ライフサイエンスコーパス: ventricular dysfunction

1 otensin-converting enzyme inhibitor for left ventricular dysfunction).

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

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

4 elevated pulmonary blood pressures and right ventricular dysfunction.

5 DLST are important metabolic players in left ventricular dysfunction.

6 and possibly contributing to, diastolic left ventricular dysfunction.

7 who are hemodynamically stable without right ventricular dysfunction.

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

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

10 ical therapy for patients with ischemic left ventricular dysfunction.

11 les of cardiac fibroblasts in remodeling and ventricular dysfunction.

12 dial infarction characterized by severe left ventricular dysfunction.

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

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

15 amilial cardiomyopathy, and severity of left ventricular dysfunction.

16 ly after cardiac procedures in patients with ventricular dysfunction.

17 olution to heart failure or symptomatic left ventricular dysfunction.

18 lmonary hypertension caused by systolic left ventricular dysfunction.

19 velop significant myocardial injury and left ventricular dysfunction.

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

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

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

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

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

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

26 vents are associated with the development of ventricular dysfunction.

27 less myocardial salvage, and more pronounced ventricular dysfunction.

28 de progressive heart failure and severe left ventricular dysfunction.

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

30 n zebrafish embryos caused cardiac edema and ventricular dysfunction.

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

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

33 ailure patients across the continuum of left ventricular dysfunction.

34 11 patients who developed grade 2 or 3 left ventricular dysfunction.

35 of these structures despite persistent left ventricular dysfunction.

36 n heart failure across the continuum of left ventricular dysfunction.

37 o sensitize the heart to ischemic insult and ventricular dysfunction.

38 accelerating adverse cardiac remodeling and ventricular dysfunction.

39 nafil treatment ameliorated DOX-induced left ventricular dysfunction.

40 , adverse remodeling, chronic apoptosis, and ventricular dysfunction.

41 oration of HF in patients with systolic left ventricular dysfunction.

42 e death, adverse ventricular remodeling, and ventricular dysfunction.

43 cing with abnormal substrate predisposing to ventricular dysfunction.

44 ricular ejection fraction, and regional left ventricular dysfunction.

45 idative stress, which may contribute to left ventricular dysfunction.

46 presence of coronary artery disease and left ventricular dysfunction.

47 uration, and heart failure in the setting of ventricular dysfunction.

48 p is linear with respect to severity of left ventricular dysfunction.

49 anagement of diseases that are precursors to ventricular dysfunction.

50 with stable coronary artery disease and left-ventricular dysfunction.

51 All had significant right ventricular dysfunction.

52 -1alpha can worsen systolic overload induced ventricular dysfunction.

53 valve regurgitation, pulmonary and systemic ventricular dysfunction.

54 to expected haemodynamic sequelae from left ventricular dysfunction.

55 ith pulmonary embolism and evidence of right ventricular dysfunction.

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

57 leads to excessive dilatative remodeling and ventricular dysfunction.

58 ary pulmonary hypertension secondary to left ventricular dysfunction.

59 to mediate the myocardial fibrosis and left ventricular dysfunction.

60 compared in patients with and without right ventricular dysfunction.

61 es myocardial fibrosis and improves the left ventricular dysfunction.

62 coronary artery disease and significant left ventricular dysfunction.

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

64 lmonary microvasculature culminated in right ventricular dysfunction.

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

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

67 rovokes left ventricular remodeling and left ventricular dysfunction.

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

69 .6-3.9]), septic shock (2.7 [1.5-4.8]), left ventricular dysfunction (2.7 [1.6-5.0]), administration

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

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

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

73 Ventricular dysfunction adversely affects transplant-fre

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

75 ty of such an approach in patients with left ventricular dysfunction after myocardial infarction.

76 n stable heart failure outpatients with left ventricular dysfunction after myocardial infarction.

77 n stable heart failure outpatients with left ventricular dysfunction after myocardial infarction.

78 Left ventricular dysfunction after successful cardiopulmonary

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

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

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

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

83 undergone the Fontan palliation may develop ventricular dysfunction and arrhythmias, but the mechani

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

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

86 Right ventricular dysfunction and congestive states may contri

87 n patients with heart failure caused by left ventricular dysfunction and could be the first in class

88 expressed in adult mice (V1A-TG(Ind)), left ventricular dysfunction and dilatation were also seen, a

89 l in a broad selection of patients with left ventricular dysfunction and either demonstrated or antic

90 before PCI in all patients with severe left ventricular dysfunction and extensive coronary disease.

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

92 P has been shown to be reliable in detecting ventricular dysfunction and heart failure in adults.

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

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

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

96 ecommended in patients with symptoms of left ventricular dysfunction and in other settings, but the r

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

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

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

100 l valve repair to CABG in patients with left ventricular dysfunction and moderate to severe MR may im

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

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

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

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

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

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

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

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

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

110 s, leading to attenuation of MI-induced left ventricular dysfunction and remodeling.

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

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

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

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

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

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

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

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

119 t include atrial fibrillation, profound left ventricular dysfunction, and after mechanical prosthetic

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

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

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

123 ensive intracellular aggregates, accelerated ventricular dysfunction, and early mortality.

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

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

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

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

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

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

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

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

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

133 with mildly symptomatic heart failure, left ventricular dysfunction, and wide QRS complex compared w

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

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

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

137 dentifies diabetes and heart failure or left ventricular dysfunction as potential risk factors for bl

138 8 patients with pulmonary embolism had right ventricular dysfunction, as assessed by measurement of N

139 ; 95% confidence interval, 1.59-5.49), right ventricular dysfunction, as evidenced by fractional area

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

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

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

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

144 Right ventricular dysfunction, but not functional RV hypertrop

145 tients with coronary artery disease and left ventricular dysfunction, but this relationship was not s

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

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

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

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

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

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

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

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

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

155 ganic nitrate attenuates doxorubicin-induced ventricular dysfunction, cell death, oxidative stress, a

156 Ischemic heart disease as the cause of ventricular dysfunction (chi-square test: 34.9 and 7.4;

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

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

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

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

161 Patients with systolic left ventricular dysfunction die progressively from congestiv

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

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

164 Patients (n = 301) had severe left ventricular dysfunction (ejection fraction < or = 30%) a

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

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

167 Non-dose-limiting toxicities included left ventricular dysfunction, elevated thyroid stimulating ho

168 In patients with left ventricular dysfunction enrolled in the MADIT-CRT trial,

169 n be useful in diagnosing and treating right ventricular dysfunction, especially when associated with

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

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

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

173 ediction over baseline risk factors and left ventricular dysfunction (global chi(2) 207.5 versus 169.

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

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

176 yssynchrony on outcome in patients with left ventricular dysfunction, heart failure, or both after my

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

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

179 95% CI, 2.3-27.1; P=0.001) and subpulmonary ventricular dysfunction (HR, 3.0; 95% CI, 1.2-12.6; P=0.

180 1.97; p = 0.009), and heart failure or left ventricular dysfunction (HR: 1.32; 95% CI: 1.01 to 1.73;

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

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

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

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

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

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

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

188 red myocytes as well as hypertrophy and left ventricular dysfunction in experimental heart failure se

189 tributing to maladaptive remodeling and left ventricular dysfunction in hearts subjected to chronic s

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

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

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

193 diac energy production is a primary cause of ventricular dysfunction in sepsis.

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

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

196 a/reperfusion injury and improvement of left ventricular dysfunction in the failing heart after myoca

197 Hypoxia causes left ventricular dysfunction in the human heart, but the bioc

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

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

200 The degree of left ventricular dysfunction in this setting is often out of

201 resenting early in life to asymptomatic left ventricular dysfunction in those diagnosed during adulth

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

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

204 tients with coronary artery disease and left ventricular dysfunction in whom coronary-artery bypass g

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

206 61+/-7 and 61+/-7 mm, P<0.0001), more right ventricular dysfunction, increased epicardial fat thickn

207 Left ventricular dysfunction is a known predictor of ventricu

208 Acute left ventricular dysfunction is a major complication of cardi

209 Right ventricular dysfunction is a powerful determinant of pro

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

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

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

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

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

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

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

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

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

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

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

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

222 to heart failure, such as chamber dilation, ventricular dysfunction, lung edema, cardiac fibrosis, a

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

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

225 d longer-term outcomes in patients with left ventricular dysfunction (LVD).

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

227 Left ventricular dysfunction, mediated by ventricular interde

228 on, age <3 months at BD, moderate or greater ventricular dysfunction, moderate or greater atrioventri

229 Right ventricular dysfunction, moderate-severe tricuspid regur

230 Radiographically, significant left ventricular dysfunction, myocardial delayed enhancement

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

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

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

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

235 Strikingly, these defects preceded the left ventricular dysfunction of heart disease and failure in

236 Left ventricular dysfunction often precedes symptoms, needing

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

238 Eligible patients had right ventricular dysfunction on echocardiography or computed

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

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

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

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

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

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

245 4; P=0.034), moderate to severe subpulmonary ventricular dysfunction (OR, 3.4; 95% CI, 1.1-10.2; P=0.

246 5-7.9; P=0.004), moderate to severe systemic ventricular dysfunction (OR, 3.4; 95% CI, 1.1-10.4; P=0.

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

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

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

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

251 =0.03), mitral valve surgery (P=0.02), right ventricular dysfunction (P=0.03), and higher mean pulmon

252 eath after accounting for risk factors, left ventricular dysfunction, pharmacological stress, and sym

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

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

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

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 Advanced right ventricular dysfunction reduces the likelihood of clinic

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

261 high-risk patients (e.g. patients with left ventricular dysfunction, reoperation, elderly, multimorb

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

263 s in a preclinical model of postinfarct left ventricular dysfunction results in formation of new card

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

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

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

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

268 ventilation, nine patients presented a right ventricular dysfunction (right ventricular end-diastolic

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

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

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

272 experiments in 17 pigs with postinfarct left ventricular dysfunction showed CDC doses > or =10(7) but

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

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

275 amenable to CABG, and dominant anterior left ventricular dysfunction that was amenable to surgical ve

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

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

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

279 Screening for right ventricular dysfunction using goal-directed echocardiogr

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

281 Left ventricular dysfunction was associated with higher eryth

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

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

284 Postischemic left ventricular dysfunction was created by repetitive left c

285 No right ventricular dysfunction was observed.

286 Left ventricular dysfunction was present in 21.5% of patients

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

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

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

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

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

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

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

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

295 tients with coronary artery disease and left ventricular dysfunction who were enrolled in a randomize

296 II enrolled 1232 patients with ischemic left ventricular dysfunction who were randomized to ICD and n

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