ライフサイエンスコーパス: precordial

1 et was epicardium, 0.46; body surface, 0.47; precordial, 0.17; and optimal leads, 0.11.

2 y, was epicardium, 0.91; body surface, 0.84; precordial, 0.72; and optimal leads, 0.81.

3 ational autoencoder (VAE) that reconstructed precordial 6-lead ECG using limb 6-lead ECG.

4 from 4 lead sets: epicardial, body surface, precordial, and a 6-lead optimal set.

5 Precordial blows in sports and daily activities can trig

6 tion from ventricular fibrillation following precordial blows.

7 n of the interval between discontinuation of precordial compression and delivery of the first electri

8 Cardiopulmonary resuscitation, including precordial compression and mechanical ventilation, was s

9 animals were successfully resuscitated with precordial compression and mechanical ventilation.

10 coronary perfusion pressure generated during precordial compression and pupil diameter was documented

11 nd mitral valve closing and opening followed precordial compression and relaxation.

12 herefore serves to minimize interruptions of precordial compression and the myocardial damage caused

13 t combined with epinephrine treatment during precordial compression and then alone in a prolonged car

14 the concept that stroke volumes generated by precordial compression are quantitatively related to the

15 The stroke volume index produced by precordial compression averaged 0.45 mL/kg or approximat

16 of untreated VF, mechanical ventilation and precordial compression began.

17 dy was to measure stroke volumes produced by precordial compression during cardiopulmonary resuscitat

18 Interruptions of precordial compression for rhythm analyses that exceed 1

19 eated ventricular fibrillation and 8 mins of precordial compression in 13 animals, seven of which wer

20 umed for a "hands off" interval during which precordial compression is discontinued to allow for auto

21 If VF was not reversed, a 1-min interval of precordial compression preceded a second sequence of up

22 lation was not reversed, a 1-min interval of precordial compression preceded a second sequence of up

23 We confirmed that precordial compression produces approximately one third

24 Precordial compression together with mechanical ventilat

25 mins of untreated ventricular fibrillation, precordial compression was begun and continued for 6 min

26 e ventricular fibrillation in each instance, precordial compression was begun coincident with mechani

27 Precordial compression was begun together with mechanica

28 One minute after injection of the compound, precordial compression was begun together with mechanica

29 val of between 3 and 5 mins of untreated VF, precordial compression was begun.

30 n was restored in each of 5 animals in which precordial compression was delayed for 3 seconds before

31 on-decompression (Lifestick resuscitator) or precordial compression was initiated.

32 Precordial compression was maintained at 80 per minute t

33 The precordial compression was performed with a pneumaticall

34 Mechanical ventilation and precordial compression were initiated after 8 mins of un

35 ogressive decreases in stroke volumes during precordial compression were predictive of unsuccessful r

36 was monitored and artifacts produced during precordial compression were removed by digital filtering

37 untreated for 3 minutes before the start of precordial compression, mechanical ventilation, and atte

38 untreated for 7 minutes before the start of precordial compression, mechanical ventilation, and atte

39 r 6 mins before attempted resuscitation with precordial compression, mechanical ventilation, and elec

40 P < .01) than that generated by conventional precordial compression.

41 nstraints caused by artifacts resulting from precordial compression.

42 to the right atrium 2 min after the start of precordial compression.

43 rognosticator that would be displayed during precordial compression.

44 variation in the hands-off interval between precordial compressions and shock delivery was observed,

45 particular, the "hands-off" interval between precordial compressions and subsequent defibrillation sh

46 ested whether spectral-phase analysis of the precordial ECG enabled identification of periodic activa

47 by marked ST-segment elevation in the right precordial ECG leads and is associated with a high incid

48 terized by ST-segment elevation in the right precordial ECG leads and is frequently accompanied by an

49 ists of an ST-segment elevation in the right precordial ECG leads, a shorter-than-normal QT interval,

50 Precordial ECGs were recorded from 15 ischemic cardiomyo

51 explored the mechanisms linking clinical and precordial echocardiographic predictors to thromboemboli

52 coved' ST segment elevations in the anterior precordial electrocardiogram leads, which occasionally r

53 terized by ST-segment elevation in the right precordial electrocardiographic leads and a high inciden

54 h right ventricular volume overload when the precordial examination is inconclusive.

55 Right bundle-branch block and precordial injury pattern in V1 through V3 is common in

56 otio cordis, or sudden death following blunt precordial injury.

57 anifest a TWI pattern different from that of precordial ischemic TWI, thereby discriminating between

58 QRSp was quantified for each precordial lead as the total number of low-amplitude def

59 annular VAs by lower prevalence of positive precordial lead concordance.

60 table voltage amplitude increases across all precordial lead measurements.

61 haracteristics, including QRS morphology and precordial lead morphology, can help distinguish between

62 In the overall cohort, precordial lead QRS complexes were most salient with hig

63 p = 0.0004), a more depressed ST-segment in precordial lead V5 (p = 0.0002), and a higher coronary a

64 eversed QTUc prolongation, especially in the precordial leads (quinidine, 590+/-79 to 479+/-35 [+/-SD

65 coved-type ST-segment elevation in the right precordial leads (V1 to V3; type 1 Brugada electrocardio

66 T-wave inversions in right precordial leads are relatively rare in the general popu

67 elevation (type 1 Brugada pattern) in right precordial leads at therapeutic concentrations in 2 pati

68 there was a dominant frequency gradient from precordial leads facing the scar region to the contralat

69 ildren (5.7%) and was localized in the right precordial leads in 131 (4.7%).

70 y via saliency mapping revealed that lateral precordial leads influence all outcome predictions, with

71 ary disease, increasing STdep in the lateral precordial leads is associated with increasing LV mass a

72 pattern and ST elevation (STE) in the right precordial leads of the ECG.

73 normalities of repolarization in the lateral precordial leads of the electrocardiogram, as manifested

74 e-branch block and ST elevation in the right precordial leads of the surface ECG.

75 pattern of ST-segment elevation in the right precordial leads should not be seen as a marker of a spe

76 easured ST depression (STdep) in the lateral precordial leads to the presence of left ventricular hyp

77 T-wave inversion in right precordial leads V(1) to V(3) is a relatively common fin

78 T-wave inversions in right precordial leads V(1) to V(3) were present in 54 (0.5%)

79 nts displayed extensive T-wave inversions in precordial leads V1 through V4, with either persistent o

80 T wave inversion in infero-lateral and left precordial leads were the most common ECG abnormalities.

81 T QRS morphologies were measured in limb and precordial leads with electronic calipers.

82 nly present with ST-segment elevation in the precordial leads, chest pain, relatively minor elevation

83 ncy spectral area computed from conventional precordial leads, like coronary perfusion pressure and e

84 ccentric hypertrophy increased amplitudes in precordial leads, minimally affecting limb leads, while

85 Eccentric hypertrophy primarily affected the precordial leads, showing notable voltage amplitude incr

86 a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high

87 se characterized by T-wave inversions in the precordial leads, transient QT prolongation in some, and

88 terized by ST segment elevation in the right precordial leads, V1-V3 (unrelated to ischemia or struct

89 II, III, aVR, and aVF and the mid to lateral precordial leads.

90 d sinus rhythm and ST depression in the left precordial leads.

91 elevation and T-wave inversion in the right precordial leads.

92 attern and ST-segment elevation in the right precordial leads.

93 x (the time to the maximum deflection in the precordial leads/QRS duration) was the largest in LV sum

94 A delayed precordial maximum deflection index > or =0.55 identifie

95 Recognition of a prolonged precordial maximum deflection index and early use of tra

96 ar arrhythmia, inverted T-waves in the right precordial or lateral leads, and/or family history of su

97 The value of precordial or transesophageal echocardiography in additi

98 specific for the evaluation of patients with precordial or transthoracic wounds (sensitivity 100%, sp

99 examinations were performed on patients with precordial or transthoracic wounds or blunt abdominal tr

100 ical manifestations may be non-specific with precordial pain, simulating an acute coronary syndrome,

101 us display of frontal (limb) and horizontal (precordial) plane leads.

102 However, slowed initial precordial QRS activation, as quantified by a novel metr

103 included the following: syncope; Q waves or precordial QRS amplitudes <1.8 mV; 3 abnormal SAECG para

104 omponents that influenced model predictions (precordial QRS complexes for all outcomes; T waves for L

105 RMVTs with a precordial R wave transition at or before lead V2 are co

106 nts had a QRS configuration during RMVT with precordial R wave transitions at or before lead V2.

107 n resuscitated after receiving three or more precordial shocks were randomly assigned to receive 300

108 likely to initiate VF than impacts at other precordial sites (5 of 55; 9%, p = 0.02).

109 lectrocardiographic criteria, including left precordial ST segment depression, complete atrioventricu

110 erized by ventricular fibrillation and right precordial ST segment elevation on ECG.

111 plete atrioventricular heart block and right precordial ST segment elevation.

112 Precordial T-wave alternans increased from 0.04 +/- 0.02

113 was the only independent predictor for right precordial T-wave inversion (odds ratio, 3.6; 95% confid

114 Postpacing precordial T-wave inversion (TWI), known as cardiac memo

115 The prevalence of right precordial T-wave inversion decreased significantly with

116 ic LV dysfunction had higher odds of lateral precordial T-wave inversions (odds ratio, 18.4; 95% conf

117 nce interval, 1.21-4.01; P=0.01) and lateral precordial T-wave inversions (odds ratio, 9.87; 95% conf

118 Right precordial T-wave inversions did not predict increased m

119 ern that allows discrimination from ischemic precordial T-wave inversions regardless of the coronary

120 ranch block pattern, QRS duration </=175 ms, precordial transition >/=V1, and maximum deflection inde

121 ECG inconsistencies such as late precordial transition (TZ) and discordant QRS axis may n

122 notch in the middle of the QRS in all cases, precordial transition at </=lead V3 in 7 patients, and a

123 bundle branch block, inferior axis and early precordial transition can be ablated in the majority of

124 ace ECG pattern of patients with OTVT with a precordial transition in lead V(3) who underwent success

125 /- 34 ms, p = 0.006), more often exhibited a precordial transition in lead V(6) (3 of 17 [18%] vs. 0

126 A PVC precordial transition occurring later than the sinus rhy

127 bundle branch block, inferior axis and early precordial transition with Rs or R in V2 or V3.

128 from RVOT origin in patients with lead V(3) precordial transition.

129 ischemic group consisted of 47 patients with precordial TWI identified among 228 consecutive patients

130 ositive or isoelectric T(I), and (3) maximal precordial TWI>TWI(III) was 92% sensitive and 100% speci

131 nown as cardiac memory (CM), mimics ischemic precordial TWI, and there are no established ECG criteri

132 ific for CM, discriminating it from ischemic precordial TWI.

133 differences in QRS axis, limb (I, aVr), and precordial (V1, V2, V6) ECG leads.

134 modality for the evaluation of patients with precordial wounds and blunt truncal injuries because it

135 ity of US in the evaluation of patients with precordial wounds and hypotensive patients with blunt to