ライフサイエンスコーパス: structural heart disease

1 luation for minimally invasive therapies for structural heart disease.

2 tients with documented paroxysmal AF without structural heart disease.

3 urden in patients with paroxysmal AF without structural heart disease.

4 aluation suggests the presence of associated structural heart disease.

5 ds may reflect the presence of an underlying structural heart disease.

6 compare this with reference patients without structural heart disease.

7 ation and in pediatric patients with complex structural heart disease.

8 of ventricular arrhythmias in patients with structural heart disease.

9 ses the risk of heart failure in adults with structural heart disease.

10 ential MRI measurements in the evaluation of structural heart disease.

11 ar localization are present in many forms of structural heart disease.

12 of sudden cardiac death in children without structural heart disease.

13 f 61 kg (range 2 to 130 kg), with 69% having structural heart disease.

14 mmunity's understanding of the many forms of structural heart disease.

15 race and player position and judged free of structural heart disease.

16 fibrillation duration and is not affected by structural heart disease.

17 of ventricular function and assess causes of structural heart disease.

18 ring at slower pacing rates in patients with structural heart disease.

19 llation (AF), particularly in the setting of structural heart disease.

20 No association was found with structural heart disease.

21 A large atrial septal defect was the only structural heart disease.

22 udies have included subjects with underlying structural heart disease.

23 een shown to initiate VF in patients without structural heart disease.

24 tachycardias often occur in patients without structural heart disease.

25 nd heart failure, but also for some forms of structural heart disease.

26 ng AS with low cardiac output state or other structural heart disease.

27 AVA) on recurrent VF events in patients with structural heart disease.

28 mean age of 45 +/- 13 years who did not have structural heart disease.

29 arly true for VT, including patients without structural heart disease.

30 requent cause of syncope in patients without structural heart disease.

31 oth prospective and retrospective studies of structural heart disease.

32 Fifty-five patients (79%) had structural heart disease.

33 weight, age, center size, or the presence of structural heart disease.

34 tening arrhythmias, often in the presence of structural heart disease.

35 ablation of VT occurring in the presence of structural heart disease.

36 enges in accessing state-of-the-art care for structural heart disease.

37 entricular tachycardia (VT) in patients with structural heart disease.

38 EP substrates associated with infarction and structural heart disease.

39 as are most likely to occur in patients with structural heart disease.

40 s rhythm maps in 6 patients who did not have structural heart disease.

41 nts had electrical heart disease followed by structural heart disease.

42 hlete nearly always occur in the presence of structural heart disease.

43 al flutter (Fl) in patients with and without structural heart disease.

44 minations of pregnancy because the fetus had structural heart disease.

45 clinical practice occur in patients who have structural heart disease.

46 f cardiac arrest in persons without apparent structural heart disease.

47 re negative for ischemia and had no signs of structural heart disease.

48 hy, idiopathic ventricular fibrillation, and structural heart disease.

49 sine-sensitive VT occurs in patients without structural heart disease.

50 reasingly important role in the diagnosis of structural heart disease.

51 ricular tachycardia (VT) in patients without structural heart disease.

52 lar outflow tract (RVOT) in patients without structural heart disease.

53 major cause of sudden death in patients with structural heart disease.

54 without a history of atrial flutter, AF, or structural heart disease.

55 d isolated TR without significant underlying structural heart disease.

56 ality assessment and more final diagnoses of structural heart disease.

57 ncing age, cardiometabolic risk factors, and structural heart disease.

58 ventions for the management of patients with structural heart disease.

59 natriuretic peptide levels, and evidence of structural heart disease.

60 0%, elevated natriuretic peptide levels, and structural heart disease.

61 iverse health system to detect many forms of structural heart disease.

62 g arrhythmogenic substrates in patients with structural heart disease.

63 ed families from Lagos, Nigeria, affected by structural heart disease.

64 ortic disease, dyslipidemias, and congenital/structural heart disease.

65 natriuretic peptide levels, and evidence of structural heart disease.

66 tes 64% of incessant FAT in patients without structural heart disease.

67 chocardiography to improve underdiagnosis of structural heart disease.

68 in several subgroups including those without structural heart disease.

69 VCs) most frequently occur in the context of structural heart disease.

70 rity of malignant VTs occur in patients with structural heart disease.

71 cardiac conditions including functional and structural heart disease.

72 rioventricular block or sinus arrest, and no structural heart disease.

73 were male (range, 50% to 74%), and <10% had structural heart disease.

74 rticularly among younger AF patients without structural heart disease.

75 between AADs in younger AF patients without structural heart disease.

76 these left VAs in patients with and without structural heart disease.

77 y for pulmonary vein isolation and 17 had no structural heart disease.

78 younger patients with paroxysmal AF and mild structural heart disease.

79 ue of 99.4% (97.8-99.8%) were seen for major structural heart disease.

80 so far only has been shown in patients with structural heart disease.

81 d of transcatheter interventions in acquired structural heart diseases.

82 association between the presence of ECs and structural heart disease (15.3% in patients without ECs

83 plant, and mechanical support, 21 related to structural heart disease, 21 related to congenital heart

84 of sustained outflow tract VT without overt structural heart disease, 24 had left ventricular outflo

85 y prevention (68.0% vs 62.4%; P = 0.002) and structural heart disease (84.9% vs 76.8%; P < 0.001).

86 n assessment of patients with chest pain and structural heart diseases, although more refined CT tech

87 Structural heart disease and a patent foramen ovale are

88 r fibrillation that occurs in a patient with structural heart disease and an abnormal serum potassium

89 ast majority of cardiac arrest patients have structural heart disease and are commonly treated with a

90 ongly linked to the presence and severity of structural heart disease and are strongly prognostic in

91 with nonreversible cardiac causes including structural heart disease and arrhythmia syndromes.

92 Among patients with structural heart disease and at least 1 hemodynamically

93 cause of emerging therapeutic procedures for structural heart disease and atrial fibrillation ablatio

94 -center study was performed on patients with structural heart disease and both VT and VF, with incide

95 election for device therapy in patients with structural heart disease and Brugada syndrome.

96 istry enhanced pediatric, nonatherosclerotic structural heart disease and congenital heart disease (C

97 nism, and management of VT in the setting of structural heart disease and discuss the evolving role o

98 -based transcatheter interventions targeting structural heart disease and emphasize the importance of

99 ILVNC, provided they had no other associated structural heart disease and fulfilled all the accompany

100 dures in 22 patients (ischemic, n = 11) with structural heart disease and hemodynamically unstable VT

101 In patients with structural heart disease and ICD-documented SMVT, using

102 r arrhythmias that occur in patients without structural heart disease and in the absence of the long

103 mplex 3-dimensional relationships present in structural heart disease and in their capacity to adequa

104 oponin T (cTnT) are strongly associated with structural heart disease and increased risk of death and

105 In patients with unexplained syncope, structural heart disease and inducible sustained ventric

106 ardiac troponin proteins are associated with structural heart disease and predict incident cardiovasc

107 ed episodes of atrial fibrillation, or both (structural heart disease and previous atrial fibrillatio

108 Patients with structural heart disease and SMVT documented by an ICD-E

109 ICD implantation to include patients with no structural heart disease and spontaneous ventricular tac

110 a highly sensitive assay was associated with structural heart disease and subsequent risk for all-cau

111 les predicted development of a complication (structural heart disease and the presence of multiple ta

112 nagement strategy differs between those with structural heart disease and those without.

113 iants associated with severe arrhythmias and structural heart diseases and investigated whether these

114 ling the human heart offer new insights into structural heart diseases and the engineering of complex

115 Forty of 68 (58%) patients had structural heart disease, and 21/40 (53%) patients were

116 tricular ejection fraction >40%, evidence of structural heart disease, and elevated N-terminal pro-B-

117 ular ejection fraction of >=40%, evidence of structural heart disease, and elevated natriuretic pepti

118 terventional cardiologists with expertise in structural heart disease, and imaging experts.

119 g individuals with type 2 diabetes mellitus, structural heart disease, and impaired exercise capacity

120 persistent (n = 121) AF, with no substantial structural heart disease, and in normal sinus rhythm at

121 a range of novel therapeutic procedures for structural heart disease, and represents a promising adv

122 4 weeks who were 14 days old or less, had no structural heart disease, and required assisted ventilat

123 of PAF, ejection fraction, left atrial size, structural heart disease, and the ablation technique, on

124 rmalized in reference to 47 controls with no structural heart disease, and the diagnostic area under

125 cular hypertrophy, and a composite model for structural heart disease; and 1 negative control AI-ECG

126 n, which may contribute to why patients with structural heart disease are at higher risk for ventricu

127 Patients with structural heart disease are at increased risk of advers

128 th more AF burden and less severe underlying structural heart disease are more likely to experience l

129 Patients with structural heart disease are predisposed to arrhythmias

130 tion (ie, T-wave alternans) in patients with structural heart disease are unknown.

131 ans should ask patients about any history of structural heart disease, arrhythmia, and syncope.

132 in older patients or in patients with known structural heart disease, arrhythmia, or certain electro

133 ses of multidetector CT in the assessment of structural heart disease, as well as evolving periproced

134 ntricular fibrillation who have no definable structural heart disease associated with a right bundle

135 with replacement fibrosis and progression of structural heart disease before symptoms is fundamental

136 Ten key structural heart disease building blocks can be identifi

137 icular arrhythmias (VAs) and those caused by structural heart disease can originate from the papillar

138 s cardiac conditions, such as arrhythmias or structural heart disease (cardiac syncope), or other cau

139 ormal heart, VT that occurs in patients with structural heart disease carries an elevated risk for su

140 Among the various structural heart diseases causing stroke, the role of pa

141 rosthetic paravalvular leaks referred to our structural heart disease center with congestive heart fa

142 r Tbx5 resulted in an increased incidence of structural heart disease, confirming that normal heart d

143 These include the evaluation of structural heart diseases, congenital heart diseases, pe

144 The underlying structural heart disease consisted of dilated cardiomyop

145 tive coronary artery disease and who have no structural heart disease continue to be a common occurre

146 ith 36 age- and sex-matched subjects with no structural heart disease (control group), as well as 36

147 mber of procedures, sex, and the presence of structural heart disease correlate with outcome success.

148 e heart team for complex coronary artery and structural heart disease could serve as a model for the

149 ficantly lower than arrhythmia patients with structural heart disease (CRP, 0.23 mg/dL) but higher th

150 r dying in the first year of life because of structural heart disease; details included the postal ar

151 Age, sex, race, or structural heart disease did not affect this proportion

152 rdiography should be performed to screen for structural heart disease (eg, unsuspected cardiomyopathy

153 abnormality divided our patients who had no structural heart disease (except 3 patients with mild le

154 y explain why arrhythmia-prone patients with structural heart disease exhibit T-wave alternans at low

155 disturbances, for patients with significant structural heart disease, for patients receiving a drug

156 for sustained monomorphic VT associated with structural heart disease from 2008 to 2012, sustained VT

157 is a common cause of death in patients with structural heart disease, genetic mutations, or acquired

158 lation for ventricular tachycardia (VT) from structural heart disease has a significant risk of recur

159 f sudden or total mortality in patients with structural heart disease, has been limited by a substant

160 Transcatheter therapies in structural heart disease have evolved tremendously over

161 When patients with VT and structural heart disease have no VT or nonclinical VT on

162 nfidence interval, 1.024-3.846; P<0.04), and structural heart disease (hazard ratio 1.874; 95% confid

163 1.027-1.553; P = 0.027), and the presence of structural heart disease (HR, 1.236; 95% CI, 1.003-1.524

164 Timely diagnosis of structural heart disease improves patient outcomes, yet

165 As the appreciation of structural heart disease in children and adults has incr

166 ement in cases of dilated cardiomyopathy and structural heart disease in infants.

167 CGs acquired in patients without preexisting structural heart disease in the year 2010, 11% were clas

168 ath seemed less likely to be associated with structural heart disease in women compared with men (58.

169 l resuscitation as well as less frequency of structural heart disease in women compared with men.

170 tricular remodeling, with high prevalence of structural heart disease, including left ventricular hyp

171 rred approach for training and assessment of structural heart disease interventional skills.

172 nvolving the expanding role of cardiac CT in structural heart disease interventions.

173 -16 years; ejection fraction, 49+/-13%) with structural heart disease, intramural scar was detected b

174 tion of genetic risk remains unexplained for structural heart disease involving the interventricular

175 ed for myocarditis (IRR, 1.36; P < .001) and structural heart disease (IRR, 1.16; P < .001) than for

176 valve replacement (IRR, 2.07; P < .001) and structural heart disease (IRR, 1.44; P < .001) compared

177 ients with myocardial injury and significant structural heart disease, irrespective of the diagnosis

178 Structural heart disease is a rapidly evolving field, an

179 The increased incidence of arrhythmias in structural heart disease is accompanied by remodeling of

180 ablation of ventricular tachycardia (VT) in structural heart disease is challenging because of nonin

181 Early detection of structural heart disease is critical to improving outcom

182 Structural heart disease is highly prevalent in patients

183 ventricular tachycardia (VT) associated with structural heart disease is more difficult than ablation

184 d right ventricular pacing in adults without structural heart disease is not fully characterized and

185 associated with incident HF, HF subtypes, or structural heart disease is unknown.

186 udy in patients with unexplained syncope and structural heart disease is usually assigned diagnostic

187 II receptor blockade (ARB) in patients with structural heart disease is well established.

188 thletes with life-threatening arrhythmias or structural heart disease known to put the athlete at ris

189 less likely than men to have a diagnosis of structural heart disease (LV dysfunction or coronary art

190 gation is well described in patients without structural heart disease (mainly idiopathic ventricular

191 e arrhythmias that occur in patients without structural heart disease, metabolic/electrolyte abnormal

192 In the absence of overt structural heart disease, most left ventricular outflow

193 ; LR, 7.3 [95% CI, 2.4-22]), or known severe structural heart disease (n = 222; range of sensitivity,

194 al diagnosis of CP (n=28), RCM (n=30), or no structural heart disease (n=34).

195 ar complexes in patients without significant structural heart disease (n=75, primary end point) was 9

196 n age 59 +/- 14.5 years, 219 men [71%]) with structural heart disease, New York Heart Association fun

197 Thirty-three patients with structural heart disease (NICM, n = 16; ICM, n = 17) ref

198 tive heart failure, conduction disorder, and structural heart disease occurred in the initial follow-

199 ntricular tachycardia (VT) in the setting of structural heart disease often requires extensive substr

200 ults with and without new-onset AFib without structural heart disease or >= moderate TR at baseline w

201 ession in samples from 5 individuals without structural heart disease or AF.

202 n of syncope is the presence (or absence) of structural heart disease or an abnormal electrocardiogra

203 In the setting of structural heart disease or an abnormal electrocardiogra

204 logic participants, without known underlying structural heart disease or cardiac symptoms, underwent

205 eristics of inducible AF in patients without structural heart disease or clinical AF and the effect o

206 d AF is common in patients in the absence of structural heart disease or clinical AF, and its inciden

207 s on the basis of the presence or absence of structural heart disease or heart failure, electrocardio

208 Structural heart disease or inadvertent pacing in scar w

209 late to cardiovascular disease cohorts where structural heart disease or ischemia may influence repol

210 ycardia and sudden death in patients without structural heart disease or QT prolongation has been rep

211 icated in the guidelines for reasons such as structural heart disease or renal function.

212 se (OR, 2.08), heart failure (OR, 5.01), and structural heart disease (OR, 4.59).

213 ed fall risk is associated with medications, structural heart disease, orthostatic hypotension, and a

214 ith ablation-refractory VT in the setting of structural heart disease over a broad range of left vent

215 related to higher, whereas absence of known structural heart disease (P=0.003) to lower incidence of

216 Patients with structural heart disease, paced rhythms, and bundle bran

217 block in detail, approaches specific to the structural heart disease patient, the need for cross-dis

218 o ensure appropriate and timely treatment of structural heart disease patients; 2) to minimize the ri

219 ibrillation, left atrium area, hypertension, structural heart disease, presence of left common trunk,

220 Patients with structural heart disease presenting for VT radiofrequenc

221 pective observational registry of women with structural heart disease, providing a uniquely large stu

222 was enrolled, regardless of the presence of structural heart disease, PVC morphology, or previous ab

223 ation would be suitable for patients without structural heart disease receiving class IC drugs, patie

224 Management of arrhythmias in patients with structural heart disease remains a challenge.

225 The accuracy of ECG imaging (ECGI) in structural heart disease remains uncertain.

226 ry ventricular tachycardia in the setting of structural heart disease results in frequent implantable

227 High-risk structural heart disease (severe left ventricular dysfun

228 ted BAV (BAV group) and 867 patients without structural heart disease (SHD) (no-SHD group).

229 ICD) shocks in small series of patients with structural heart disease (SHD) and recurrent ventricular

230 lar (LV) dysfunction, regardless of previous structural heart disease (SHD) diagnosis, PVC morphology

231 oposed echocardiographic (ECHO) criteria for structural heart disease (SHD) in dialysis patients.

232 onic-clonic seizures (GTSZ) with and without structural heart disease (SHD) remains controversial lea

233 Seven patients had structural heart disease (SHD), one of whom died.

234 Identifying structural heart diseases (SHDs) early can change the co

235 participants were free of HF risk factors or structural heart disease (Stage 0), 52% were categorized

236 ation for ascertainment of adverse events in structural heart disease studies.

237 and further excluding those with subclinical structural heart disease (subcohort 2).

238 art by autopsy, most common in athletes) and structural heart disease such as coronary artery disease

239 the clinical routine to assess patients with structural heart diseases such as aortic coarctation wit

240 f sudden cardiac deaths can be attributed to structural heart diseases, such as hypertrophic cardiomy

241 h prevalence of clinical conditions, such as structural heart disease, that can enhance the pro-arrhy

242 In adult patients without structural heart disease, the atrial ERP was measured be

243 In 20 patients without structural heart disease, the atrial ERP was measured be

244 In patients with and without structural heart disease, the formation of stable rotors

245 In coronary angiography patients without structural heart disease, the minor A allele of rs168999

246 with an adverse prognosis in the setting of structural heart disease, the relationship between AT/AF

247 survival in a large number of patients with structural heart disease treated in the setting of a ded

248 nd broad application of this and other novel structural heart disease treatment modalities in the fut

249 s in place of clinical event adjudication in structural heart disease trials.

250 Of 200 consecutive patients with VT and structural heart disease undergoing ablation, 11 had cli

251 jects of this study were 19 patients without structural heart disease undergoing an electrophysiology

252 Consecutive patients with structural heart disease undergoing VT ablation using th

253 ighteen patients (age 44+/-12 years) without structural heart disease underwent right atrial electroa

254 Age- and sex-adjusted structural heart disease variables associated with death

255 Overall 30-day mortality in the structural heart disease VT group reached 5.0% (patients

256 ent 722 ablation procedures, 473 (65.5%) for structural heart disease VT in the period 2006 to 2012.

257 Procedures for structural heart disease VT versus idiopathic VT had a s

258 Further evaluation of patients for structural heart disease was clinically driven, not prot

259 Structural heart disease was more severe in patients wit

260 Structural heart disease was present in 36% of infants,

261 Structural heart disease was present in 76% of patients.

262 At least 1 measure of structural heart disease was present in 93% of patients.

263 e occurrence of sudden cardiac arrest due to structural heart disease was uncommon during participati

264 sleep or after exercise, and the absence of structural heart disease, we hypothesized a developmenta

265 nset AF (n = 1747) or SR (n = 29 623) and no structural heart disease were identified.

266 tients with documented paroxysmal AF without structural heart disease were randomized to placebo or 4

267 Thirty-four patients without structural heart diseases were randomly assigned for a s

268 ent of refractory ventricular arrhythmias in structural heart disease when other treatment modalities

269 ome); and syncope in the setting of advanced structural heart disease when thorough invasive and noni

270 r having undiagnosed, clinically significant structural heart disease while outperforming single-dise

271 e against HF in patients without established structural heart disease who were receiving trastuzumab

272 ts (mean age +/- SD 65 +/- 14 years; 43 with structural heart disease) who underwent an attempt at ra

273 ial tachycardias occurring in the absence of structural heart disease will arise along the CT.

274 nction over 12 months among patients who had structural heart disease with no or mild HF symptoms.

275 -7.7 years; 81% women; 56% without diagnosed structural heart disease) with syncope of unknown origin