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1 y failure, one thromboembolic event, and one sudden death).
2 syncope, 7 near-drowning, and 3 resuscitated sudden death).
3 that SCT is associated with exertion-related sudden death.
4 entricular arrhythmias and can predispose to sudden death.
5 Illicit fentanyl use is associated with sudden death.
6 odels to identify patients at higher risk of sudden death.
7 f internal cardiac defibrillators to prevent sudden death.
8 diomyopathy, heart failure, arrhythmias, and sudden death.
9 ed by aortic dilation and rupture leading to sudden death.
10 are associated with cardiac arrhythmias and sudden death.
11 cular death, HF hospitalization, and aborted sudden death.
12 ardiomyopathy, Takotsubo cardiomyopathy, and sudden death.
13 patients with inherited cardiomyopathies and sudden death.
14 chemic changes were noted in SCA mice before sudden death.
15 (HCM), largely because of the possibility of sudden death.
16 ic disease responsible for heart failure and sudden death.
17 heart disease, 528 from stroke, and 893 from sudden death.
18 ar diastolic heart disease, dysrhythmia, and sudden death.
19 nostic value for both cardiac death (CD) and sudden death.
20 myopathies complicated by frequent premature sudden death.
21 ith all-cause mortality, vascular death, and sudden death.
22 T syndrome (LQTS) is associated with risk of sudden death.
23 nfluence the risk of cardiac arrhythmias and sudden death.
24 d individuals to ventricular arrhythmias and sudden death.
25 aches designed to restore life to victims of sudden death.
26 block, presenting clinically as syncope, and sudden death.
27 isk of arrhythmia, premature RV failure, and sudden death.
28 r, associated with an increased incidence of sudden death.
29 s to mitral regurgitation, heart failure and sudden death.
30 -four children (60%) had a family history of sudden death.
31 (2+) sensitivity, and high susceptibility to sudden death.
32 ng arterial aneurysms, which may manifest as sudden death.
33 some patients to debilitating morbidity and sudden death.
34 n artery that can lead to vessel rupture and sudden death.
35 se of ventricular tachyarrhythmias (VTs) and sudden death.
36 hythmogenic disorder that causes syncope and sudden death.
37 overly conservative management can result in sudden death.
38 e 2 (SENP2) develop spontaneous seizures and sudden death.
39 rance, risk of progressive heart failure and sudden death.
40 ical mortality was most frequently caused by sudden death.
41 cytes, cardiac dysfunction, arrhythmias, and sudden death.
42 ventricular arrhythmias, heart failure, and sudden death.
43 8) and/or TdP (n=68; 11% fatal), and 99 with sudden death.
44 s, developmental delay, and elevated risk of sudden death.
45 and increased risk of cardiac arrhythmia and sudden death.
46 ding symptoms or recognized risk factors for sudden death.
47 verse effects, including rare occurrences of sudden death.
48 ar arrhythmias leading to cardiac arrest and sudden death.
49 iers of hERG/R148W may be at risk of cardiac sudden death.
50 ffected individuals to fatal arrhythmias and sudden death.
51 d individuals to ventricular arrhythmias and sudden death.
52 opulations are at greater risk to succumb to sudden death.
53 milial evaluation following a young person's sudden death.
54 often of cardiovascular causes, particularly sudden death.
55 iologic studies in MVP patients with aborted sudden death.
56 ch patient) and how to treat them to prevent sudden death.
57 ypoketotic hypoglycemia, cardiomyopathy, and sudden death.
58 s ratio=1.4-4.7; P<0.05) with aLQTS, TdP, or sudden death.
59 creasing the risk of cardiac arrhythmias and sudden death.
60 ed susceptibility to cardiac arrhythmias and sudden death.
61 hich can lead to ventricular arrhythmias and sudden death.
62 enotypes, including spontaneous seizures and sudden death.
63 fentanyl-induced ventricular arrhythmias and sudden death.
64 nges modeling bipolar disorder, epilepsy and sudden death.
65 n myocardial territory supplied by a SVG, or sudden death.
66 CI) increases the risk of cardiomyopathy and sudden death.
67 uid index value) were seen in 62.8% cases of sudden deaths.
69 tient-years; 1.19; 1.03-1.39, p=0.0201), and sudden death (1.68 vs 1.12 events per 100 patient-years;
70 of 2 years, 11 AACEs (2.5%) were detected: 5 sudden deaths (1.1%) and 6 spontaneous ventricular tachy
72 (9.3%): 37 (35%) due to HF, 25 (23%) due to sudden death, 15 (14%) due to other cardiovascular (CV)
73 patient (10 outpatient, 985 hospitalized, 17 sudden death), 25 food, 18 dust/soils, and 35 other stra
75 arrhythmias are rare but are associated with sudden death; 9) early- and late-onset ND abnormalities
81 was driven by reductions in out-of-hospital sudden death and hospitalized ST-segment-elevation myoca
82 e was driven by decreases in out-of-hospital sudden death and hospitalized ST-segment-elevation myoca
83 es have shown an association between risk of sudden death and left ventricular maximal wall thickness
84 Fallot was associated with a minimal risk of sudden death and low rate of reintervention for right ve
87 nged its natural history, with prevention of sudden death and reversal of HF, thereby restoring quali
90 recommended programming accounted for 56% of sudden deaths and 11% of all deaths during the study per
92 anism, and cause of death in the majority of sudden deaths and in almost 20% of nonsudden deaths.
93 magnetic conditions a series of entanglement sudden-deaths and revivals occur between the two qubits.
94 ts in the ibrutinib plus obinutuzumab group (sudden death) and one (1%) of 115 patients in the chlora
95 , 19 at low risk [age 30 (7.5); 12 males] of sudden death, and 15 healthy controls [age 37 (16); seve
96 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
98 prednisone group (gastric ulcer perforation, sudden death, and cerebrovascular accident) and the plac
99 onary heart disease overall, out-of-hospital sudden death, and hospitalized ST-segment-elevation and
100 usly admitted to hospital, presumably due to sudden death, and in patients with poor left ventricular
101 f cardiovascular injury and the incidence of sudden death, and MR blockade decreases the risk of card
103 ardioverter-defibrillators for prevention of sudden death, and other contemporary treatment options.
104 gnificantly associated with (1) total death, sudden death, and pacemaker implantation in a model, inc
105 cardioverter-defibrillator for prevention of sudden death are mainstays of therapy when deemed necess
109 hondria as potential therapeutic targets for sudden death associated with cardiovascular disease.
112 pairment, testicular dysgenesis in males and sudden death at infant age by brainstem-mediated cardior
114 ce showed markedly increased mortality, with sudden death beginning after 5 weeks and 100% mortality
115 </=5.7%, those with a SPRM-predicted risk of sudden death below the median had no reduction in mortal
116 with an increased risk of heart failure and sudden death, but its risk in patients with preserved le
117 The leading cause of mortality in HFpEF is sudden death, but little is known about the underlying m
118 r all decedents and within the categories of sudden death, cancer, congestive heart failure or chroni
119 hippocampus/amygdala and parahippocampus in sudden death cases and people at high risk, when compare
120 ents with a genetic form of exercise-induced sudden death (catecholaminergic polymorphic ventricular
121 WCD) for use and effectiveness in preventing sudden death caused by ventricular tachyarrhythmia or fi
123 brovascular accident) and the placebo group (sudden death, cerebrovascular accident, and pneumonia),
124 was performed (composite clinical outcome of sudden death, class III/IV heart failure, left ventricul
125 blockade of PI4KA in adult animals leads to sudden death closely correlating with the drug's ability
126 ver, despite its rarity and absence in large sudden death cohorts, TKOS remains a malignant and poten
127 type 1 patients is associated with total and sudden deaths, conduction defects, left ventricular dysf
130 by doxorubicin plus cyclophosphamide group), sudden death (docetaxel plus capecitabine followed by do
131 defibrillator discharges, resuscitated from sudden death, documented stroke, and admission for conge
132 luding implantable defibrillators to prevent sudden death, drugs and surgical myectomy (or, alternati
133 s in neonates, provoking brain damage and/or sudden death due to apnea episodes and cardiorespiratory
135 diac repolarization, associated high risk of sudden death due to ventricular tachycardia, and congeni
138 ex, clinical presentation, family history of sudden death, ethnicity, and deprivation index did not p
142 ge, NYHA functional class, family history of sudden death (FHSD), syncope, atrial fibrillation, non-s
145 ttributed to coronary heart disease, stroke, sudden death from an unknown cause, or a combination of
149 gical connection between epilepsy itself and sudden death have fuelled increased attention to this ph
150 t explained by a substantially lower risk of sudden death (hazard ratio, 0.53 [0.43-0.65]; P<0.001).
151 onary syndrome, fatal myocardial infarction, sudden death, heart failure, coronary artery revasculari
152 alth-care expenditure as a result of stroke, sudden death, heart failure, unplanned hospital admissio
153 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
154 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
155 : 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)
156 ortic dissections are a preventable cause of sudden death if individuals at risk are identified and s
157 e patients (related to heart failure in 38%, sudden death in 5%, and other cardiovascular reason in 2
159 etes mellitus, and (2) all end points except sudden death in a model including all baseline character
161 cular tachycardia (CPVT), a leading cause of sudden death in apparently healthy individuals exposed t
163 uch sources as the U.S. National Registry of Sudden Death in Athletes (which uses news media, Interne
164 rts) from both the U.S. National Registry of Sudden Death in Athletes and the National Collegiate Ath
173 ibrillators (ICDs) for primary prevention of sudden death in patients with an ejection fraction (EF)
174 ibrillator (ICD) is effective for preventing sudden death in patients with hypertrophic cardiomyopath
175 of death due to ventricular tachyarrhythmias/sudden death in patients with nonischemic dilated cardio
177 reases the risk of cardiovascular events and sudden death in patients with reduced glomerular filtrat
178 ventricular arrhythmias are a major cause of sudden death in patients with structural heart disease.
179 To explore the role of cardiac problems in sudden death in RTT, we characterized cardiac rhythm in
180 ting the increased risk for exertion-related sudden death in SCT carriers is unlikely related to fitn
184 table arrhythmia syndrome or risk factor for sudden death in the context of other cardiac pathology.
186 for and challenges of risk stratification of sudden death in the heart failure patient and discusses
187 h to pre-participation screening for risk of sudden death in the older athlete is a complex issue and
190 sorder long QT syndrome (LQTS) can result in sudden death in the young or remain asymptomatic into ad
191 iomyopathy (HCM) is the most common cause of sudden death in the young, although not all patients eli
195 is of clinical importance given the risk of sudden death in these patients, but so far contradictory
198 ects the fact that ARVC is a common cause of sudden death in young people and that sudden death may b
200 Methods to predict a higher or lower risk of sudden death include the detection of myocardial fibrosi
201 l Risk Model (SPRM) for proportional risk of sudden death, including death from ventricular arrhythmi
202 linked to severe diseases with high risk for sudden death, including epileptic encephalopathy and car
206 association of ventricular arrhythmias with sudden death led to significant investigation with antia
208 As measurement of LVWT impacts diagnosis and sudden death management, CMR should be considered as par
209 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.
213 sustained ventricular tachycardia (n=1), or sudden death (n=1), compared with none of athletes with
214 red in 18 patients (3%; 0.54%/y): arrhythmic sudden death (n=12), progressive heart failure and heart
215 itis and hepatitis, respiratory failure, and sudden death [n=1 each]), six (2%) patients in the durva
217 cluding death (heart failure related, n=142; sudden death, n=71; and noncardiac, n=22) or cardiac tra
218 Although mechanisms of fentanyl-related sudden death need further investigation, blockade of hER
219 imaging, coronary obstruction, arrhythmias, sudden death, neoaortic regurgitation and dilation, neur
220 The overwhelming majority of sports-related sudden deaths occur among those older than 35 years of a
223 frequency with which cardiovascular-related sudden death occurs in competitive athletes importantly
225 e interval, 1.6-9.7) and a family history of sudden death (odds ratio, 3.2; 95% confidence interval,
227 ecameron contains a novella that details the sudden death of a young man called Gabriotto, including
230 ith adverse disease complications, including sudden death or heart failure death and a generally adve
231 eart failure (aHR, 2.24; 95% CI, 2.05-2.43), sudden death or ventricular arrhythmia (aHR, 1.69; 95% C
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 d by variants found in genes associated with sudden death-predisposing catecholaminergic polymorphic
237 many HCM patients, making the likelihood of sudden death prevention a reality and fulfilling the asp
238 oung, although not all patients eligible for sudden death prevention with an implantable cardioverter
239 table cardioverter-defibrillators (ICDs) for sudden death prevention, heart transplantation for end-s
240 e for HCM has demonstrated the potential for sudden death prevention, predominantly in adult patients
241 implantable cardioverter-defibrillators for sudden death prevention, thereby creating the opportunit
242 s, and one patient assigned fluoxetine had a sudden death (primary cause) with multiple sclerosis and
243 Children referred for a family history of sudden death receive cardiac disease diagnoses (14%), bu
244 trastructural changes, and long-term risk of sudden death remain unresolved and need further research
246 l fibrosis, although its role in stratifying sudden death risk in subgroups of HCM patients remains i
247 orphology index has the potential to improve sudden death risk stratification and patient selection f
248 its major disease pathways (i.e., arrhythmic sudden death risk; progressive heart failure [HF] due to
249 progressive heart failure (n=17); arrhythmic sudden death (SD) (n=17); and embolic stroke (n=2).
254 epth of 10x across 90% of nucleotides within sudden death-susceptibility genes in 100% of parental ex
263 to a number of diseases, including epilepsy, sudden death syndromes like SUDEP and SIDS, and cardiac
264 inant syndrome of ventricular arrhythmia and sudden death that can present with divergent clinical fe
265 UDEP excludes other forms of seizure-related sudden death that might be mechanistically related (eg,
267 le cardioverter-defibrillators (ICDs) reduce sudden death, these patients die of heart failure (HF) o
269 nd 39 females) with >/=1 HCM risk factor for sudden death underwent S-ICD ECG screening at rest and o
272 ion of CIED alerts were noted when comparing sudden deaths versus nonsudden deaths (p < 0.001), defib
273 al and cardiac magnetic resonance studies in sudden death victims and patients with arrhythmic MVP.
277 veillance of all genes (N=100) implicated in sudden death was performed to identify putative pathogen
282 diac mortality, heart failure mortality, and sudden death were 25.2%, 14.9%, 10.3%, 12.2%, and 2.1%,
285 sinus bradycardia, spontaneous seizure, and sudden death were detected in RQ/+ mutant mice in vivo;
286 Patients referred for a family history of sudden death were evaluated in a retrospective review fr
288 t failure morbidity or a cause of arrhythmic sudden death; when treated, it is associated with low di
290 function of hERG causes long QT syndrome and sudden death, which occur in patients with cardiac ische
291 high-risk patients susceptible to arrhythmic sudden death with a sensitivity of only 33%, leaving man
293 autopsy studies report an associated risk of sudden death with interarterial anomalous left coronary
294 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 history of ventricular fibrillation (VF) and sudden death without electrocardiographic or echocardiog
298 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.