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

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

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

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

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

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

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

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

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

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

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

11 No association was found with structural heart disease.

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

13 udies have included subjects with underlying structural heart disease.

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

15 tachycardias often occur in patients without structural heart disease.

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

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

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

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

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

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

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

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

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

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

26 EP substrates associated with infarction and structural heart disease.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 rticularly among younger AF patients without structural heart disease.

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

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

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

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

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

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

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

50 luation for minimally invasive therapies for structural heart disease.

51 tients with documented paroxysmal AF without structural heart disease.

52 cardiac conditions including functional and structural heart disease.

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

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

55 compare this with reference patients without structural heart disease.

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

57 of ventricular arrhythmias in patients with structural heart disease.

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

59 d of transcatheter interventions in acquired structural heart diseases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 4 weeks who were 14 days old or less, had no structural heart disease, and required assisted ventilat

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

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

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

87 Patients with structural heart disease are predisposed to arrhythmias

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

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

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

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

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

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

94 Ten key structural heart disease building blocks can be identifi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 Transcatheter therapies in structural heart disease have evolved tremendously over

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

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

116 1.027-1.553; P = 0.027), and the presence of structural heart disease (HR, 1.236; 95% CI, 1.003-1.524

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

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

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

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

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

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

123 -16 years; ejection fraction, 49+/-13%) with structural heart disease, intramural scar was detected b

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

125 Structural heart disease is a rapidly evolving field, an

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

127 Structural heart disease is highly prevalent in patients

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 Structural heart disease or inadvertent pacing in scar w

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

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

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

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

149 Patients with structural heart disease presenting for VT radiofrequenc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 -7.7 years; 81% women; 56% without diagnosed structural heart disease) with syncope of unknown origin