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3 all, all-cause mortality also was lower with paroxysmal (3.0%/year) compared with persistent (4.4%/ye
4 ; mean left atrial diameter, 43+/-5 mm) with paroxysmal (36 of 50 patients; 72%) or short-standing (<
5 trium diameter, 45+/-6 mm) with a history of paroxysmal (40/66, 61%) or persistent atrial fibrillatio
6 ulants were used less often in patients with paroxysmal (53%) and new onset (16%) AF than in patients
7 tive patients (mean age, 61+/-10 years) with paroxysmal (550) or persistent atrial fibrillation (583)
8 +/-11 years) undergoing catheter ablation of paroxysmal (59%) or persistent (41%) AF, the ACE inserti
11 bolic event was lower in those patients with paroxysmal AF (1.49%/year), compared with persistent (1.
12 tients with persistent AF than in those with paroxysmal AF (41.1 +/- 28.0 vs. 33.2 +/- 22.8, p = 0.04
14 malities (cryptogenic 37% vs 45%; p=0.18) or paroxysmal AF (6% vs 10%; p=0.17) at baseline or of new
16 which 226 (74%) were confined to symptomatic paroxysmal AF (average, 5+/-5; range, 1 to >20), whereas
17 - 10 years, 186 males) randomized those with paroxysmal AF (n = 115) to CPVI or HFSA-only (noninferio
20 al [CI], 1.89-3.60), 2.1-fold higher odds of paroxysmal AF (odds ratio, 2.14; 95% CI, 1.45-3.16) and,
21 fold higher odds of persistent compared with paroxysmal AF (odds ratio, 2.19; 95% CI, 1.66-2.88).
22 y AF (OR = 2.07, 95% CI 1.59-2.68), and with paroxysmal AF (OR = 1.98, 95% CI 1.44-2.74) and chronic
25 ex for AF patients was 0.6 +/- 0.5 mm Hg/mL (paroxysmal AF 0.51 +/- 0.4 and persistent AF 0.73 +/- 0.
28 xt below) over 12 weeks in 134 patients with paroxysmal AF and implanted pacemakers where AF burden (
29 d at preferred sites in 10% of patients with paroxysmal AF and in 35% of patients with persistent AF.
34 g-term single procedure success rates in non-paroxysmal AF are disappointingly low for current stepwi
35 ocardiographic abnormalities and subclinical paroxysmal AF at baseline in patients with index events
36 ared with patients without AF, patients with paroxysmal AF at randomization had a higher risk of the
37 ange 0-12.8) and was higher in patients with paroxysmal AF compared with patients without a history o
39 442 (69%) males and 328 (51%) patients with paroxysmal AF equally distributed between the 2 groups.
43 he substrate occurs and is more effective in paroxysmal AF rather than persistent or permanent AF.
44 In ENGAGE AF-TIMI 48 trial, patients with paroxysmal AF suffered fewer thromboembolic events and d
45 cantly worse in patients with persistent and paroxysmal AF than in controls (Repeatable Battery for t
46 ient participants with confirmed symptomatic paroxysmal AF that required cardioversion (n = 428), at
47 (STOP AF) trial randomized 245 patients with paroxysmal AF to medical therapy versus cryoballoon-base
50 HF patients with a history of AF, those with paroxysmal AF were at greater risk of HF hospitalization
52 /= 80 years, prior myocardial infarction and paroxysmal AF were independent predictors of OAC non-use
53 involving 127 treatment-naive patients with paroxysmal AF were randomized at 16 centers in Europe an
54 152 patients undergoing de novo ablation for paroxysmal AF were randomized to 2 different treatment a
55 Patients with drug-refractory, symptomatic paroxysmal AF were randomly assigned to either incomplet
56 miR-25 were lower in atria of patients with paroxysmal AF when compared with patients in sinus rhyth
58 f 291 hypertensive patients with symptomatic paroxysmal AF who were scheduled to undergo pulmonary ve
59 ost study enrolled patients with symptomatic paroxysmal AF with an initial 3-month noninterventional
62 tal of 152 patients (age, 60+/-11 years; 63% paroxysmal AF) undergoing PV isolation for AF were studi
63 56.9 +/- 11.8 years, 63.9% male, 69.2% with paroxysmal AF) who were arrhythmia-free at 12 months (ex
66 group 1: two events (0.87%) in patients with paroxysmal AF, 4 (2.3%) in patients with persistent AF,
68 of SCI was present in 80 patients (89%) with paroxysmal AF, 83 (92%) with persistent AF (paroxysmal v
69 are those with normal structural hearts and paroxysmal AF, although those with congestive heart fail
70 ernans was more prevalent in persistent than paroxysmal AF, and absent in controls (P=0.018 APD; P=0.
71 r the treatment of patients with symptomatic paroxysmal AF, for whom at least one antiarrhythmic drug
74 longer AF duration, with more prevalent non-paroxysmal AF, higher CHADS2/CHA2DS2-VASc score, and ora
75 approach generally agreed on for those with paroxysmal AF, optimal techniques for the ablation of no
77 rotein is elevated in atria of patients with paroxysmal AF, suggesting that microRNA-mediated post-tr
78 st rate-dependent amplification, followed by paroxysmal AF, with marked rate dependence, and undetect
89 ng catheter ablation for symptomatic AF (66% paroxysmal AF; age, 58+/-10 years; left atrial area, 27+
90 ulation (N=2069; 66% men; 60+/-10 years; 62% paroxysmal AF; mean CHADS2, 1.2+/-0.9; CHA2DS2-VASc, 2.1
95 onal cohort study of patients diagnosed with paroxysmal and persistent AF (undergoing their first cat
99 ) and cognitive performance in patients with paroxysmal and persistent atrial fibrillation (AF) and c
101 l FIRM-guided ablation procedures (n=24; 50% paroxysmal) at University of California, Los Angeles Med
105 e of pulmonary vein (PV) antrum isolation in paroxysmal atrial fibrillation (AF) patients over more t
106 cts with symptomatic, persistent/high-burden paroxysmal atrial fibrillation (AF) were enrolled at 6 c
112 observed in 70 patients (16.1%) before TAVR: paroxysmal atrial fibrillation (AF)/atrial tachycardia (
113 lloon Pulmonary Vein Ablation of Symptomatic Paroxysmal Atrial Fibrillation (MACPAF) study, serial 3-
115 line within 5 years (odds ratio [OR]: 12.7), paroxysmal atrial fibrillation (OR: 5.19), subtherapeuti
117 t the hypothesis that PP1 is dysregulated in paroxysmal atrial fibrillation (PAF) at the level of its
118 atients; 60 patients undergoing ablation for paroxysmal atrial fibrillation (PAF), 30 patients underg
121 g persistent atrial fibrillation (LPeAF), or paroxysmal atrial fibrillation (PAF); if right atrial si
122 CH Catheter for the Treatment of Symptomatic Paroxysmal Atrial Fibrillation (SMART-AF) trial using sh
124 ustained ventricular tachycardia [n=1], fast paroxysmal atrial fibrillation [n=1], symptomatic bradyc
125 nt Cryoablation Balloon for the Treatment of Paroxysmal Atrial Fibrillation [Stop AF]; NCT00523978).
126 on and find out whether it could improve the paroxysmal atrial fibrillation ablation results in human
128 blanking period after catheter ablation for paroxysmal atrial fibrillation but calls into question t
129 or pulmonary vein isolation in patients with paroxysmal atrial fibrillation has demonstrated encourag
130 for ablation of drug refractory, symptomatic paroxysmal atrial fibrillation in 172 participants recru
132 ersus single tip wide area catheter ablation-paroxysmal atrial fibrillation is the first multinationa
133 for atrial fibrillation and represented with paroxysmal atrial fibrillation or atrial tachycardia und
136 before radiofrequency catheter ablation for paroxysmal atrial fibrillation significantly reduces the
137 dergoing radiofrequency catheter ablation of paroxysmal atrial fibrillation to receive remote IPC or
140 ive patients (61+/-8 years old, 41 men) with paroxysmal atrial fibrillation underwent PVI using Carto
142 patients with symptomatic, drug-refractory, paroxysmal atrial fibrillation were enrolled in a prospe
144 iofrequency energy delivery in patients with paroxysmal atrial fibrillation who undergo PVI and leads
145 e treatment of patients with drug-refractory paroxysmal atrial fibrillation, and there was no signifi
146 pain syndrome, hypertension, and refractory paroxysmal atrial fibrillation, for which she had underg
147 ated in cryptogenic stroke, including occult paroxysmal atrial fibrillation, patent foramen ovale, ao
150 is study, in patients undergoing ablation of paroxysmal atrial fibrillation, was to: (1) identify fac
151 inferiority study included 140 patients with paroxysmal atrial fibrillation, which was refractory to
162 hepatic failure (3%), liver abscesses (3%), paroxysmal atrial tachycardia (3%), thoracic pain (3%),
166 mbination-known as infantile convulsions and paroxysmal choreoathetosis (ICCA)-are related autosomal
168 es, presence of cough >/=14 days (20.5%) and paroxysmal coughing spells (33.3%) at diagnosis were unc
171 ss of brain disorders that usually result in paroxysmal disorders, although their role in other neuro
172 d in an autosomal dominant fashion and cause paroxysmal disturbances of neurological function, althou
174 , peripheral manifestations, and stereotypic paroxysmal dizziness spells are common with LGI1-IgG.
175 dysfunction is a rare disorder that leads to paroxysmal dizziness, fatigue, and syncope because of a
177 studies have been carried out on each of the paroxysmal dyskinesia genes, to date there has been no l
178 wo of PNKD) in a series of 145 families with paroxysmal dyskinesias as well as in a series of 53 pati
179 ng group of episodic movement disorders, the paroxysmal dyskinesias, and study of the causative genes
180 weeks) or late (>6 weeks after ablation) and paroxysmal (either spontaneous conversion or treated wit
183 ve of 16 patients developed additional brief paroxysmal episodes in puberty, either dystonic/dyskinet
186 l kinesigenic dyskinesia or choreoathetosis, paroxysmal exercise-induced dyskinesia, and paroxysmal n
190 syndromes such as inherited erythromelalgia, paroxysmal extreme pain disorder, and small-fibre neurop
191 pain (CIP); (2) primary erythromelalgia; (3) paroxysmal extreme pain disorder; (4) febrile seizures a
192 ion in which trigeminal stimulation triggers paroxysmal facial pain, affects defensive peripersonal s
193 progressive condition, occurring first in a paroxysmal form, then in persistent, and then long-stand
194 (>/=7 consecutive days of AF >/=23 hours/d), paroxysmal (>/=1 day with AF >/=6 hours), or no/little A
199 CHA(2)DS(2)-VASC score of 4.5+/-1.2 and was paroxysmal in 26 (25.0%), persistent in 8 (7.7%), and pe
200 ears, the predominant arrhythmia pattern was paroxysmal in 62.3%, persistent in 28.2%, and permanent
201 Postrandomization AF/AT, which remained paroxysmal in 69.5%, did not reduce biventricular pacing
202 amilial infantile epilepsy (41.7%; n = 602), paroxysmal kinesigenic dyskinesia (38.7%; n = 560) and i
204 Benign familial infantile seizures (BFIS), paroxysmal kinesigenic dyskinesia (PKD), and their combi
205 be subdivided into three clinical syndromes: paroxysmal kinesigenic dyskinesia or choreoathetosis, pa
206 x patients with 16p11.2 microdeletions and a paroxysmal kinesigenic dyskinesia phenotype have been re
207 nfantile convulsions and choreoathetosis and paroxysmal kinesigenic dyskinesia, confirming a common d
208 ssociated with variable phenotypes including paroxysmal kinesigenic dyskinesia, paroxysmal non-kinesi
209 ), PRRT2 has been identified as the cause of paroxysmal kinesigenic dystonia and other genes, such as
210 clinical triad of epilepsy, dysarthria, and paroxysmal kinesigenic dystonia, and a high titer of Cas
212 e 21 105 patients were categorized as having paroxysmal (<7 days duration), persistent (>/=7 days but
213 UT1-DS experienced a mean of 30.8 (+/- 27.7) paroxysmal manifestations (52% motor events) at baseline
214 a 90% clinical improvement in non-epileptic paroxysmal manifestations and a normalised brain bioener
217 f 219 AF patients referred for ablation (59% paroxysmal, mean CHA2DS2VASc score 1.7 +/- 1.4) were enr
220 n various regions of the brain, resulting in paroxysmal movement disorders and seizure phenotypes.
225 ts, 61%; 64.0+/-10.0 years) with symptomatic paroxysmal (n=345; 42%) or persistent atrial fibrillatio
226 during (induced) AF in 10 patients with AF (paroxysmal: n=3; persistent: n=4; and longstanding persi
227 d interictal function are unaffected in many paroxysmal neurological channelopathies, possibly explai
229 6; 95% confidence interval [CI], 1.30-2.12), paroxysmal nocturnal dyspnea (odds ratio 1.95; 95% CI, 1
230 among self-reported PE, 2-pillow orthopnea, paroxysmal nocturnal dyspnea, left and right ventricular
232 5 monoclonal antibody (mAb) for treatment of paroxysmal nocturnal hemoglobinuria (PNH) and atypical h
233 predisposes individuals to disorders such as paroxysmal nocturnal hemoglobinuria (PNH) and atypical h
234 , has been shown to prevent complications of paroxysmal nocturnal hemoglobinuria (PNH) and improve qu
242 he mechanism of bone marrow failure (BMF) in paroxysmal nocturnal hemoglobinuria (PNH) is not yet kno
243 vivo measurements of complement activity in paroxysmal nocturnal hemoglobinuria (PNH) patients on ec
244 ate that the erythrocytes from patients with paroxysmal nocturnal hemoglobinuria (PNH) undergoing ecu
245 lood, Krawitz et al report on a patient with paroxysmal nocturnal hemoglobinuria (PNH) who does not h
250 ctivation on erythrocytes from patients with paroxysmal nocturnal hemoglobinuria (PNH); the authors d
251 mAb approved for treatment of patients with paroxysmal nocturnal hemoglobinuria and atypical hemolyt
252 from other TMAs based on the hypothesis that paroxysmal nocturnal hemoglobinuria cells are more sensi
253 ease we demonstrated that FB28.4.2 protected paroxysmal nocturnal hemoglobinuria erythrocytes from co
254 tients with chronic hemolysis suffering from paroxysmal nocturnal hemoglobinuria in which the acquire
255 a 5-fold-enhanced complement regulation on a paroxysmal nocturnal hemoglobinuria patient's erythrocyt
256 ically relevant AP-mediated disease model of paroxysmal nocturnal hemoglobinuria, mini-FH largely out
257 omide-treated erythrocytes that recapitulate paroxysmal nocturnal hemoglobinuria, PspCN enhanced prot
259 val = 1.06-1.13), which is intronic to PNKD (paroxysmal non-kinesigenic dyskinesia) and TMBIM1 (trans
260 including paroxysmal kinesigenic dyskinesia, paroxysmal non-kinesigenic dyskinesia, episodic ataxia a
263 trial tissue was obtained from patients with paroxysmal or chronic AF and from control subjects in si
266 ation, and oxidative stress in patients with paroxysmal or persistent AF not receiving conventional a
268 l-arm study in 337 patients with symptomatic paroxysmal or persistent AF within 6 months of enrollmen
274 ous leiomyomas can be associated with severe paroxysmal pain in which nerve conduction may have a key
275 enetic pain disorders that range from severe paroxysmal pain to a congenital inability to sense pain.
277 nch block, Left atrium >/=47 mm, Type of AF [paroxysmal, persistent or long-standing persistent], and
278 investigated outcomes related to type of AF (paroxysmal, persistent or permanent, or new onset) in 2
280 n symptoms, the type of atrial fibrillation (paroxysmal, persistent, or long-standing persistent), pa
284 s of all three genes, but around half of our paroxysmal series remain genetically undefined implying
286 as the single causative gene for a group of paroxysmal syndromes of infancy, including epilepsy, par
288 trial tachyarrhythmia and (2) progression of paroxysmal to (long-standing) persistent/permanent AF du
290 progression of atrial fibrillation (AF) from paroxysmal to persistent forms remains a major clinical
292 childhood periodic syndromes include benign paroxysmal torticollis, benign paroxysmal vertigo, abdom
293 tremor, tardive tremor and rabbit syndrome, paroxysmal tremors (hereditary chin tremor, bilateral hi
295 d postcontrast ventricular T1 time, AF type (paroxysmal versus persistent), AF duration, and body mas
297 nclude benign paroxysmal torticollis, benign paroxysmal vertigo, abdominal migraine, and cyclic vomit
298 ersistent, p = 0.59), and 41 (46%) controls (paroxysmal vs. controls and persistent vs. controls, p <
300 paroxysmal AF, 83 (92%) with persistent AF (paroxysmal vs. persistent, p = 0.59), and 41 (46%) contr
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