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 No cardiac structural or valvular abnormalities were observed after treatment wit

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

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

6 Treatment with NOACs in patients with non-valvular AF that undergo cardioversion seems to be as sa

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

8 rivaroxaban in a Korean population with non-valvular AF.

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

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

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

12 r, the specific impact of such neosinuses on valvular and root biomechanics and the potential influen

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

14 ithout a history of ischemic heart disease), valvular, and end-organ disease were followed up for the

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

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

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

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

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

20 he prognostic impact of all levels of native valvular AS.

21 in patients with ischaemic stroke due to non-valvular atrial fibrillation (AF) is unknown.

22 e and systemic embolism in patients with non-valvular atrial fibrillation (AF), but actual data are n

23 veness and safety in Asian patients with non-valvular atrial fibrillation (AF).

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

25 patients with venous thromboembolism and non-valvular atrial fibrillation have had minimal representa

26 te oral anticoagulation in patients with non-valvular atrial fibrillation is a longstanding, common,

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

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

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

30 l acute ischaemic strokes are related to non-valvular atrial fibrillation, the most common cardiac ar

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

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

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

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

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

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

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

38 17 patients (39.5%) had the degree of aortic valvular calcification documented on CT or echocardiogra

39 efects including BAV, valvular stenosis, and valvular calcification in murine models.

40 Valvular calcification is associated with the developmen

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

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

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

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

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

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

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

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

49 active metabolite MBP and the development of valvular-cardiovascular disease states.

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

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

52 data were provided as infective endocarditis valvular complications (classified as abscess or pseudoa

53 p Lp(a) tertile had increased progression of valvular computed tomography calcium score (n = 51; 309

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

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

56 sease may help prevent progression to severe valvular damage.

57 icularly in people with predisposing cardiac valvular damage.

58 Congenital valvular defects are prevalent among newborns and can ca

59 peutic modality in the management of various valvular defects.

60 ique holds major promise in the diagnosis of valvular degeneration and the surveillance of patients w

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

62 The main pathogeneses were valvular disease (36%) and hypertension (28%).

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

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

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

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

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

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

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

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

71 om and adult participants with aortic and/or valvular disease who were enrolled between May and Augus

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

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

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

75 ing atherosclerosis, pulmonary hypertension, valvular disease, and fibroelastosis.

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

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

78 myocardial infarction, atrial fibrillation, valvular disease, and revascularization procedures).

79 ased age, male sex, acute coronary syndrome, valvular disease, carotid disease, hyperlipidemia, hyper

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

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

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

83 logy ranging from congenital to vascular and valvular disease, particularly in structural heart inter

84 r cysts, intracranial aneurysms, and cardiac valvular disease, show that ADPKD is a systemic disorder

85 l infarction, cardiomyopathies, arrhythmias, valvular disease, thromboembolic disease, aortic disease

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

87 osis, coronary heart disease, heart failure, valvular disease, venous disease, and peripheral artery

88 prone to developing severe aortic disease or valvular disease.

89 g former drinkers and those with significant valvular disease.

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

91 mic heart disease, heart failure, and severe valvular disease.

92 ng therapeutic alternative for patients with valvular disease.

93 sis, livedo racemosa, or APS-related cardiac valvular disease.

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

95 lve prolapse (MVP) is one of the most common valvular disorders.

96 The aortic flow and valvular dynamics associated with these thinner valvular

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

98 Valvular dynamics showed stable valvular area in systole

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

100 providing powerful prediction of subsequent valvular dysfunction and highlighting patients at risk o

101 w that reduced VIC formation correlates with valvular dysfunction and severe retrograde blood flow th

102 urgitation (TR) in the absence of left-sided valvular dysfunction are often managed nonoperatively.

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

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

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

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

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

108 n vivo approaches, a population of human pre-valvular endocardial cells (HPVCs) can be derived from p

109 e, we report that GATA2 is not necessary for valvular endothelial cell (VEC) differentiation.

110 l changes of valvular interstitial cells and valvular endothelial cells associated with MVP developme

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

112 nduced endothelial-mesenchymal transition in valvular endothelial cells, resulting in increased prote

113 mal transition and proteoglycan secretion in valvular endothelial cells.

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

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

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

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

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

119 DS1 genotype and AS may implicate effects on valvular fatty acids.

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

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

122 es analysis time and improves reliability of valvular flow quantification with four-dimensional flow

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

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

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

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

127 4%), pulmonary vascular disease (1.2%-7.1%), valvular heart disease (5.0%-9.8%), and renal failure (7

128 ysplasia (ARVD, 17%), postmyocarditis (14%), valvular heart disease (8%), congenital heart disease (2

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

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

131 Background: Valvular heart disease (VHD) is an important cause of mo

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

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

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

135 of the atrium is described in patients with valvular heart disease and is associated with an increas

136 Mitral regurgitation (MR) is a common valvular heart disease and is the second most frequent i

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

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

139 herapeutic options for calcific vascular and valvular heart disease are invasive transcatheter proced

140 ations for clinicians to diagnose and manage valvular heart disease as well as supporting documentati

141 been the standard of care for patients with valvular heart disease for many decades, but transcathet

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

143 This executive summary of the valvular heart disease guideline provides recommendation

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

145 Many recommendations from the earlier valvular heart disease guidelines have been updated with

146 cture: Many recommendations from the earlier valvular heart disease guidelines have been updated with

147 Valvular heart disease has recently become an increasing

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

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

150 egurgitation (MR) is the most common type of valvular heart disease in patients over the age of 75 in

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

152 Aortic stenosis is the most common valvular heart disease in the United States.

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

154 uropean Society of Cardiology guidelines for valvular heart disease included changes in the definitio

155 Valvular heart disease is a major cause of morbidity and

156 Valvular heart disease is observed in approximately 2% o

157 Patients with valvular heart disease often have left ventricular diast

158 s generally well tolerated, with no observed valvular heart disease or pulmonary arterial hypertensio

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

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

161 Valvular heart disease was defined as history or baselin

162 rditis, coronary artery disease, stroke, and valvular heart disease were also observed for multiple c

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

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

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

166 Managing severe valvular heart disease with mechanical valve replacement

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

168 ng conditions (for example, hypertension and valvular heart disease) or coronary artery disease.

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

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

171 rest in establishing best practices in TAVR, valvular heart disease, and cardiovascular implantable e

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

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

174 tabolic & Lipid Disorders, Rhythm Disorders, Valvular Heart Disease, and Vascular Medicine (1-100).

175 vention, Rhythm Disorders & Thromboembolism, Valvular Heart Disease, and Vascular Medicine (1-100).

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

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

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

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

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

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

182 mended first-line test for the assessment of valvular heart disease, but cardiovascular magnetic reso

183 lve stenosis (AVS), which is the most common valvular heart disease, causes a progressive narrowing o

184 African American, and to have hypertension, valvular heart disease, diabetes, hypothyroidism, AIDS,

185 anaemia, chronic kidney disease, presence of valvular heart disease, left ventricular ejection fracti

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

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

188 , hypertension treatment, diabetes mellitus, valvular heart disease, prevalent myocardial infarction,

189 linically relevant 5-HT-related pathologies (valvular heart disease, pulmonary arterial hypertension)

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

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

192 ease, chronic obstructive pulmonary disease, valvular heart disease, tobacco use, and alcohol abuse.

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

194 amyloid deposits in patients with AF without valvular heart disease, which represents the most common

195 newer options for diagnosis and treatment of valvular heart disease.

196 tions than previously appreciated, including valvular heart disease.

197 and quality of echocardiographic studies for valvular heart disease.

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

199 ociated with improved concordance in grading valvular heart disease.

200 ccredited laboratories for the evaluation of valvular heart disease.

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

202 Aortic stenosis is the most frequent valvular heart disease.

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

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

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

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

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

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

209 ost challenging encountered in patients with valvular heart disease.

210 newer options for diagnosis and treatment of valvular heart disease.

211 f coronary artery disease, hypertension, and valvular heart disease.

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

213 ease, or Group 2 PH, includes heart failure, valvular heart diseases, and congenital heart diseases.

214 Trabeculation and valvular hyperplasia were diminished in hearts of embryo

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

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

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

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

219 plications, we aimed to detect acute Q fever valvular injury to improve therapeutic management.

220 ed data from patients with acute Q fever and valvular injury.

221 nosis (AS), patients often show extra-aortic valvular injury.

222 otrophin-1) to be a mediator of Aldo-induced valvular interstitial cell activation and proteoglycan s

223 Aldo enhanced valvular interstitial cell activation markers and induce

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

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

226 nto the valves affects the biology of aortic valvular interstitial cells (VICs) remains to be elucida

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

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

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

230 ypic, molecular, and histological changes of valvular interstitial cells and valvular endothelial cel

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

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

233 ls; inference of gene regulatory networks in valvular interstitial cells positions Adamts19 in a high

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

235 Lp(a) induced osteogenic differentiation of valvular interstitial cells, mediated by OxPL and inhibi

236 nvestigated the effects of Lp(a) and OxPL on valvular interstitial cells.

237 ing highlight Adamts19 as a novel marker for valvular interstitial cells; inference of gene regulator

238 Patients with severe native VHD or previous valvular intervention were enrolled prospectively across

239 2028 patients (28.0%) had undergone previous valvular intervention.

240 require early and more frequent vascular and valvular interventions and reinterventions, in particula

241 l figure in mitral VHD and late referral for valvular interventions suggest the need to improve furth

242 Valvular interventions were performed in 2150 patients d

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

244 ers of valve interstitial cells of different valvular layers, demonstrating cell specificity.

245 thoracic echocardiography (TTE) identified a valvular lesion of acute Q fever endocarditis without un

246 tity, acute Q fever endocarditis, defined as valvular lesion potentially caused by C. burnetii: veget

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

248 The frequency of valvular monitoring by transthoracic echocardiography is

249 dogenous synthesis of n-3 PUFA and increased valvular n-3 PUFA content, exhibited reduced valve calci

250 tentially caused by C. burnetii: vegetation, valvular nodular thickening, rupture of chorda tendinae,

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

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

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

254 ntage of defining the hemodynamic effects of valvular or device infection.

255 e) activity in myocardium from patients with valvular or ischemic heart disease and heart failure wit

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

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

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

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

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

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

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

263 is with unstable angina, acute endocarditis, valvular regurgitation with impending heart failure), 10

264 ight ventricular function, hemodynamics, and valvular regurgitation.

265 on of hemodynamically significant shunts and valvular regurgitation.

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

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

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

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

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

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

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

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

274 edictors of mortality in patients undergoing valvular replacement surgery.

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

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

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

278 Infundibular with pulmonary valvular stenosis was the most common type of stenosis (

279 Aortic bicuspidy, valvular stenosis, and insufficiency were considered as

280 ish, and aortic valve defects including BAV, valvular stenosis, and valvular calcification in murine

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

282 ed the impact of LP placement on cardiac and valvular structure and function.

283 l factors that alter proper functionality of valvular substructures.

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

285 pulation and are the most common reasons for valvular surgery because no drug-based treatments exist.

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

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

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

289 nt ischemic attack, intracranial bleeding or valvular surgery.

290 .6 years), 69% were men, and 36% had planned valvular surgery.

291 , mechanically demanding, and highly dynamic valvular system remains poorly understood.

292 V conical deformation does not cause notable valvular tenting.

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

294 in the endocardium is indispensable for the valvular tissue remodeling in the heart.

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

296 vular dynamics associated with these thinner valvular tissues have not been previously identified and

297 Moderate to intense (18)F-FDG valvular uptake was also associated with worse outcome (

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