ライフサイエンスコーパス: sudden death

1 syncope, 7 near-drowning, and 3 resuscitated sudden death).

2 ed susceptibility to cardiac arrhythmias and sudden death.

3 (HCM), largely because of the possibility of sudden death.

4 ic disease responsible for heart failure and sudden death.

5 heart disease, 528 from stroke, and 893 from sudden death.

6 ar diastolic heart disease, dysrhythmia, and sudden death.

7 nostic value for both cardiac death (CD) and sudden death.

8 myopathies complicated by frequent premature sudden death.

9 ith all-cause mortality, vascular death, and sudden death.

10 enotypes, including spontaneous seizures and sudden death.

11 T syndrome (LQTS) is associated with risk of sudden death.

12 d individuals to ventricular arrhythmias and sudden death.

13 aches designed to restore life to victims of sudden death.

14 block, presenting clinically as syncope, and sudden death.

15 isk of arrhythmia, premature RV failure, and sudden death.

16 nges modeling bipolar disorder, epilepsy and sudden death.

17 r, associated with an increased incidence of sudden death.

18 s to mitral regurgitation, heart failure and sudden death.

19 -four children (60%) had a family history of sudden death.

20 (2+) sensitivity, and high susceptibility to sudden death.

21 ng arterial aneurysms, which may manifest as sudden death.

22 some patients to debilitating morbidity and sudden death.

23 n artery that can lead to vessel rupture and sudden death.

24 se of ventricular tachyarrhythmias (VTs) and sudden death.

25 hythmogenic disorder that causes syncope and sudden death.

26 overly conservative management can result in sudden death.

27 e 2 (SENP2) develop spontaneous seizures and sudden death.

28 rance, risk of progressive heart failure and sudden death.

29 ical mortality was most frequently caused by sudden death.

30 cytes, cardiac dysfunction, arrhythmias, and sudden death.

31 ventricular arrhythmias, heart failure, and sudden death.

32 and increased risk of cardiac arrhythmia and sudden death.

33 ding symptoms or recognized risk factors for sudden death.

34 verse effects, including rare occurrences of sudden death.

35 ar arrhythmias leading to cardiac arrest and sudden death.

36 iers of hERG/R148W may be at risk of cardiac sudden death.

37 ffected individuals to fatal arrhythmias and sudden death.

38 , marked QT prolongation, and a high risk of sudden death.

39 or cardiac arrhythmias, cardiomyopathies, or sudden death.

40 ge to cardiac myocytes, and in some animals, sudden death.

41 hmia, cardiomyopathy, or a family history of sudden death.

42 heart blocks, thromboembolic phenomena, and sudden death.

43 can lead to fatal ventricular arrhythmias or sudden death.

44 evelopment of heart failure, arrhythmia, and sudden death.

45 l occlusion resulting in tissue ischemia and sudden death.

46 e to cardiac myocytes, and, in some animals, sudden death.

47 ions and normal function are at low risk for sudden death.

48 licted individuals to cardiac arrhythmia and sudden death.

49 CI) increases the risk of cardiomyopathy and sudden death.

50 cute chest syndrome, multiorgan failure, and sudden death.

51 haracterized by stress-triggered syncope and sudden death.

52 iving Tbx3 mutants are at increased risk for sudden death.

53 is a plausible candidate gene for premature sudden death.

54 ng loss of fast conduction, arrhythmias, and sudden death.

55 ic cardiomyopathy and confer a high risk for sudden death.

56 that SCT is associated with exertion-related sudden death.

57 entricular arrhythmias and can predispose to sudden death.

58 odels to identify patients at higher risk of sudden death.

59 f internal cardiac defibrillators to prevent sudden death.

60 ed by aortic dilation and rupture leading to sudden death.

61 are associated with cardiac arrhythmias and sudden death.

62 cular death, HF hospitalization, and aborted sudden death.

63 patients with inherited cardiomyopathies and sudden death.

64 chemic changes were noted in SCA mice before sudden death.

65 uid index value) were seen in 62.8% cases of sudden deaths.

66 sports participation (2), family history of sudden death (1), and other (1).

67 tient-years; 1.19; 1.03-1.39, p=0.0201), and sudden death (1.68 vs 1.12 events per 100 patient-years;

68 of 2 years, 11 AACEs (2.5%) were detected: 5 sudden deaths (1.1%) and 6 spontaneous ventricular tachy

69 Nearly all patients with sudden death (14 of 15) had abnormal cardiac dimensions

70 (9.3%): 37 (35%) due to HF, 25 (23%) due to sudden death, 15 (14%) due to other cardiovascular (CV)

71 rting 7044 deaths, 3993 cardiac deaths, 1150 sudden deaths, 1837 myocardial infarctions, and 1490 str

72 patient (10 outpatient, 985 hospitalized, 17 sudden death), 25 food, 18 dust/soils, and 35 other stra

73 ted arrhythmia (3.4%), and family history of sudden death (4.2%) were uncommon.

74 arrhythmias are rare but are associated with sudden death; 9) early- and late-onset ND abnormalities

75 Only 1 patient had sudden death, a low annual rate of 0.06%/y.

76 tricular septal thickness, family history of sudden death, abnormal exercise blood pressure, and impl

77 Although sudden death accounted for approximately 25% to 30% of d

78 There was a 44% decline in the rate of sudden death across the trials (P=0.03).

79 Sudden death after surgery for atrial septal defect, ven

80 Family history included unexplained sudden death among relatives.

81 that refine our understanding of the risk of sudden death among Wolff-Parkinson-White patients were p

82 variability (HRV) is a major risk factor for sudden death and cardiovascular disease.

83 HCM) is prominently associated with risk for sudden death and disease progression, largely in young p

84 berta Hutterite population with a history of sudden death and found several individuals with severe f

85 polarization (ER) pattern is associated with sudden death and has been shown to be heritable.

86 was driven by reductions in out-of-hospital sudden death and hospitalized ST-segment-elevation myoca

87 e was driven by decreases in out-of-hospital sudden death and hospitalized ST-segment-elevation myoca

88 es have shown an association between risk of sudden death and left ventricular maximal wall thickness

89 Fallot was associated with a minimal risk of sudden death and low rate of reintervention for right ve

90 ticipatory planning for therapies to prevent sudden death and manage HF, is warranted.

91 mutation, clinical outcome can range between sudden death and no symptoms.

92 Baseline estimates of sudden death and radiofrequency ablation complication ra

93 nterpreting mtDNA variants in the context of sudden death and rare diseases.

94 nged its natural history, with prevention of sudden death and reversal of HF, thereby restoring quali

95 PURPOSE OF REVIEW: Unexplained sudden death and the sudden arrhythmic death syndrome (S

96 al aneurysms are at high risk for arrhythmic sudden death and thromboembolic events.

97 One death was cardiac sudden death and two were due to sepsis.

98 recommended programming accounted for 56% of sudden deaths and 11% of all deaths during the study per

99 Most sudden deaths and cardiac arrests occurred in the swim s

100 anism, and cause of death in the majority of sudden deaths and in almost 20% of nonsudden deaths.

101 Late mortality was predominantly a result of sudden deaths and myocardial infarction.

102 magnetic conditions a series of entanglement sudden-deaths and revivals occur between the two qubits.

103 , 19 at low risk [age 30 (7.5); 12 males] of sudden death, and 15 healthy controls [age 37 (16); seve

104 th from stroke, 2.1 (95% CI, 1.5 to 2.9) for sudden death, and 3.5 (95% CI, 2.9 to 4.1) for death fro

105 Two (5%) had a previous episode of aborted sudden death, and 8 (20%) had syncope.

106 onary heart disease overall, out-of-hospital sudden death, and hospitalized ST-segment-elevation and

107 usly admitted to hospital, presumably due to sudden death, and in patients with poor left ventricular

108 f cardiovascular injury and the incidence of sudden death, and MR blockade decreases the risk of card

109 at baseline and (2) the incidence of death, sudden death, and other cardiac adverse events.

110 ardioverter-defibrillators for prevention of sudden death, and other contemporary treatment options.

111 gnificantly associated with (1) total death, sudden death, and pacemaker implantation in a model, inc

112 am is also a risk factor for arrhythmias and sudden death, and the increased prevalence of QT prolong

113 cardioverter-defibrillator for prevention of sudden death are mainstays of therapy when deemed necess

114 Prior syncope and family history of sudden death are predictors of a positive genetic test.

115 artery aneurysms, myocardial infarction, and sudden death as a result of the illness.

116 Aborted sudden death as the first manifestation of the disease o

117 hondria as potential therapeutic targets for sudden death associated with cardiovascular disease.

118 The cumulative incidence of sudden death at 90 days after randomization was 2.4% in

119 t stopped all medications after pPCI), and 1 sudden death at home 9 months after pPCI.

120 fibrillator discharge, and resuscitated from sudden death) at 30 days, 1 year, and 2 years was 0%, 1.

121 ce showed markedly increased mortality, with sudden death beginning after 5 weeks and 100% mortality

122 </=5.7%, those with a SPRM-predicted risk of sudden death below the median had no reduction in mortal

123 gs do not provide sufficient protection from sudden death, but do have a role in reducing arrhythmias

124 with an increased risk of heart failure and sudden death, but its risk in patients with preserved le

125 The leading cause of mortality in HFpEF is sudden death, but little is known about the underlying m

126 r all decedents and within the categories of sudden death, cancer, congestive heart failure or chroni

127 hippocampus/amygdala and parahippocampus in sudden death cases and people at high risk, when compare

128 ents with a genetic form of exercise-induced sudden death (catecholaminergic polymorphic ventricular

129 WCD) for use and effectiveness in preventing sudden death caused by ventricular tachyarrhythmia or fi

130 Under conditions studied, sudden deaths caused by insulin-induced severe hypoglyce

131 blockade of PI4KA in adult animals leads to sudden death closely correlating with the drug's ability

132 type 1 patients is associated with total and sudden deaths, conduction defects, left ventricular dysf

133 Rates of sudden death declined substantially over time among ambu

134 d worse cardiac function, than those in whom sudden death did not occur.

135 by doxorubicin plus cyclophosphamide group), sudden death (docetaxel plus capecitabine followed by do

136 defibrillator discharges, resuscitated from sudden death, documented stroke, and admission for conge

137 luding implantable defibrillators to prevent sudden death, drugs and surgical myectomy (or, alternati

138 s in neonates, provoking brain damage and/or sudden death due to apnea episodes and cardiorespiratory

139 In college student-athletes, risk of sudden death due to cardiovascular disease is relatively

140 diac repolarization, associated high risk of sudden death due to ventricular tachycardia, and congeni

141 Two important causes of sudden death during endurance races are arrhythmic death

142 ex, clinical presentation, family history of sudden death, ethnicity, and deprivation index did not p

143 sease-related morbidity/mortality, including sudden death, even with conventional risk factors.

144 The sudden death event rate was 4.7%/year.

145 perative complications (n=2), and arrhythmic sudden death events (n=5, 1.2% [0.20%/y]).

146 generally carry an excellent prognosis, rare sudden death events have been reported.

147 The rate of sudden death fell from 12.15% with conventional care to

148 ge, NYHA functional class, family history of sudden death (FHSD), syncope, atrial fibrillation, non-s

149 EG suppression, cardiorespiratory arrest and sudden death following a seizure.

150 ttributed to coronary heart disease, stroke, sudden death from an unknown cause, or a combination of

151 Only 5 of the 100 interrogated sudden death genes hosted actionable pathogenic mutation

152 laining the poor prognosis and propensity to sudden death has been elusive.

153 The risk of sudden death has changed over time among patients with s

154 opathy, but recurrent heart failure and late sudden death have been reported.

155 gical connection between epilepsy itself and sudden death have fuelled increased attention to this ph

156 alth-care expenditure as a result of stroke, sudden death, heart failure, unplanned hospital admissio

157 mortality (HR, 1.29 [1.05-1.59]; P=0.02) and sudden death (HR, 1.83 [1.24-2.69]; P<0.01) compared wit

158 rd ratio [HR], 1.58 [1.22-2.04]; P<0.01) and sudden death (HR, 2.12 [1.33-3.39]; P<0.01), compared wi

159 : 0.29; 95% CI: 0.12 to 0.73; p = 0.005) and sudden death (HR: 0.46; 95% CI: 0.20 to 1.07; p = 0.065)

160 ortic dissections are a preventable cause of sudden death if individuals at risk are identified and s

161 ical, 1 eccentric), and prognosis (premature sudden death in 2 individuals compared with survival to

162 e patients (related to heart failure in 38%, sudden death in 5%, and other cardiovascular reason in 2

163 etes mellitus, and (2) all end points except sudden death in a model including all baseline character

164 associated with ventricular arrhythmias and sudden death in animal models and humans.

165 cular tachycardia (CPVT), a leading cause of sudden death in apparently healthy individuals exposed t

166 diomyopathy (HCM), a disease associated with sudden death in apparently healthy young adults.

167 success of radiofrequency ablation, and (3) sudden death in asymptomatic patients with WPW.

168 uch sources as the U.S. National Registry of Sudden Death in Athletes (which uses news media, Interne

169 rts) from both the U.S. National Registry of Sudden Death in Athletes and the National Collegiate Ath

170 ardiographic screening for the prevention of sudden death in athletes.

171 LQTS is a known cause of sudden death in childhood, adolescence and young adultho

172 reliably define the incidence and causes of sudden death in college student-athletes.

173 l/ox-CaMKII pathway contributes to increased sudden death in diabetic patients after myocardial infar

174 ROS contribute to sudden death in diabetics after myocardial infarction by

175 Adjusted hazard ratios for sudden death in each trial group were calculated with th

176 s that were associated with the incidence of sudden death in fasted CD36(-/-) mice.

177 ting events, the incidence of sports-related sudden death in older adults is expected to rise.

178 in all-cause mortality, vascular death, and sudden death in patients with AF.

179 ibrillators (ICDs) for primary prevention of sudden death in patients with an ejection fraction (EF)

180 of death due to ventricular tachyarrhythmias/sudden death in patients with nonischemic dilated cardio

181 Reports of sudden death in patients with normalized left ventricula

182 reases the risk of cardiovascular events and sudden death in patients with reduced glomerular filtrat

183 To explore the role of cardiac problems in sudden death in RTT, we characterized cardiac rhythm in

184 ting the increased risk for exertion-related sudden death in SCT carriers is unlikely related to fitn

185 in the increased incidence of arrhythmia and sudden death in the ageing population.

186 ciated with life-threatening arrhythmias and sudden death in the athlete.

187 table arrhythmia syndrome or risk factor for sudden death in the context of other cardiac pathology.

188 for and challenges of risk stratification of sudden death in the heart failure patient and discusses

189 h to pre-participation screening for risk of sudden death in the older athlete is a complex issue and

190 represents the latest molecular autopsy for sudden death in the young (SDY).

191 sorder long QT syndrome (LQTS) can result in sudden death in the young or remain asymptomatic into ad

192 iomyopathy (HCM) is the most common cause of sudden death in the young, although not all patients eli

193 HCM is the most common cause of sudden death in the young.

194 ssel occlusions, myocardial infarctions, and sudden death in these mice.

195 is of clinical importance given the risk of sudden death in these patients, but so far contradictory

196 ucleoside (AICAR) prevents this heat-induced sudden death in this mouse model.

197 common cardiomyopathies and a major cause of sudden death in young athletes.

198 en without autopsy, familial screening after sudden death in young patients is effective.

199 cardiomyopathy is the most frequent cause of sudden death in young people (including trained athletes

200 ects the fact that ARVC is a common cause of sudden death in young people and that sudden death may b

201 Most sudden deaths in triathletes happened during the swim se

202 irect cause of death (right heart failure or sudden death) in 37 (44%) patients; PH contributed to bu

203 Methods to predict a higher or lower risk of sudden death include the detection of myocardial fibrosi

204 l Risk Model (SPRM) for proportional risk of sudden death, including death from ventricular arrhythmi

205 Sudden death is associated with failure of postnatal org

206 Sudden death is rare.

207 association of ventricular arrhythmias with sudden death led to significant investigation with antia

208 culated infrared absorption rates assuming a sudden-death limit.

209 As measurement of LVWT impacts diagnosis and sudden death management, CMR should be considered as par

210 use of sudden death in young people and that sudden death may be the first manifestation of the disea

211 teral prefrontal cortex (Brodmann Area 9) of sudden death medication-free individuals post mortem.

212 risk of all-cause mortality, cardiac death, sudden death, myocardial infarction, or stroke based on

213 te pericardial effusion (n = 1), unexplained sudden death (n = 2), and late strokes thought to be non

214 r therapy, postnatal cardiac arrest (n=4) or sudden death (n=1) was common among subjects with fetal/

215 ients experienced arrhythmic events, such as sudden death (n=1), appropriate implantable cardioverter

216 sustained ventricular tachycardia (n=1), or sudden death (n=1), compared with none of athletes with

217 red in 18 patients (3%; 0.54%/y): arrhythmic sudden death (n=12), progressive heart failure and heart

218 with CTCAE terms: disease progression [n=3], sudden death [n=1], and not specified [n=1]).

219 cluding death (heart failure related, n=142; sudden death, n=71; and noncardiac, n=22) or cardiac tra

220 imaging, coronary obstruction, arrhythmias, sudden death, neoaortic regurgitation and dilation, neur

221 The overwhelming majority of sports-related sudden deaths occur among those older than 35 years of a

222 Over the 10-year study period, 182 sudden deaths occurred (age 20 +/- 1.7 years; 85% male;

223 frequency with which cardiovascular-related sudden death occurs in competitive athletes importantly

224 e interval, 1.6-9.7) and a family history of sudden death (odds ratio, 3.2; 95% confidence interval,

225 The sudden death of a previously healthy young individual is

226 ecameron contains a novella that details the sudden death of a young man called Gabriotto, including

227 that frequently is identified only after the sudden death of apparently healthy individuals.

228 The sudden death of young individuals is commonly attributed

229 ith adverse disease complications, including sudden death or heart failure death and a generally adve

230 on between current or recent PI exposure and sudden death or nonhemorrhagic stroke (adjusted rate rat

231 eart failure (aHR, 2.24; 95% CI, 2.05-2.43), sudden death or ventricular arrhythmia (aHR, 1.69; 95% C

232 ssion was used to examine trends in rates of sudden death over time.

233 n by fewer deaths from myocardial infarction/sudden death (P<0.001) but not heart failure (P=0.85).

234 ructural changes potentially attributable to sudden death pathogenesis were present on magnetic reson

235 ed a longer mitral annulus disjunction in 50 sudden death patients with MVP and LV fibrosis than in 2

236 eases in heart failure-related mortality and sudden death (period 4 versus 1: HR, 0.10; P<001 and HR,

237 Concerns about hGH-associated sudden death persist, but recent studies show either abs

238 d by variants found in genes associated with sudden death-predisposing catecholaminergic polymorphic

239 oung, although not all patients eligible for sudden death prevention with an implantable cardioverter

240 table cardioverter-defibrillators (ICDs) for sudden death prevention, heart transplantation for end-s

241 e for HCM has demonstrated the potential for sudden death prevention, predominantly in adult patients

242 implantable cardioverter-defibrillators for sudden death prevention, thereby creating the opportunit

243 a poor prognosis secondary to a high risk of sudden death previously attributed to ventricular tachya

244 drug treatment and prediction of the risk of sudden death remain fairly primitive.

245 trastructural changes, and long-term risk of sudden death remain unresolved and need further research

246 rhythmias, important causes of suffering and sudden death, remains an unmet goal for biomedical resea

247 A total of 135 sudden deaths, resuscitated cardiac arrests, and trauma-

248 sk and significantly decreased 1- and 3-year sudden death risk compared with era 1.

249 mptoms, including 135 with >/=1 conventional sudden death risk factors and 50 (37%) with late gadolin

250 l fibrosis, although its role in stratifying sudden death risk in subgroups of HCM patients remains i

251 orphology index has the potential to improve sudden death risk stratification and patient selection f

252 nced by improvements in overall survival and sudden death risk.

253 its major disease pathways (i.e., arrhythmic sudden death risk; progressive heart failure [HF] due to

254 progressive heart failure (n=17); arrhythmic sudden death (SD) (n=17); and embolic stroke (n=2).

255 n suggested as the cause of up to a third of sudden death (SD) cases.

256 symptoms without the increased incidence of sudden death seen in adults treated with PDE3i.

257 lains the reported cardiac abnormalities and sudden death seen in humans with SCA.

258 Overall, 17 sudden death-susceptibility gene variants were identifie

259 epth of 10x across 90% of nucleotides within sudden death-susceptibility genes in 100% of parental ex

260 s of ultrarare, nonsynonymous variants in 99 sudden death-susceptibility genes.

261 AACEs included postdischarge sudden death, sustained ventricular tachycardia, and ven

262 liforme is a soil borne pathogen that causes sudden death syndrome (SDS) in soybean plants.

263 Sudden death syndrome (SDS), caused by Fusarium virgulif

264 ulation in Fusarium virguliforme that causes sudden death syndrome in soybean.

265 to F. virguliforme, the pathogen that causes sudden death syndrome.

266 to a number of diseases, including epilepsy, sudden death syndromes like SUDEP and SIDS, and cardiac

267 d ventricular tachycardia, a risk factor for sudden death) than is high LGE-SI.

268 inant syndrome of ventricular arrhythmia and sudden death that can present with divergent clinical fe

269 UDEP excludes other forms of seizure-related sudden death that might be mechanistically related (eg,

270 Sudden deaths that occurred out of hospital accounted fo

271 or specific disorders with increased risk of sudden death, the benefit of identifying such disorders

272 Cardiomyopathy patients are at risk of sudden death, typically from scar-related abnormalities

273 nd 39 females) with >/=1 HCM risk factor for sudden death underwent S-ICD ECG screening at rest and o

274 alized for pneumonia are at greater risk for sudden death up to 1 year after infection.

275 01 genes implicated in cardiac disorders and sudden death using a postmortem blood sample.

276 ion of CIED alerts were noted when comparing sudden deaths versus nonsudden deaths (p < 0.001), defib

277 red using established enzymatic methods, and sudden death was adjudicated using medical records, deat

278 adolescents with HCM judged at high risk for sudden death was assembled.

279 The rate of sudden death was not higher among patients with a recent

280 veillance of all genes (N=100) implicated in sudden death was performed to identify putative pathogen

281 Sudden death was reported in 3583 patients.

282 sease; however, right ventricular failure or sudden death was the sole cause of death in less than ha

283 diac mortality, heart failure mortality, and sudden death were 25.2%, 14.9%, 10.3%, 12.2%, and 2.1%,

284 The cumulative incidence rates of sudden death were assessed at different time points afte

285 on, and family history of cardiac disease or sudden death were collected.

286 sinus bradycardia, spontaneous seizure, and sudden death were detected in RQ/+ mutant mice in vivo;

287 All-cause mortality and sudden death were significantly lower in era 2 and 3 com

288 re at higher risk of all-cause mortality and sudden death when compared with those without CAD.

289 t failure morbidity or a cause of arrhythmic sudden death; when treated, it is associated with low di

290 Sudden death, where no end point illness is overt, is ob

291 function of hERG causes long QT syndrome and sudden death, which occur in patients with cardiac ische

292 larly in decisions for primary prevention of sudden death with implantable defibrillators.

293 ents likely to achieve primary prevention of sudden death with implantable defibrillators.

294 autopsy studies report an associated risk of sudden death with interarterial anomalous left coronary

295 arrhythmic death syndrome (SADS) describes a sudden death with negative autopsy and toxicological ana

296 etion of Slc8b1 in adult mouse hearts causes sudden death, with less than 13% of affected mice surviv

297 The RISP cKO had a sudden death, with minimal behavioral changes.

298 history of ventricular fibrillation (VF) and sudden death without electrocardiographic or echocardiog

299 neous disorders with the common phenotype of sudden death without explanation upon postmortem investi

300 uction in mortality from other CV causes and sudden death, without apparent impact on HF deaths.