibiaxial stretch, valvular interstitial cells on stiff substrates decrease

224 signaling mediators colocalized primarily to valvular interstitial cells suggesting autocrine/paracri

225 cells that line the leaflet surface and the valvular interstitial cells that populate the valve extr

226 extracellular matrix production in cultured valvular interstitial cells was dependent on SMAD2/3 and

227 cimens, cultured valve tissues, and cultured valvular interstitial cells were obtained from patients

228 new, more quantitative methods for assessing valvular involvement and the combination of parameters t

229 ease remains unclear, although regression of valvular lesions after the end of treatment has been rep

230 h malignancies, autoimmune diseases, cardiac valvular lesions, and in patients on mechanical circulat

231 of hypercholesterolemia, superoxide levels, valvular lipid deposition, and myofibroblast activation

232 The frequency of valvular monitoring by transthoracic echocardiography is

233 fication (AVC) is the intrinsic mechanism of valvular obstruction leading to aortic stenosis (AS) and

234 generative AS is conditioned by the upstream valvular obstruction that dampens forward and backward c

235 l tree's behavior could be influenced by the valvular obstruction.

236 rely reduced ejection fraction not caused by valvular or ischemic heart disease.

237 Clinical VTE and the evidence for the valvular origin of venous thrombosis are reviewed.

238 dure was associated with excellent long-term valvular outcomes and survival, regardless of the need f

239 ntricular trabeculation, septal defects, and valvular overgrowth.

240 With surgical removal of valvular PFE, the valve was preserved in 92 (98%).

241 vely useful in the execution of percutaneous valvular procedures and evaluation of their results.Clin

242 reased 30-day mortality rate, but concurrent valvular procedures increased the risk to 8.5%.

243 Of these, 47 patients had concurrent valvular procedures, 15 patients had simultaneous closur

244 rature on prosthetic valve function and para-valvular regurgitation (PVR) after trans-catheter aortic

245 itral and tricuspid valve disease, primarily valvular regurgitation assessment, with an emphasis on t

246 disease in 3.8% (newly identified in 2.2%), valvular regurgitation or stenosis in 28.0% (newly ident

247 on of hemodynamically significant shunts and valvular regurgitation.

248 o 21 years) and tabulated visible shunts and valvular regurgitation.

249 ight ventricular function, hemodynamics, and valvular regurgitation.

250 s) are upregulated in CAVD and contribute to valvular remodeling and calcification.

251 ent fibroblasts are unable to support normal valvular remodeling and establishment of a mature cardia

252 lunar valves) is required for late gestation valvular remodeling, mesenchymal apoptosis, and proper v

253 Advantages of valvular repair compared with replacement include lower

254 of contact with raw fish and with history of valvular repair in an unaffected heart valve.

255 ic surgery, of which coronary artery bypass, valvular repair, and pulmonary thromboendarterectomy wer

256 IE were older age, male sex, drug abuse, and valvular replacement after an initial episode of IE.

257 rial endocarditis and 1267 (11.4%) underwent valvular replacement surgery (tissue valve, 44.3%; nonti

258 ture is limited on the long-term outcomes of valvular replacement surgery and the choice of prosthesi

259 edictors of mortality in patients undergoing valvular replacement surgery.

260 sis (AS) is the most common cause of cardiac valvular replacement surgery.

261 We outline current management strategies for valvular rheumatic heart disease on the basis of either

262 ristics of the vessel wall within the venous valvular sinus are assessed in turn.

263 y increased expression of EPCR and TM in the valvular sinus endothelium as opposed to the vein lumena

264 However, the possible contribution of the valvular sinus endothelium has received little attention

265 our hypothesis and suggest that variation in valvular sinus thromboresistance may be an important fac

266 tion posed regarding the link between venous valvular stasis-associated hypoxia and thrombosis.

267 illance within 1 year for moderate or severe valvular stenosis (64 [15.0%]), and routine surveillance

268 Aortic valvular stenosis (AS) is the most common cause of cardi

269 now possible to instantaneously abolish the valvular stenosis and to measure the resulting changes i

270 real-time accurate assessment of cardiac and valvular structural and functional abnormalities makes t

271 many asymptomatic individuals with abnormal valvular structure and/or aortic root dilation.

272 l factors that alter proper functionality of valvular substructures.

273 idence interval [CI], 2.304-3.145), previous valvular surgery (OR, 1.525; 95% CI, 1.375-1.692), reimp

274 s an understanding of these problems so that valvular surgery can be considered when appropriate.

275 er mortality observed in patients undergoing valvular surgery compared with medical therapy alone (20

276 839 (61.7% [95% CI, 59.2%-64.3%]) underwent valvular surgery during the index hospitalization.

277 ly associated with 1-year mortality, whereas valvular surgery during the initial hospitalization was

278 emodynamic parameters in patients undergoing valvular surgery has failed to explain these symptoms.

279 ned recommendations on the optimal timing of valvular surgery in patients with IE and recent stroke s

280 (95% CI, 26.0%-32.2%) in patients undergoing valvular surgery vs 58.4% (95% CI, 54.1%-62.6%) in those

281 al therapy and subsequent mortality, whereas valvular surgery was associated with lower in-hospital a

282 Valvular surgery was performed in 25 patients (45%), inc

283 Age, prior history, valvular surgery, and left atrial pathology and dysfunct

284 uding functional mitral regurgitation, prior valvular surgery, hypertrophic cardiomyopathy, rheumatic

285 hythmia, heart failure, endocarditis, during valvular surgery, pulmonary hypertension, noncardiac cau

286 .6 years), 69% were men, and 36% had planned valvular surgery.

287 of patients were men, and 51.8% had planned valvular surgery.

288 V conical deformation does not cause notable valvular tenting.

289 ht ventricular shape widening with increased valvular tenting.

290 Conversely, PHTN-FTR is determined by valvular tethering with tenting linked to RV elongation

291 trial enlargement, atrial tissue masses, and valvular thickening at 4 weeks of age, as well as diasto

292 additional mice had no external evidence of valvular thickening.

293 tween the cells that give rise to septal and valvular tissues and hence partition the heart.

294 of Stat3 in hematopoietic cells and cardiac valvular tissues leads to myeloid progenitor hyperplasia

295 underlie the formation of cardiac septal and valvular tissues thus has important implications for the

296 (P<0.0001) and area (P<0.0001), and reduced valvular-to-annular ratio (P=0.006).

297 was independently determined by inspiratory valvular-to-annular ratio (P=0.026) and inspiratory chan

298 Eleven computed tomography-based measures of valvular/vascular calcification, adiposity, and muscle a

299 rmine how commonly acute Q fever could cause valvular vegetations associated with antiphospholipid an

300 Antiphospholipid antibody syndrome with valvular vegetations in acute Q fever is a new clinical