ライフサイエンスコーパス: right ventricle

1 ventricular septal defect, and double outlet right ventricle.

2 care must be taken to support the unassisted right ventricle.

3 t ventricle but less well for lesions in the right ventricle.

4 ization and displacement of the aorta to the right ventricle.

5 mmatory foci, that is, at the surface of the right ventricle.

6 oventricular valve defects and double outlet right ventricle.

7 d by ventricular arrhythmias and an abnormal right ventricle.

8 ventricular drain that was inserted into the right ventricle.

9 to be destined to form the outflow tract and right ventricle.

10 oss and fibrofatty tissue replacement of the right ventricle.

11 es rise to the outflow tract and much of the right ventricle.

12 mon atrioventricular canal and double outlet right ventricle.

13 , resulting in a common trunk overriding the right ventricle.

14 teins, is fibroadipocytic replacement of the right ventricle.

15 consecutive patients with VA origins in the right ventricle.

16 us stroke; and known thrombus in the left or right ventricle.

17 ow tract, atrioventricular canal, and future right ventricle.

18 ty, and inherent difficulties in imaging the right ventricle.

19 iac myocytes that typically manifests in the right ventricle.

20 ted cardiomyopathy and unique defects in the right ventricle.

21 ar dysplasia preferentially impacts the thin right ventricle.

22 ietal band is one of the muscle bands in the right ventricle.

23 t may benefit lung vessels and the remodeled right ventricle.

24 of preload, and progressive dilation of the right ventricle.

25 and 22 (81%) had no antegrade flow from the right ventricle.

26 ion in demembranated trabeculae from the rat right ventricle.

27 y well suited for noninvasive imaging of the right ventricle.

28 d in 69% and 84%, respectively, covering the right ventricle.

29 -attenuation lesion at the inner wall of the right ventricle.

30 as open under water and air escaped from the right ventricle.

31 raordinary endurance exercise may injure the right ventricle.

32 ion increases myocyte number in the neonatal right ventricle.

33 xercise training seem to injure the systemic right ventricle.

34 ubule network integrity in both the left and right ventricles.

35 nce interval, -0.58 to -0.31); double-outlet right ventricle, -0.48 (95% confidence interval, -0.87 t

36 m for the right atrium, 2.7+/-1.2 mm for the right ventricle, 1.8+/-1.0 mm for the left atrium, and 2

37 eft ventricle (124+/-27 vs 79+/-12 mL/m(2)), right ventricle (127+/-28 vs 83+/-14 mL/m(2)), left atri

38 1.1 +/- 12.0 versus 46.0 +/- 6.6%, P < 0.05; right ventricle: 29.4 +/- 12.3 versus 46.3 +/- 5.3%, P <

39 ns were delivered to 3 separate sites in the right ventricle (30 W, 60 seconds, 17 mL/min irrigation)

40 um (39.7+/-4.2 to 42.3+/-4.3 ms; P=0.01) and right ventricle (48.1+/-2.5 to 53.3+/-5.3 ms; P<0.01).

41 lation comprised more patients with dominant right ventricle (66% vs. 36%) and hypoplastic left heart

42 not yet well established, mainly because the right ventricle, a common target of the disease, present

43 s derived from neonatal mouse heart left and right ventricles, a total of 45 167 unique transcripts w

44 malrotation, overriding aorta, double outlet right ventricle, aberrant semilunar valve development, b

45 quality in 74% of left ventricle and 84% of right ventricle acquisitions and performs better than SS

46 ving a chronically implanted single-chamber (right ventricle) active fixation leadless pacemaker.

47 In pulmonary hypertension, the right ventricle adapts to the increasing vascular load b

48 mediated deletion resulted in double outlet right ventricle alignment heart defects.

49 were included in this analysis (3501 for the right ventricle analysis).

50 nging from overriding aorta to double-outlet right ventricle and dextro-transposition of the great ar

51 There is reliable remodeling of the excluded right ventricle and good function of the left ventricle.

52 y vascular resistance (PVR), effects reverse right ventricle and left ventricle remodeling, improves

53 defined as the angle between the base of the right ventricle and LV free wall, using the crest of the

54 on data suggests that the progenitors of the right ventricle and outflow tract invert their position

55 The right ventricle and outflow tract of the developing hear

56 s are incorporated into the cardiac outflow (right ventricle and outflow tract).

57 e second heart field (SHF) gives rise to the right ventricle and outflow tract, yet its evolutionary

58 he second heart field (SHF) give rise to the right ventricle and primitive outflow tract (OFT).

59 to the outflow tract and the majority of the right ventricle and provides an embryological context fo

60 in D2, cyclin A2, and Cdk4 expression in the right ventricle and that the Cyclin D2 and Cdk4 promoter

61 to be primarily determined by factors in the right ventricle and tricuspid valve and not the timing o

62 poorly looped hearts with aberrantly formed right ventricles and defective atrioventricular cushion

63 e imaging for the assessment of the left and right ventricles and of indexes of aortic function.

64 ing ventricular noncompaction, double outlet right ventricles and ventricular septal defects.

65 tricular septal defect, double outlet of the right ventricle) and brain defects but not midline fusio

66 ith cardiac defects, including double outlet right ventricle, and atrial and ventricular septal defec

67 ac function, maintenance of perfusion to the right ventricle, and correction of any physiologically d

68 ulmonic infundibulum associated with a small right ventricle, and increased OFT mesenchyme with failu

69 entricular subendocardium and subepicardium, right ventricle, and peripheral tissues in a canine mode

70 efects such as tetralogy of Fallot, systemic right ventricle, and univentricular hearts.

71 ype B, aortic arch hypoplasia, double-outlet right ventricle, and ventricular septal defect.

72 ts in decreased myocyte proliferation in the right ventricle, and we identified numerous cell cycle g

73 The median right ventricle:aortic pressure ratio after repair was 0

74 egments sensed from a conventional pacemaker right ventricle apical lead, and alerted patients to det

75 s to identify which patients with a systemic right ventricle are at risk for clinical events.

76 the basis for predominant involvement of the right ventricle are unknown.

77 a broad spectrum of CHD, including systemic right ventricles, are similar to those in ischemic heart

78 xtensive surgery in the atria and leaves the right ventricle as the systemic ventricle.

79 lasia or lack of the outflow tract (OFT) and right ventricle as well as the inflow tract, dysplasia o

80 ies of the pulmonary vascular system and the right ventricle, as well as their coupling, as important

81 ld (SHF) contribute to the outflow tract and right ventricle, as well as to parts of the left ventric

82 esults in tricuspid atresia with hypoplastic right ventricle associated with the loss of AVC myocardi

83 ansposition of great arteries, double-outlet right ventricle, atrioventricular septal defects, and ca

84 y in the right ventricular outflow tract and right ventricle basal regions.

85 Some emphasized right ventricle-based shunts as a 'cause' of improving r

86 (univentricular heart with a right atrial to right ventricle bioprosthesis in 3, Ebstein's anomaly of

87 entricular end-diastolic pressure, and lower right ventricle/body weight and lung/body weight ratios,

88 sma norepinephrine levels, lung/body weight, right ventricle/body weight, and left ventricular end-di

89 Electroanatomic mapping of the right ventricle, both endocardially and epicardially, an

90 ralogy of Fallot focuses on isthmuses in the right ventricle but may be hampered by hypertrophied myo

91 he disease has an early predilection for the right ventricle, but recognition of left-dominant and bi

92 endurance athletes with special focus on the right ventricle by contrast-enhanced cardiovascular magn

93 a; airway fibrosis; vascular remodeling; and right ventricle cardiac hypertrophy.

94 rized by echocardiography and left ventricle/right ventricle catheter-derived variables.

95 red with placebo in patients with a systemic right ventricle caused by congenitally or surgically cor

96 physiological studies on cardiomyocytes from right ventricle demonstrated a shorter action potential

97 mutation embryos disrupted cardiac looping, right ventricle development, and ablated IKr activity at

98 The primary endpoint was right ventricle diameter at the third rhythm analysis: 3

99 This study aimed to compare right ventricle diameter during resuscitation from cardi

100 nography were able to detect a difference in right ventricle diameter of approximately 10 mm with a s

101 related (rho=0.378, P<.01) with the ratio of right ventricle diameter to left ventricle diameter (RV/

102 rd rhythm analysis during resuscitation, the right ventricle diameter was 32 mm (95% CI, 29-35) in th

103 The right ventricle diameter was measured.

104 During induction of cardiac arrest, the right ventricle dilated in all groups (p < 0.01 for all)

105 These findings indicate that right ventricle dilation may be inherent to cardiac arre

106 sinus diverticulum and one a right atrium to right ventricle diverticulum.

107 contributing to development of double outlet right ventricle (DORV) and ventricular septal defects (V

108 icular septal defect (VSD) and double-outlet right ventricle (DORV).

109 , and heart defects, including double-outlet right ventricle (DORV).

110 Dilation of the right ventricle during cardiac arrest and resuscitation

111 hat occur in the heart and in particular the right ventricle during WLS, and give an indication of th

112 ical studies have mostly focused on modeling right ventricle dysfunction or failure and pulmonary art

113 Preterm birth was associated with a small right ventricle (end diastolic volume, 79.8+/-13.2 versu

114 lume, 156+/-26 versus 172+/-28 mL, P<0.001), right ventricle (end-diastolic area=27.0+/-4.8 versus 28

115 Right ventricle enlargement and dysfunction were found i

116 ubstrate identification consisted in mapping right ventricle epicardial surface before and after flec

117 ada syndrome, AES is commonly located in the right ventricle epicardium and ajmaline exposes its exte

118 Extensive areas of AES were found in the right ventricle epicardium, which were wider in group 1

119 , including obliteration of the lumen of the right ventricle, excessive hyperplasia and apoptosis of

120 se in pulmonary arterial pressure leading to right ventricle failure caused sudden death.

121 However, right ventricle failure is a major predictor of outcomes

122 cord, with abnormal mucosa also seen in the right ventricle (Fig 1).

123 nfundibular pouch and in some regions of the right ventricle forming secondary pouches.

124 exercise group and control group (change in right ventricle free wall peak velocity E' exercise grou

125 in the differentiation of outflow tract and right ventricle from progenitors of the second heart fie

126 Analysis of a biopsy sample of the right ventricle from the proband showed markedly decreas

127 onary arterial hypertension and in lungs and right ventricles from rats exposed to hypoxia.

128 f circulating histones on left ventricle and right ventricle function at clinically relevant concentr

129 proposed to use these agents to support the right ventricle function in pulmonary hypertension.

130 lmonary arterial pressure and improvement of right ventricle function.

131 Patients with a systemic right ventricle had elevated BNP levels, and positive co

132 graphic assessment of diseases affecting the right ventricle has lagged behind that of the left ventr

133 eceptor blockers in patients with a systemic right ventricle has not been elucidated.

134 ion of the great arteries (TGA) and systemic right ventricles have premature congestive heart failure

135 (HR, 7.1; P=0.0043), single morphologically right ventricle (HR, 10.5; P=0.0429), and higher right a

136 ed, right ventricle pressures increased, and right ventricle hypertrophy and pulmonary changes occurr

137 the right ventricular systolic pressure and right ventricle hypertrophy.

138 ived to adulthood with spontaneous eccentric right ventricle hypertrophy.

139 Deletion of Hand2 in mice results in right ventricle hypoplasia and embryonic lethality.

140 y connection in 135 (51.7%); right atrium to right ventricle in 25 (9.6%); and total cavopulmonary co

141 ntified: 1) scars involving the subtricuspid right ventricle in 46 patients (group A); and 2) scars r

142 es that IUGR also leads to impairment of the right ventricle in addition to the left ventricle classi

143 explains the predominant involvement of the right ventricle in ARVC.

144 30 s) were created on the epicardium of the right ventricle in eight mongrel dogs.

145 derlying molecular mechanisms of the failing right ventricle in PAH?

146 urrently no approved therapies targeting the right ventricle in pulmonary hypertension.

147 tionated electrical activity recorded in the right ventricle in the setting of BrS.

148 e of structural differences between left and right ventricles in vulnerability to electric shocks in

149 w presents new insights into the role of the right ventricle independently and in conjunction with th

150 The native aortic root was excised from the right ventricle infundibulum and inserted into the left

151 3.65 m s(-1)) were identified in the left or right ventricle initially with mechanical stimulation an

152 on cardiovascular magnetic resonance at the right ventricle insertion site.

153 ar heart to give rise to the majority of the right ventricle, interventricular septum, and outflow tr

154 ysplasia/cardiomyopathy (ARVC), in which the right ventricle is "replaced" by fibrofatty tissue, resu

155 he great arteries, worsening of the systemic right ventricle is accompanied by clinical events such a

156 is study was to test the hypothesis that the right ventricle is more dilated during resuscitation fro

157 In pulmonary hypertension, the status of the right ventricle is one of the most important predictors

158 Factor images (right ventricle, left ventricle, and myocardium) were su

159 iables that differentiated these groups were right ventricle:left ventricle inflow angle, LV width/LV

160 The angle of right ventricle/LV inflow and other surrogates of inflow

161 ariable between the 3 cluster groups was the right ventricle:LV inflow angle (partial R(2)=0.86), def

162 The resultant increased work of the right ventricle may cause right heart failure and liver

163 Monophasic APs were recorded in the right ventricle (n = 62) and/or left ventricle (n = 9) a

164 dentified by micro-CT included double outlet right ventricle (n=36), transposition of the great arter

165 ified in the right atrium (n=25) than in the right ventricle (n=5).

166 rvival, yet eventual failure of the systemic right ventricle necessitates cardiac transplantation in

167 argeted to the right atrium, His bundle, and right ventricle of 10 mongrel dogs (23 to 32 kg) via a 1

168 atriuretic peptide B is also observed in the right ventricle of AC patients.

169 d, respectively, into the left ventricle and right ventricle of dogs to record endocardial activation

170 ygen consumption (MVO2) of the hypertrophied right ventricle of IPAH patients can be measured using P

171 s whether MVO2 can also be determined in the right ventricle of IPAH patients from the clearance of (

172 ilure may be defined as the inability of the right ventricle of the heart to provide adequate blood f

173 , which contributes to the outflow tract and right ventricle of the heart, is defined in part by expr

174 e cells contributed to the outflow tract and right ventricle of the heart.

175 yte diameters are significantly increased in right ventricles of AC patients.

176 entricular septal defects with double outlet right ventricle or overriding aorta.

177 tients, especially in patients with systemic right ventricles or single ventricle physiology.

178 m but not in left ventricular subepicardium, right ventricle, or noncardiac tissues from the same ani

179 At cardiac repair, a transannular patch for right ventricle outlet reconstruction was required in 44

180 malalignment defects including double-outlet right ventricle, overriding aorta and pulmonary stenosis

181 left ventricle, E12 values were lower in the right ventricle (P=0.037) and left ventricular outflow t

182 tract (P<0.001) and higher in left ventricle-right ventricle pairs (P=0.021) and left ventricular epi

183 eplacement of myocytes, predominantly in the right ventricle.Phenotypic expression of ARVC is variabl

184 Although structural abnormalities of the right ventricle predominate, it is well recognized that

185 laterals unifocalized, and higher postrepair right ventricle pressure.

186 equently, endothelin-1 production increased, right ventricle pressures increased, and right ventricle

187 logy, previous intracardiac repair, systemic right ventricle, pulmonary hypertension, pulmonary regur

188 The right ventricle-pulmonary artery (RVPA) shunt may improv

189 domized to modified Blalock-Taussig shunt or right ventricle-pulmonary artery shunt (RVPAS) found bet

190 the Norwood procedure (hazard ratio, 2.0 for right ventricle-pulmonary artery shunt versus modified B

191 ure to a modified Blalock-Taussig shunt or a right ventricle-pulmonary artery shunt.

192 H is determined largely by the status of the right ventricle, rather than the levels of pulmonary art

193 unctional consequences on left ventricle and right ventricle remain unclear.

194 function is dependent on LV health, the IUGR right ventricle remains poorly studied.

195 ental arrest and latent myopathy of left and right ventricles, respectively.

196 In contrast, the right ventricle responds to endurance training with ecce

197 croarray-based gene ontology analysis of the right ventricle revealed that a number of MCT-altered ge

198 These patients had mildly dilated right ventricles (right ventricular end-diastolic volume

199 e English language by using the search words right ventricle, right ventricular failure, pulmonary hy

200 [IQR: 14.4 to 103.8 pmol/l]) and a systemic right ventricle (RV) (31.1 pmol/l [IQR: 21.8 to 56.0 pmo

201 These patients have a systemic right ventricle (RV) and are at risk of arrhythmia, prem

202 The geometry of the right ventricle (RV) and left ventricle (LV) may alter t

203 bowing (VSB), ratio between the diameters of right ventricle (RV) and left ventricle (LV), and emboli

204 uencies (DFs) during MVT were similar in the right ventricle (RV) and left ventricle (LV).

205 T, and was associated with distension of the right ventricle (RV) and reduced cardiac output.

206 intervals and activation timings across the right ventricle (RV) body, outflow tract (RVOT), and lef

207 Outcomes after right ventricle (RV) decompression in infants with pulmo

208 enetic protein receptor type 2 (BMPR2) gene, right ventricle (RV) dysfunction is associated with RV l

209 t with digoxin attenuated the development of right ventricle (RV) hypertrophy and prevented the pulmo

210 It has been shown that right ventricle (RV) hypertrophy involves significant co

211 The systemic right ventricle (RV) in HLHS is subject to significant c

212 te the recognition of a critical role of the right ventricle (RV) in many aspects of cardiovascular m

213 less, gradual dysfunction and failure of the right ventricle (RV) in the systemic circulation remain

214 herosclerosis) performed cMRIs with complete right ventricle (RV) interpretation on 4,062 participant

215 However, the management of the borderline right ventricle (RV) is controversial, and there may be

216 The right ventricle (RV) is of lesser importance in acquired

217 The right ventricle (RV) is the major determinant of functio

218 have been identified at early stages in the right ventricle (RV) of infants with HLHS, although the

219 n) performed, which leaves the morphological right ventricle (RV) supporting the systemic circulation

220 The ability of the right ventricle (RV) to adapt to hypoxia in children wit

221 ere is minimal data on the adaptation of the right ventricle (RV) to pressure and volume overload and

222 Right ventricle (RV) to pulmonary artery (PA) conduits a

223 1.67+/-6.03 mmHg, P<0.01), an attenuation of right ventricle (RV) to whole heart (WH) wt ratios (0.22

224 Speckle-derived strain of the right ventricle (RV) was utilized to detect occult abnor

225 d along 4 anatomic axes: left ventricle (LV)-right ventricle (RV), LV:apico-basal, LV:anterior-poster

226 ng left ventricular pacing varies within the right ventricle (RV).

227 volumes for the left ventricle (LV) and the right ventricle (RV).

228 rly myocardium of the outflow tract (OT) and right ventricle (RV).

229 w tract (OFT), LV, atrium and SV but not the right ventricle (RV).

230 y showed a filling defect at the apex of the right ventricle (RV).

231 dilation, with consequent compression of the right ventricle (RV); hydrops and low cardiac output are

232 evels (P < .001), larger left (P = .023) and right ventricles (RV; P = .002), and worse RV function (

233 n (SVR) trial randomized infants with single right ventricles (RVs) undergoing a Norwood procedure to

234 ay ventricular septal defects, double outlet right ventricle, semilunar valve hyperplasia and aortic

235 Studies of longitudinal axis function of the right ventricle show that contractile function improveme

236 f SSFP and TSE BB images of the left and the right ventricles showed a significant improvement with r

237 s increasingly shifted opinion away from the right ventricle shunt as a 'cause' of improved results.

238 The survival of the right ventricle shunt group is slightly higher at 3 year

239 , identifying this as a marker of a systemic right ventricle (SRV) that may most tolerate (and possib

240 great arteries (TGA) patients with systemic right ventricles (SRVs).

241 omyopathy phenotype, involving both left and right ventricles, suggesting that loss of the VIP gene o

242 ategies based on staged procedures, with the right ventricle supporting both systemic and pulmonary c

243 d with LV outflow tract obstruction loss and right ventricle systolic impairment.

244 The changes are greater in the right ventricle than previously observed in the left ven

245 ventricle exerts biomechanical stress on the right ventricle that can progress into heart failure.

246 xpression of structural abnormalities in the right ventricle that may have genetic, infective, or inf

247 ndary at the future junction of the left and right ventricles that arises prior to morphogenesis.

248 ontain a rudimentary outflow tract but not a right ventricle, the existence and function of SHF-like

249 d upregulation of Gremlin 1 mRNA in lung and right ventricle tissue compared with normoxic controls.

250 trum of septation defects from double outlet right ventricle to common arterial trunk in mutants.

251 he native positive inotropic response of the right ventricle to increased afterload.

252 The median right ventricle to left ventricle diameter ratio was 1.3

253 l have been demonstrated with the use of the right ventricle to pulmonary artery (RV-PA) conduit comp

254 The use of a right ventricle to pulmonary artery (RV-PA) conduit in t

255 lody TPVR within the Contegra conduit in the right ventricle to pulmonary artery position.

256 the modified Blalock-Taussig shunt (MBTS) or right ventricle to pulmonary artery shunt (RVPAS).

257 h to the Norwood procedure, which utilizes a right ventricle to pulmonary artery shunt or Sano modifi

258 allot is determined by the adaptation of the right ventricle to the physiological sequelae of the rig

259 tern of LGE localized at the junction of the right ventricle to the septum was respectively observed

260 Angioplasty and stent placement in right ventricle-to-pulmonary artery (RV-PA) conduits hav

261 The optimal treatment for dysfunctional right ventricle-to-pulmonary artery (RV-PA) conduits is

262 Eligible patients with dysfunctional right ventricle-to-pulmonary artery conduits were screen

263 and effective in patients with dysfunctional right ventricle-to-pulmonary artery conduits.

264 Following Melody valve implant, the peak right ventricle-to-pulmonary artery gradient decreased f

265 al was better for the Norwood procedure with right ventricle-to-pulmonary artery shunt (RVPAS) compar

266 hybrid palliation (Blalock-Tausig shunt 591, right ventricle-to-pulmonary artery shunt 640, and hybri

267 nificant change is a renewed interest in the right ventricle-to-pulmonary artery shunt as the source

268 odel, whereas a 5-mm conduit was used in the right ventricle-to-pulmonary artery shunt model.

269 operation with a modified Blalock-Tausig or right ventricle-to-pulmonary artery shunt.

270 e with modified Blalock-Taussig shunt versus right-ventricle-to-pulmonary-artery shunt, 14-month neur

271 omparing outcomes in 549 infants with single right ventricle undergoing a Norwood procedure randomize

272 SVR) trial randomized subjects with a single right ventricle undergoing a Norwood procedure to a modi

273 fatty-fibrous myocardial replacement of the right ventricle, ventricular arrhythmias, and right vent

274 ited cardiac defects including double-outlet right ventricle, ventricular septal defect (VSD), atriov

275 ld (SHF) led to trabeculation defects in the right ventricle, ventricular septal defect, persistent t

276 heart deformations, including double outlet right ventricle, ventricular-septal defects, and pericar

277 ds for better image quality were greater for right ventricle versus left ventricle (odds ratio, 1.8;

278 in the relative numbers of BMD cells in the right ventricle wall as compared with the left ventricle

279 In the mouse studies, both the left and right ventricle walls were clearly observable, as were t

280 The right ventricle was dilated during resuscitation from ca

281 However, the right ventricle was dilated, irrespective of the cause o

282 ing groups at the third rhythm analysis, the right ventricle was larger for hypovolemia than for prim

283 The right ventricle was more dilated during resuscitation wh

284 canine model, a full thickness defect in the right ventricle was repaired with either Dacron or ECM.

285 drogenase activity, left ventricular weight, right ventricle weight, and left ventricular mass after

286 Intact rat trabeculae from the right ventricle were mounted between a force transducer

287 cines and full-volume 3DTTE data sets of the right ventricle were used to measure end-diastolic volum

288 Some of the BMD cells in the right ventricle were vascular cells and cardiomyocytes.

289 e significantly reduced the size of left and right ventricles, whereas that of DN-Lats2 caused hypert

290 er exercise training might injure a systemic right ventricle which is loaded with every heartbeat.

291 y, it had multiple beneficial effects on the right ventricle, which included suppression of pathologi

292 and cardiomyocyte loss predominantly in the right ventricle, which is associated with life-threateni

293 nt state of three-dimensional imaging of the right ventricle will be highlighted along with the chall

294 highly penetrant phenotype of double outlet right ventricle with a concurrent ventricular septal def

295 3.86 m s(-1)) were identified in the left or right ventricle with a stimulating electrode.

296 We examined the right ventricle with cardiac magnetic resonance imaging

297 (RCM) is characterized by nondilated left or right ventricle with diastolic dysfunction.

298 maker that is nonsurgically implanted in the right ventricle with the use of a catheter.

299 rdium versus subendocardium in both left and right ventricles, with lower levels in Hey2(+/-) mice co

300 h block had delayed activation in the entire right ventricle, without ST-segment elevation, fractiona