ライフサイエンスコーパス: ventricular dysfunction

1 clophosphamide are both associated with left ventricular dysfunction.

2 valve regurgitation, pulmonary and systemic ventricular dysfunction.

3 to expected haemodynamic sequelae from left ventricular dysfunction.

4 ith pulmonary embolism and evidence of right ventricular dysfunction.

5 mechanics may help in the early diagnosis of ventricular dysfunction.

6 leads to excessive dilatative remodeling and ventricular dysfunction.

7 ary pulmonary hypertension secondary to left ventricular dysfunction.

8 to mediate the myocardial fibrosis and left ventricular dysfunction.

9 compared in patients with and without right ventricular dysfunction.

10 es myocardial fibrosis and improves the left ventricular dysfunction.

11 coronary artery disease and significant left ventricular dysfunction.

12 t), and only 5.1% of patients had mild right ventricular dysfunction.

13 lmonary microvasculature culminated in right ventricular dysfunction.

14 y low 30-day mortality in patients with left ventricular dysfunction.

15 and heart failure (HF) in patients with left ventricular dysfunction.

16 rovokes left ventricular remodeling and left ventricular dysfunction.

17 c indicators of worse hemodynamics and right ventricular dysfunction.

18 ertrophy-related signal activation, and left ventricular dysfunction.

19 elevated pulmonary blood pressures and right ventricular dysfunction.

20 and possibly contributing to, diastolic left ventricular dysfunction.

21 and from acute myocardial damage to chronic ventricular dysfunction.

22 who are hemodynamically stable without right ventricular dysfunction.

23 tion beyond clinical data and degree of left ventricular dysfunction.

24 e syndromes, or they can be chronic, such as ventricular dysfunction.

25 ical therapy for patients with ischemic left ventricular dysfunction.

26 les of cardiac fibroblasts in remodeling and ventricular dysfunction.

27 se of old age, comorbidities, or severe left ventricular dysfunction.

28 to persistent AF, with no evidence for left ventricular dysfunction.

29 amilial cardiomyopathy, and severity of left ventricular dysfunction.

30 ly after cardiac procedures in patients with ventricular dysfunction.

31 olution to heart failure or symptomatic left ventricular dysfunction.

32 lmonary hypertension caused by systolic left ventricular dysfunction.

33 velop significant myocardial injury and left ventricular dysfunction.

34 de (O55B5, 10 mg/kg), inducing systolic left ventricular dysfunction.

35 an attenuate age-dependent induction of left ventricular dysfunction.

36 re, pneumonia, atrial fibrillation, and left ventricular dysfunction.

37 ing (MRI) tagging before the onset of global ventricular dysfunction.

38 ted with Vcl deficiency, before the onset of ventricular dysfunction.

39 vents are associated with the development of ventricular dysfunction.

40 less myocardial salvage, and more pronounced ventricular dysfunction.

41 n cardiomyocytes, metabolic alterations, and ventricular dysfunction.

42 resistive, load and may contribute to right ventricular dysfunction.

43 n sensitize the heart to ischemic injury and ventricular dysfunction.

44 fficacy of TAVI in patients with severe left ventricular dysfunction.

45 ailure patients across the continuum of left ventricular dysfunction.

46 LVEF, independent from the severity of left ventricular dysfunction.

47 ave a high likelihood of developing systemic ventricular dysfunction.

48 ion, and 5 with incessant VA associated with ventricular dysfunction.

49 and ICD therapy in patients with severe left ventricular dysfunction.

50 s in the myocardium and correlates with left ventricular dysfunction.

51 DLST are important metabolic players in left ventricular dysfunction.

52 dial infarction characterized by severe left ventricular dysfunction.

53 s 31%, and 60% had moderate or greater right ventricular dysfunction.

54 de progressive heart failure and severe left ventricular dysfunction.

55 n zebrafish embryos caused cardiac edema and ventricular dysfunction.

56 intracoronary route in 17 patients with left ventricular dysfunction 1.5 to 3 months after myocardial

57 .6-3.9]), septic shock (2.7 [1.5-4.8]), left ventricular dysfunction (2.7 [1.6-5.0]), administration

58 y chain 6, in 2 patients who developed right ventricular dysfunction 3 to 11 years postoperatively.

59 pe (5/26 [19%] versus 3/73 [4%]; P=0.02) and ventricular dysfunction (6/26 [23%] versus 4/73 [6%]; P=

60 were older and had higher prevalence of left ventricular dysfunction (67% versus 13% of fascicular VA

61 Ventricular dysfunction adversely affects transplant-fre

62 The mechanism responsible for left ventricular dysfunction after cardiac surgery is only pa

63 ondary mitral regurgitation (MR) due to left ventricular dysfunction, also known as functional MR, is

64 Asymptomatic left ventricular dysfunction (ALVD) is present in 3-6% of the

65 lines are at high risk for asymptomatic left ventricular dysfunction (ALVD), subsequent heart failure

66 gic receptor (betaAR) polymorphisms and left ventricular dysfunction-an important cause of allograft

67 ization therapy in patients with severe left ventricular dysfunction and a QRS duration <120 millisec

68 er imaging techniques are required to assess ventricular dysfunction and adverse myocardial remodelli

69 inical assessment alone for identifying left ventricular dysfunction and aortic or mitral valve disea

70 xample, whereas uninsured patients with left ventricular dysfunction and CAD were less likely to rece

71 therapy agents with the development of left ventricular dysfunction and cardiomyopathy, is an issue

72 regurgitation is frequently associated with ventricular dysfunction and carries a high mortality.

73 Right ventricular dysfunction and congestive states may contri

74 ommon in many lung diseases leading to right ventricular dysfunction and death.

75 tachycardia (FAT), if untreated, can lead to ventricular dysfunction and heart failure (tachycardia-i

76 ardial infarction (AMI) with subsequent left ventricular dysfunction and heart failure continues to b

77 the peripartum period and is marked by left ventricular dysfunction and heart failure.

78 ideration of discontinuing asymptomatic left ventricular dysfunction and HF screening in low-risk sur

79 ISO-induced left ventricular dysfunction and hypertrophic remodeling, inc

80 lmonary hypertension caused by systolic left ventricular dysfunction and improved cardiac index and p

81 in nonimmunosuppressed rats ameliorates left ventricular dysfunction and improves remodeling via favo

82 to further explore the significance of right ventricular dysfunction and investigate potential explan

83 rome (TTS) is characterized by an acute left ventricular dysfunction and is associated with life-thre

84 t data demonstrate promising effects on left ventricular dysfunction and left ventricular ejection fr

85 n in the heart is sufficient to provoke left ventricular dysfunction and left ventricular remodeling.

86 omatic high-risk patients with ischemic left ventricular dysfunction and multivessel coronary artery

87 latory ventilation+15, 15 patients had right ventricular dysfunction and nine had right ventricular f

88 ent left ventricular apical ballooning, left ventricular dysfunction and normal or near-normal corona

89 ate the association between early, postnatal ventricular dysfunction and outcome among infants with C

90 diastolic dysfunction grade II or III, right ventricular dysfunction and pericardial effusions.

91 asma levels of MBG are associated with right ventricular dysfunction and predict worse long-term clin

92 Treatment with losartan reduced left ventricular dysfunction and prevented increased extracel

93 d not have these comorbidities, whereas left ventricular dysfunction and prior cardiac operation were

94 In the Cox proportional hazards model, right ventricular dysfunction and pulmonary hypertension were

95 es mellitus, a positive troponin assay, left-ventricular dysfunction and regional wall motion abnorma

96 et therapeutic approach also attenuated left ventricular dysfunction and remodeling post-MI (left ven

97 tive strategy attenuated development of left ventricular dysfunction and remodeling post-transverse a

98 al function was associated with reduced left ventricular dysfunction and remodeling, as well as incre

99 diameter ratio on CT as indicators of right ventricular dysfunction and reported that recurrent veno

100 rative echocardiography, in particular right ventricular dysfunction and restrictive left ventricular

101 ed the interferon response and improved left ventricular dysfunction and survival.

102 PARR-2 randomized patients with severe left ventricular dysfunction and suspected CAD being consider

103 ter a 5-year follow-up in patients with left ventricular dysfunction and suspected CAD, overall, PET-

104 stand longitudinal differences in interstage ventricular dysfunction and their subsequent impact on t

105 cement (LGE), is associated to a progressive ventricular dysfunction and worse prognosis.

106 Severe ventricular dysfunction and/or pulmonary hypertension ma

107 ith compound heterozygosity (3 with systolic ventricular dysfunction), and 4 with MYH6-FLNC synergist

108 ts with stable coronary artery disease, left ventricular dysfunction, and a heart rate of 70 beats pe

109 ly effective anticancer drug but cause acute ventricular dysfunction, and also induce late-onset card

110 with large acute myocardial infarction, left ventricular dysfunction, and at high risk of developing

111 rk Heart Association functional class, right ventricular dysfunction, and atrial fibrillation (HR: 0.

112 Interstage transplant-free survival, ventricular dysfunction, and AVVR were equivalent among

113 f the AMI, older age, lower hemoglobin, left ventricular dysfunction, and chronic heart failure.

114 re resistant to the cardiac remodeling, left ventricular dysfunction, and early death observed in the

115 diac fibroblasts leads to fibrogenesis, left ventricular dysfunction, and excessive scarring in the i

116 diac fibroblasts leads to fibrogenesis, left ventricular dysfunction, and excessive scarring in the i

117 eft ventricular ejection fraction<50%, right ventricular dysfunction, and heart rate/respiratory rate

118 ciated with increased CACS, subclinical left ventricular dysfunction, and increased pulse pressure.

119 ure, accentuates post-MI remodeling and left ventricular dysfunction, and increases the progression t

120 ients with mild heart-failure symptoms, left ventricular dysfunction, and left bundle-branch block, e

121 intolerance, atrial tachyarrhythmias, right ventricular dysfunction, and pulmonary hypertension incr

122 udies had fewer comorbidities, had less left ventricular dysfunction, and received more inappropriate

123 re beneficial in patients with acquired left ventricular dysfunction, and recent findings have sugges

124 ts in 14 centers for cardiogenic shock, left ventricular dysfunction, and severe inflammatory state.

125 and sudden deaths, conduction defects, left ventricular dysfunction, and supraventricular arrhythmia

126 h history of ventricular tachycardia or left ventricular dysfunction appear to be associated with a h

127 mechanisms contributing to progressive left ventricular dysfunction are matched by stem cell activit

128 Patients with ventricular dysfunction as a consequence of FAT were not

129 e significant univariable predictors of left ventricular dysfunction as assessed by an ejection fract

130 8 patients with pulmonary embolism had right ventricular dysfunction, as assessed by measurement of N

131 ; 95% confidence interval, 1.59-5.49), right ventricular dysfunction, as evidenced by fractional area

132 modynamic instability, newly recognized left ventricular dysfunction, as well as imaging during the s

133 hat re-examine this in patients without left ventricular dysfunction, as well as in patients with sta

134 as associated with oxidative stress and left ventricular dysfunction assessed by electron spin resona

135 e excess risk for CHF, and asymptomatic left ventricular dysfunction asymptomatic period.

136 observed in patients without transient left ventricular dysfunction at H24.

137 Circulatory failure, ventricular dysfunction, atrioventricular valve regurgit

138 ning of dietary fatty acids (DFAs) with left ventricular dysfunction, both of which are improved by m

139 y documented coronary artery disease or left ventricular dysfunction, but blacks had more prevalent c

140 Right ventricular dysfunction, but not functional RV hypertrop

141 and KCNQ1OT1 improved the prediction of left ventricular dysfunction by a model, including demographi

142 ductive nature of scar tissue contributes to ventricular dysfunction by electrically uncoupling viabl

143 ere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction (CADUCEUS) trial revealed that c

144 ere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction (CADUCEUS) trial, we enrolled pa

145 ere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction [CADUCEUS]; NCT00893360).

146 Increased LGE burden and right ventricular dysfunction can identify LGE+ patients at hi

147 B ablation decreases the progression of left ventricular dysfunction, cardiac remodeling, and arrhyth

148 uding guideline-directed medication for left ventricular dysfunction, cardiac resynchronization thera

149 Most importantly, we show that ventricular dysfunction caused by chronic hyper-aldoster

150 Thus, in rats with left ventricular dysfunction, chronic RMH pacing improved car

151 s) experienced more transient and persistent ventricular dysfunction compared to those without advers

152 e interval, 3.3 to 5.0) of developing future ventricular dysfunction compared with those with a negat

153 Cardiac manifestations are common, including ventricular dysfunction, coronary artery dilation and an

154 decreased interstitial fibrosis, ameliorated ventricular dysfunction, decreased cardiac hypertrophy,

155 nal neural network to identify patients with ventricular dysfunction, defined as ejection fraction <=

156 ed in 16 patients (8%) and 37 (16%) had left ventricular dysfunction, defined as left ventricular eje

157 nd a deterioration of exercise tolerance and ventricular dysfunction did not predict mortality.

158 ith atrial remodeling in the context of left ventricular dysfunction due to myocardial infarction: my

159 sitagliptin protected against ischemic left ventricular dysfunction during dobutamine stress in pati

160 to investigate the underlying mechanisms of ventricular dysfunction during HF.

161 ients (age 64 +/- 10 years, n = 13 with left ventricular dysfunction) during ablation procedures for

162 t successful stenting for STEMI and had left ventricular dysfunction (ejection fraction</=48%) >/=4 d

163 t successful stenting for STEMI and had left ventricular dysfunction (ejection fraction</=48%) >/=4 d

164 s of CAD; late risk reflected diastolic left ventricular dysfunction expressed as ventricular hypertr

165 om donor mice with HF induced long-term left ventricular dysfunction, fibrosis, and hypertrophy in na

166 can induce cardiac repair and attenuate left ventricular dysfunction from both within and outside the

167 with RVP among patients without severe left ventricular dysfunction (>35%) who required permanent pa

168 sis (AS), but the prognostic impact of right ventricular dysfunction has not been well studied.

169 t failure (HF) subtended by progressive left ventricular dysfunction has received limited attention.

170 Patients with ischemic left ventricular dysfunction have higher operative risk with

171 lammatory cardiomyopathy complicated by left ventricular dysfunction, heart failure or arrhythmia is

172 multidisciplinary heart team to prevent left ventricular dysfunction, heart failure, reduced quality

173 by an experienced heart team to prevent left ventricular dysfunction, heart failure, reduced quality

174 echocardiography detects early signs of left ventricular dysfunction; however, it is unknown whether

175 95% CI, 2.3-27.1; P=0.001) and subpulmonary ventricular dysfunction (HR, 3.0; 95% CI, 1.2-12.6; P=0.

176 Left ventricular dysfunction improved significantly during fo

177 mproves survival, and, in patients with left ventricular dysfunction, improves systolic function.

178 in 12 patients (14%), and asymptomatic left ventricular dysfunction in 4 patients (5%).

179 nfarct expansion, troponin release, and left ventricular dysfunction in a swine myocardial infarction

180 irected echocardiography in diagnosing right ventricular dysfunction in acute pulmonary embolism.

181 ivists' interpretations for evaluating right ventricular dysfunction in acute pulmonary embolism.

182 ased pulmonary vascular resistance and right ventricular dysfunction in both HF phenotypes.

183 d reduce MG-induced inflammation and prevent ventricular dysfunction in diabetes.

184 of hypoplastic left heart with latent right ventricular dysfunction in individuals with a Fontan cir

185 e to exercise, may serve as a marker of left ventricular dysfunction in OHT patients.

186 ional status and to delay the progression of ventricular dysfunction in patients who are not suitable

187 for ventricular dysfunction or exacerbating ventricular dysfunction in patients with existing cardio

188 vealed hypertrophic cardiomyopathy with left ventricular dysfunction in SKO mice, and these two abnor

189 The REDEFINE trial (Right Ventricular Dysfunction in Tetralogy of Fallot: Inhibiti

190 gal nerve stimulation (VNS) can improve left ventricular dysfunction in the setting of heart failure

191 and assess the presence of longitudinal left ventricular dysfunction in these patients.

192 The diagnosis of ventricular dysfunction in TM patients differs from that

193 ocytes provoked cardiac hypertrophy and left ventricular dysfunction in vivo, whereas genetic knockdo

194 phy, dilated cardiomyopathy, and severe left ventricular dysfunction, including a marked reduction in

195 61+/-7 and 61+/-7 mm, P<0.0001), more right ventricular dysfunction, increased epicardial fat thickn

196 Left ventricular dysfunction is a known predictor of ventricu

197 Acute left ventricular dysfunction is a major complication of cardi

198 Right ventricular dysfunction is a powerful determinant of pro

199 Right ventricular dysfunction is an important and independent

200 In patients with pulmonary embolism, right ventricular dysfunction is associated with early mortali

201 cuspid regurgitation in the setting of right ventricular dysfunction is associated with poor prognosi

202 lmonary hypertension caused by systolic left ventricular dysfunction is associated with significant m

203 ary embolism using imaging presence of right ventricular dysfunction is essential for triage; however

204 tentially reversible condition in which left ventricular dysfunction is induced or mediated by atrial

205 b PET is associated with more extensive left ventricular dysfunction, ischemic compromise, and reduce

206 Patients with severe left ventricular dysfunction, ischemic heart failure, and cor

207 procedure, even in patients with severe left ventricular dysfunction, leading to a high procedural su

208 tion, and echocardiographic evidence of left ventricular dysfunction (left ventricle ejection fractio

209 ation (TIME) enrolled 120 patients with left ventricular dysfunction (left ventricular ejection fract

210 y of clinical assessment for diagnosing left ventricular dysfunction (left ventricular ejection fract

211 nary arterial pressure and resistance, right ventricular dysfunction, left ventricular compression, a

212 cular wall motion abnormalities, global left ventricular dysfunction, left ventricular diastolic dysf

213 d wild-type (WT) mice manifested severe left ventricular dysfunction, loss of heart and body mass, al

214 potential negative interaction between left ventricular dysfunction (LVD) and MSC activation.

215 To prevent left ventricular dysfunction (LVD), surgery is recommended in

216 At baseline, left ventricular dysfunction (LVEF<50%) and left atrium enlar

217 We have learned that right ventricular dysfunction may be a predictor of survival b

218 of severe heart failure symptoms (66%), left ventricular dysfunction (mean ejection fraction 46.4 +/-

219 Left ventricular dysfunction, mediated by ventricular interde

220 Right ventricular dysfunction, moderate-severe tricuspid regur

221 Radiographically, significant left ventricular dysfunction, myocardial delayed enhancement

222 ade atrioventricular block, significant left ventricular dysfunction, myocardial delayed enhancement

223 nd 1 with pulmonary regurgitation), or right ventricular dysfunction (n=2).

224 ion Window Programming in Patients With Left Ventricular Dysfunction, Non-ischemic Etiology in Primar

225 male sex, hypertension, valve disease, left ventricular dysfunction, obesity, and alcohol consumptio

226 e oxygenation (P < 0.005).Conclusions: Early ventricular dysfunction occurs frequently in CDH and is

227 ng that AVR should be discussed before right ventricular dysfunction occurs in severe AS.

228 Left ventricular dysfunction often precedes symptoms, needing

229 rdiac troponin elevation or new or worsening ventricular dysfunction on echocardiography and confirme

230 Eligible patients had right ventricular dysfunction on echocardiography or computed

231 ass, use of multiple inotropes, severe right ventricular dysfunction on echocardiography, ratio of ri

232 atients demonstrated moderate or severe left ventricular dysfunction on initial echocardiogram (80%)

233 ventricular dysfunction only (RV(dys)), left ventricular dysfunction only (LV(dys)), and combined RV

234 hierarchical groups: normal function, right ventricular dysfunction only (RV(dys)), left ventricular

235 gies were not identified as risk factors for ventricular dysfunction or AVVR.

236 MC describes AF either as the sole cause for ventricular dysfunction or exacerbating ventricular dysf

237 heir clinical value in predicting subsequent ventricular dysfunction or heart failure has not been ex

238 n Heart Association class I indication (left ventricular dysfunction or medical history of heart fail

239 For patients with left ventricular dysfunction or myocardial infarction, advanc

240 holds are the most useful for discriminating ventricular dysfunction or outcome.

241 therapies being options for those with right ventricular dysfunction or unstable hemodynamics.

242 te and to understand the reason for the left ventricular dysfunction or when there is a suspicion of

243 4; P=0.034), moderate to severe subpulmonary ventricular dysfunction (OR, 3.4; 95% CI, 1.1-10.2; P=0.

244 5-7.9; P=0.004), moderate to severe systemic ventricular dysfunction (OR, 3.4; 95% CI, 1.1-10.4; P=0.

245 of evidence of coronary artery disease, left ventricular dysfunction, or evident repolarization syndr

246 can present as acute coronary syndrome, left ventricular dysfunction, or potentially sudden cardiac d

247 cular comorbidities, renal dysfunction, left ventricular dysfunction, or significant coronary stenosi

248 MI resulted in greater left ventricular dysfunction (P<0.05), LA pressure (P<0.0003)

249 P<0.01), pulmonary hypertension and/or right ventricular dysfunction (P=0.01), and regional wall moti

250 brillators in patients with more severe left ventricular dysfunction particularly of ischemic etiolog

251 secutive series of patients with severe left ventricular dysfunction, pLVAD-supported scar VT ablatio

252 and potential efficacy in patients with left ventricular dysfunction post STEMI who are at risk for d

253 intracoronary infusion in patients with left ventricular dysfunction post STEMI.

254 -third of young patients presented with left ventricular dysfunction post-MI.

255 pressure profile to the low flow with right ventricular dysfunction profile.

256 tly higher in patients with HF-PH with right ventricular dysfunction, pulmonary vascular remodeling w

257 ization Reverses Remodeling in Systolic Left Ventricular Dysfunction], RAFT (Resynchronization-Defibr

258 6), seven males, none with a history of left ventricular dysfunction, received venoarterial extracorp

259 s I triggers (heart failure symptoms or left ventricular dysfunction) remains controversial in part d

260 patients with and without a history of left ventricular dysfunction resulting from KD-associated myo

261 ization reVErses Remodeling in Systolic left vEntricular dysfunction (REVERSE) study were evaluated i

262 ization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE) was a multicenter rand

263 ization reVErses Remodeling in Systolic left vEntricular dysfunction (REVERSE) was a multicenter, ran

264 GE (14+/-11 versus 5+/-5%, P<0.01) and right ventricular dysfunction (right ventricular EF 45+/-12 ve

265 four important abnormalities: asystole, left ventricular dysfunction, right ventricular dilation and

266 h clinically manifest CS, the extent of left ventricular dysfunction seems to be the most important p

267 (SCM) is a peculiar form of reversible left ventricular dysfunction seen predominantly in women and

268 rtery vasculature damage (Stage 3) and right ventricular dysfunction (Stage 4).

269 a 60-year-old woman with acute PE and right ventricular dysfunction (submassive PE), illustrates the

270 ssociated with impaired functional class and ventricular dysfunction suggesting chronic maladaptive p

271 sed pulmonary vascular resistance, and right ventricular dysfunction that promotes heart failure.

272 In patients without ventricular dysfunction, those with a positive AI screen

273 e who were hemodynamically stable with right ventricular dysfunction, thrombolytic therapy was associ

274 in animal models of myocardial ischemia and ventricular dysfunction through incompletely characteriz

275 ere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction) trial.

276 Screening for right ventricular dysfunction using goal-directed echocardiogr

277 -time corrected by heart rate (QTc) and left-ventricular dysfunction was also registered.

278 history of ventricular tachycardia and left ventricular dysfunction was associated with higher risk

279 d to an ischaemia-reperfusion protocol, left ventricular dysfunction was associated with uncoupling o

280 Postischemic left ventricular dysfunction was created by repetitive left c

281 Ventricular dysfunction was defined using left ventricul

282 NP value was elevated (910 pg/mL), and right ventricular dysfunction was moderate/severe in 55% of pa

283 No right ventricular dysfunction was observed.

284 Left ventricular dysfunction was present in 21.5% of patients

285 improvement was greatest when segmental left ventricular dysfunction was severe.

286 Ventricular dysfunction was significantly associated wit

287 (VT) or nonsustained VA with associated left ventricular dysfunction were enrolled at 3 centers.

288 ary vascular resistance (PVR) >4 WU or right ventricular dysfunction were excluded.

289 lmonary hypertension caused by systolic left ventricular dysfunction were randomized to double-blind

290 n more than 7 days, and severe systolic left ventricular dysfunction were stronger predictors of extu

291 ineffective cough, and severe systolic left ventricular dysfunction were the three independent facto

292 ties, left ventricular hypertrophy, and left ventricular dysfunctions were demonstrated in Group OSAH

293 ties and pulmonary hypertension and/or right ventricular dysfunction, were independently associated w

294 nerally a normal coronary angiogram and left ventricular dysfunction, which extends beyond the territ

295 he risk stratification of patients with left ventricular dysfunction who are ICD candidates, it does

296 the most severe coronary artery disease and ventricular dysfunction who derive the greatest clinical

297 sociation (NYHA) class III or IV HF and left ventricular dysfunction who were randomized to spironola

298 patients with ischemic cardiomyopathy (left ventricular dysfunction with >70% stenosis in >/=1 epica

299 lready-established myocardial remodeling and ventricular dysfunction, with few available pharmacologi

300 ts experienced some degree of segmental left ventricular dysfunction, with severity proportional to u