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1 angiotensin-converting enzyme inhibitor for left ventricular dysfunction).
2 , hypertrophy-related signal activation, and left ventricular dysfunction.
3 ith, and possibly contributing to, diastolic left ventricular dysfunction.
4 ification beyond clinical data and degree of left ventricular dysfunction.
5 d medical therapy for patients with ischemic left ventricular dysfunction.
6 because of old age, comorbidities, or severe left ventricular dysfunction.
7 ition to persistent AF, with no evidence for left ventricular dysfunction.
8 is, familial cardiomyopathy, and severity of left ventricular dysfunction.
9 as evolution to heart failure or symptomatic left ventricular dysfunction.
10 th pulmonary hypertension caused by systolic left ventricular dysfunction.
11 nd develop significant myocardial injury and left ventricular dysfunction.
12 charide (O55B5, 10 mg/kg), inducing systolic left ventricular dysfunction.
13 1), can attenuate age-dependent induction of left ventricular dysfunction.
14 failure, pneumonia, atrial fibrillation, and left ventricular dysfunction.
15 and efficacy of TAVI in patients with severe left ventricular dysfunction.
16 art failure patients across the continuum of left ventricular dysfunction.
17 , and 11 patients who developed grade 2 or 3 left ventricular dysfunction.
18 eling of these structures despite persistent left ventricular dysfunction.
19 ity in heart failure across the continuum of left ventricular dysfunction.
20 sildenafil treatment ameliorated DOX-induced left ventricular dysfunction.
21 eterioration of HF in patients with systolic left ventricular dysfunction.
22 ventricular ejection fraction, and regional left ventricular dysfunction.
23 nd oxidative stress, which may contribute to left ventricular dysfunction.
24 d by presence of coronary artery disease and left ventricular dysfunction.
25 onship is linear with respect to severity of left ventricular dysfunction.
26 T inducibility in patients with prior MI and left ventricular dysfunction.
27 y risk in patients with coronary disease and left ventricular dysfunction.
28 hormonal activation, could result in further left ventricular dysfunction.
29 elial exocytosis, myocardial infarction, and left ventricular dysfunction.
30 ients with known coronary artery disease and left ventricular dysfunction.
31 in patients with coronary artery disease and left ventricular dysfunction.
32 in patients with coronary artery disease and left ventricular dysfunction.
33 dependent on valvular function or related to left ventricular dysfunction.
34 ardiac death (SCD) in patients with ischemic left ventricular dysfunction.
35 uding severe obstructive airways disease and left ventricular dysfunction.
36 ity for PCI and in patients with diabetes or left ventricular dysfunction.
37 y a role in development of postresuscitation left ventricular dysfunction.
38 inhibitors remain the first-line therapy for left ventricular dysfunction.
39 rals and ICD therapy in patients with severe left ventricular dysfunction.
40 occurs in the myocardium and correlates with left ventricular dysfunction.
41 rget DLST are important metabolic players in left ventricular dysfunction.
42 nt in LVEF, independent from the severity of left ventricular dysfunction.
43 yocardial infarction characterized by severe left ventricular dysfunction.
44 include progressive heart failure and severe left ventricular dysfunction.
45 ition to expected haemodynamic sequelae from left ventricular dysfunction.
46 apillary pulmonary hypertension secondary to left ventricular dysfunction.
47 ssion to mediate the myocardial fibrosis and left ventricular dysfunction.
48 creases myocardial fibrosis and improves the left ventricular dysfunction.
49 with coronary artery disease and significant left ventricular dysfunction.
50 nd cyclophosphamide are both associated with left ventricular dysfunction.
51 tively low 30-day mortality in patients with left ventricular dysfunction.
52 lity and heart failure (HF) in patients with left ventricular dysfunction.
53 art provokes left ventricular remodeling and left ventricular dysfunction.
54 ents with stable coronary artery disease and left-ventricular dysfunction.
55 in patients with coronary artery disease and left-ventricular dysfunction.
56 lysis using an experimental model of chronic left-ventricular dysfunction.
57 graphy to show that MHC-Angptl4 mice develop left-ventricular dysfunction.
58 the intracoronary route in 17 patients with left ventricular dysfunction 1.5 to 3 months after myoca
59 .4 [1.6-3.9]), septic shock (2.7 [1.5-4.8]), left ventricular dysfunction (2.7 [1.6-5.0]), administra
61 VAs were older and had higher prevalence of left ventricular dysfunction (67% versus 13% of fascicul
62 NOS3 as a key mediator in the development of left ventricular dysfunction after administration of dox
64 safety of such an approach in patients with left ventricular dysfunction after myocardial infarction
65 sts in stable heart failure outpatients with left ventricular dysfunction after myocardial infarction
66 ear in stable heart failure outpatients with left ventricular dysfunction after myocardial infarction
68 We evaluated 19 patients who presented with left ventricular dysfunction after sudden emotional stre
69 f secondary mitral regurgitation (MR) due to left ventricular dysfunction, also known as functional M
71 racyclines are at high risk for asymptomatic left ventricular dysfunction (ALVD), subsequent heart fa
73 renergic receptor (betaAR) polymorphisms and left ventricular dysfunction-an important cause of allog
74 chronization therapy in patients with severe left ventricular dysfunction and a QRS duration <120 mil
75 an clinical assessment alone for identifying left ventricular dysfunction and aortic or mitral valve
76 For example, whereas uninsured patients with left ventricular dysfunction and CAD were less likely to
77 ancer therapy agents with the development of left ventricular dysfunction and cardiomyopathy, is an i
79 ion in patients with heart failure caused by left ventricular dysfunction and could be the first in c
80 to be expressed in adult mice (V1A-TG(Ind)), left ventricular dysfunction and dilatation were also se
81 rvival in a broad selection of patients with left ventricular dysfunction and either demonstrated or
82 ement before PCI in all patients with severe left ventricular dysfunction and extensive coronary dise
83 nostic information in patients with ischemic left ventricular dysfunction and has comparable accuracy
84 one may have clinical value in patients with left ventricular dysfunction and heart failure as first-
85 myocardial infarction (AMI) with subsequent left ventricular dysfunction and heart failure continues
87 econsideration of discontinuing asymptomatic left ventricular dysfunction and HF screening in low-ris
89 th pulmonary hypertension caused by systolic left ventricular dysfunction and improved cardiac index
90 tion in nonimmunosuppressed rats ameliorates left ventricular dysfunction and improves remodeling via
91 nfants and children with CHF attributable to left ventricular dysfunction and in infants with large l
92 is recommended in patients with symptoms of left ventricular dysfunction and in other settings, but
93 syndrome (TTS) is characterized by an acute left ventricular dysfunction and is associated with life
94 Recent data demonstrate promising effects on left ventricular dysfunction and left ventricular ejecti
95 mation in the heart is sufficient to provoke left ventricular dysfunction and left ventricular remode
96 mitral valve repair to CABG in patients with left ventricular dysfunction and moderate to severe MR m
97 symptomatic high-risk patients with ischemic left ventricular dysfunction and multivessel coronary ar
98 ransient left ventricular apical ballooning, left ventricular dysfunction and normal or near-normal c
99 regulatable wild-type GSK-3beta mice induced left ventricular dysfunction and premature death, accomp
101 ho did not have these comorbidities, whereas left ventricular dysfunction and prior cardiac operation
102 inhibited interstitial fibrosis, decreasing left ventricular dysfunction and regional hypocontractil
103 -2 diet therapeutic approach also attenuated left ventricular dysfunction and remodeling post-MI (lef
104 reventive strategy attenuated development of left ventricular dysfunction and remodeling post-transve
105 thelial function was associated with reduced left ventricular dysfunction and remodeling, as well as
109 After a 5-year follow-up in patients with left ventricular dysfunction and suspected CAD, overall,
110 tic importance of WRF, 2231 patients who had left ventricular dysfunction and were enrolled in the Su
111 iabetes mellitus, a positive troponin assay, left-ventricular dysfunction and regional wall motion ab
112 atients with stable coronary artery disease, left ventricular dysfunction, and a heart rate of 70 bea
113 s that include atrial fibrillation, profound left ventricular dysfunction, and after mechanical prost
114 ents with large acute myocardial infarction, left ventricular dysfunction, and at high risk of develo
115 ime of the AMI, older age, lower hemoglobin, left ventricular dysfunction, and chronic heart failure.
116 , gender, type of surgery, emergent surgery, left ventricular dysfunction, and diabetes mellitus), st
117 ce were resistant to the cardiac remodeling, left ventricular dysfunction, and early death observed i
118 n cardiac fibroblasts leads to fibrogenesis, left ventricular dysfunction, and excessive scarring in
119 n cardiac fibroblasts leads to fibrogenesis, left ventricular dysfunction, and excessive scarring in
120 associated with increased CACS, subclinical left ventricular dysfunction, and increased pulse pressu
121 rupture, accentuates post-MI remodeling and left ventricular dysfunction, and increases the progress
122 n patients with mild heart-failure symptoms, left ventricular dysfunction, and left bundle-branch blo
123 troke or transient ischemic attack, smoking, left ventricular dysfunction, and mitral regurgitation.
124 such as acute respiratory distress syndrome, left ventricular dysfunction, and pulmonary embolism, as
125 CD studies had fewer comorbidities, had less left ventricular dysfunction, and received more inapprop
126 ers are beneficial in patients with acquired left ventricular dysfunction, and recent findings have s
127 haracterized by progression toward dilation, left ventricular dysfunction, and refractory heart failu
128 e units in 14 centers for cardiogenic shock, left ventricular dysfunction, and severe inflammatory st
129 total and sudden deaths, conduction defects, left ventricular dysfunction, and supraventricular arrhy
130 ients with mildly symptomatic heart failure, left ventricular dysfunction, and wide QRS complex compa
131 R with history of ventricular tachycardia or left ventricular dysfunction appear to be associated wit
132 many mechanisms contributing to progressive left ventricular dysfunction are matched by stem cell ac
134 1 were significant univariable predictors of left ventricular dysfunction as assessed by an ejection
135 sis identifies diabetes and heart failure or left ventricular dysfunction as potential risk factors f
136 te hemodynamic instability, newly recognized left ventricular dysfunction, as well as imaging during
137 als that re-examine this in patients without left ventricular dysfunction, as well as in patients wit
138 ion was associated with oxidative stress and left ventricular dysfunction assessed by electron spin r
141 receptor blockers (ARBs) in the treatment of left ventricular dysfunction, both acutely after myocard
142 titioning of dietary fatty acids (DFAs) with left ventricular dysfunction, both of which are improved
143 th trastuzumab; three patients had recurrent left ventricular dysfunction, but 22 patients (88%) did
144 iously documented coronary artery disease or left ventricular dysfunction, but blacks had more preval
145 tropic and lusitropic effects in humans with left ventricular dysfunction, but does not alter the for
146 in patients with coronary artery disease and left ventricular dysfunction, but this relationship was
147 NRIL and KCNQ1OT1 improved the prediction of left ventricular dysfunction by a model, including demog
148 Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction (CAPRICORN) study, which en
149 ted CB ablation decreases the progression of left ventricular dysfunction, cardiac remodeling, and ar
150 including guideline-directed medication for left ventricular dysfunction, cardiac resynchronization
153 ccurred in 16 patients (8%) and 37 (16%) had left ventricular dysfunction, defined as left ventricula
155 ats with atrial remodeling in the context of left ventricular dysfunction due to myocardial infarctio
156 on by sitagliptin protected against ischemic left ventricular dysfunction during dobutamine stress in
157 e patients (age 64 +/- 10 years, n = 13 with left ventricular dysfunction) during ablation procedures
159 f hypertension, prior revascularization, and left ventricular dysfunction (ejection fraction <40%), a
160 erwent successful stenting for STEMI and had left ventricular dysfunction (ejection fraction</=48%) >
161 erwent successful stenting for STEMI and had left ventricular dysfunction (ejection fraction</=48%) >
164 ffects of CAD; late risk reflected diastolic left ventricular dysfunction expressed as ventricular hy
165 s) from donor mice with HF induced long-term left ventricular dysfunction, fibrosis, and hypertrophy
166 that can induce cardiac repair and attenuate left ventricular dysfunction from both within and outsid
168 th prediction over baseline risk factors and left ventricular dysfunction (global chi(2) 207.5 versus
169 pared with RVP among patients without severe left ventricular dysfunction (>35%) who required permane
170 heart failure (HF) subtended by progressive left ventricular dysfunction has received limited attent
173 , inflammatory cardiomyopathy complicated by left ventricular dysfunction, heart failure or arrhythmi
174 cal dyssynchrony on outcome in patients with left ventricular dysfunction, heart failure, or both aft
176 er myocardial infarction among patients with left ventricular dysfunction, heart failure, or both.
177 nced multidisciplinary heart team to prevent left ventricular dysfunction, heart failure, reduced qua
178 tion by an experienced heart team to prevent left ventricular dysfunction, heart failure, reduced qua
179 rain echocardiography detects early signs of left ventricular dysfunction; however, it is unknown whe
180 10 to 1.97; p = 0.009), and heart failure or left ventricular dysfunction (HR: 1.32; 95% CI: 1.01 to
181 f prior myocardial infarction with resultant left ventricular dysfunction identifies a group at parti
183 ms, improves survival, and, in patients with left ventricular dysfunction, improves systolic function
185 ment with sildenafil prevented apoptosis and left ventricular dysfunction in a chronic model of doxor
186 ing infarct expansion, troponin release, and left ventricular dysfunction in a swine myocardial infar
187 cultured myocytes as well as hypertrophy and left ventricular dysfunction in experimental heart failu
188 , contributing to maladaptive remodeling and left ventricular dysfunction in hearts subjected to chro
190 al stress can precipitate severe, reversible left ventricular dysfunction in patients without coronar
191 ng revealed hypertrophic cardiomyopathy with left ventricular dysfunction in SKO mice, and these two
192 rosemide would accelerate the progression of left ventricular dysfunction in the "treated" group.
193 chemia/reperfusion injury and improvement of left ventricular dysfunction in the failing heart after
195 al vagal nerve stimulation (VNS) can improve left ventricular dysfunction in the setting of heart fai
198 ose presenting early in life to asymptomatic left ventricular dysfunction in those diagnosed during a
199 diomyocytes provoked cardiac hypertrophy and left ventricular dysfunction in vivo, whereas genetic kn
200 fy patients with coronary artery disease and left ventricular dysfunction in whom coronary-artery byp
201 ertrophy, dilated cardiomyopathy, and severe left ventricular dysfunction, including a marked reducti
205 Pulmonary hypertension caused by systolic left ventricular dysfunction is associated with signific
207 a potentially reversible condition in which left ventricular dysfunction is induced or mediated by a
208 (82)Rb PET is associated with more extensive left ventricular dysfunction, ischemic compromise, and r
210 tive procedure, even in patients with severe left ventricular dysfunction, leading to a high procedur
211 ng would not be attractive if a diagnosis of left ventricular dysfunction led to significant decrease
212 ongestion, and echocardiographic evidence of left ventricular dysfunction (left ventricle ejection fr
213 Evaluation (TIME) enrolled 120 patients with left ventricular dysfunction (left ventricular ejection
214 tivity of clinical assessment for diagnosing left ventricular dysfunction (left ventricular ejection
215 entricular wall motion abnormalities, global left ventricular dysfunction, left ventricular diastolic
216 reated wild-type (WT) mice manifested severe left ventricular dysfunction, loss of heart and body mas
217 y the potential negative interaction between left ventricular dysfunction (LVD) and MSC activation.
220 survival among those with and without severe left ventricular dysfunction (LVD); 2) identify risk fac
222 ence of severe heart failure symptoms (66%), left ventricular dysfunction (mean ejection fraction 46.
226 gh-grade atrioventricular block, significant left ventricular dysfunction, myocardial delayed enhance
227 etection Window Programming in Patients With Left Ventricular Dysfunction, Non-ischemic Etiology in P
228 ging, male sex, hypertension, valve disease, left ventricular dysfunction, obesity, and alcohol consu
229 with an increased risk of echocardiographic left ventricular dysfunction (odds ratio [OR], 1.3 per q
232 of patients demonstrated moderate or severe left ventricular dysfunction on initial echocardiogram (
234 ight ventricular dysfunction only (RV(dys)), left ventricular dysfunction only (LV(dys)), and combine
236 for reasons that included coronary disease, left ventricular dysfunction or hypertrophy, and high-do
237 erican Heart Association class I indication (left ventricular dysfunction or medical history of heart
239 w state and to understand the reason for the left ventricular dysfunction or when there is a suspicio
240 ced by VPB grade, presence of recovery VPBs, left ventricular dysfunction, or an ischemic ST-segment
241 inical or radiologic signs of heart failure, left ventricular dysfunction, or both, and a documented
242 free of evidence of coronary artery disease, left ventricular dysfunction, or evident repolarization
243 that can present as acute coronary syndrome, left ventricular dysfunction, or potentially sudden card
244 iovascular comorbidities, renal dysfunction, left ventricular dysfunction, or significant coronary st
245 tely-by precipitating myocardial infarction, left-ventricular dysfunction, or dysrhythmia; and chroni
247 defibrillators in patients with more severe left ventricular dysfunction particularly of ischemic et
248 iac death after accounting for risk factors, left ventricular dysfunction, pharmacological stress, an
249 a consecutive series of patients with severe left ventricular dysfunction, pLVAD-supported scar VT ab
250 fety and potential efficacy in patients with left ventricular dysfunction post STEMI who are at risk
254 nts: those with acute myocardial infarction, left ventricular dysfunction, previous history of stroke
255 chronization Reverses Remodeling in Systolic Left Ventricular Dysfunction], RAFT (Resynchronization-D
256 (28-66), seven males, none with a history of left ventricular dysfunction, received venoarterial extr
257 class I triggers (heart failure symptoms or left ventricular dysfunction) remains controversial in p
258 n for high-risk patients (e.g. patients with left ventricular dysfunction, reoperation, elderly, mult
259 tween patients with and without a history of left ventricular dysfunction resulting from KD-associate
260 in the management of patients with systolic left ventricular dysfunction (resulting from both ischem
261 f CDCs in a preclinical model of postinfarct left ventricular dysfunction results in formation of new
262 chronization reVErses Remodeling in Systolic left vEntricular dysfunction (REVERSE) study were evalua
263 chronization reVErses Remodeling in Systolic left vEntricular dysfunction (REVERSE) was a multicenter
264 chronization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE) was a multicenter
265 tify four important abnormalities: asystole, left ventricular dysfunction, right ventricular dilation
266 s with clinically manifest CS, the extent of left ventricular dysfunction seems to be the most import
267 pathy (SCM) is a peculiar form of reversible left ventricular dysfunction seen predominantly in women
268 sion experiments in 17 pigs with postinfarct left ventricular dysfunction showed CDC doses > or =10(7
270 ocardium is common in patients with NQMI and left ventricular dysfunction, suggesting that aggressive
271 sidual TR was associated with age, right and left ventricular dysfunction, tethering distance and are
272 iving vasopressin had more postresuscitation left ventricular dysfunction than those receiving epinep
273 was amenable to CABG, and dominant anterior left ventricular dysfunction that was amenable to surgic
275 t, namely those with atrial fibrillation and left ventricular dysfunction, those with acute sustained
276 terogeneous group, ranging from asymptomatic left ventricular dysfunction to chronic decompensation w
277 role nesiritide might play in patients with left ventricular dysfunction undergoing coronary artery
279 A history of ventricular tachycardia and left ventricular dysfunction was associated with higher
280 jected to an ischaemia-reperfusion protocol, left ventricular dysfunction was associated with uncoupl
288 rdia (VT) or nonsustained VA with associated left ventricular dysfunction were enrolled at 3 centers.
289 om pulmonary hypertension caused by systolic left ventricular dysfunction were randomized to double-b
290 9) with prior myocardial infarction (MI) and left ventricular dysfunction were referred for defibrill
291 lation more than 7 days, and severe systolic left ventricular dysfunction were stronger predictors of
292 tion, ineffective cough, and severe systolic left ventricular dysfunction were the three independent
293 rmalities, left ventricular hypertrophy, and left ventricular dysfunctions were demonstrated in Group
294 ve generally a normal coronary angiogram and left ventricular dysfunction, which extends beyond the t
295 ces the risk stratification of patients with left ventricular dysfunction who are ICD candidates, it
296 of patients with coronary artery disease and left ventricular dysfunction who were enrolled in a rand
297 ADIT-II enrolled 1232 patients with ischemic left ventricular dysfunction who were randomized to ICD
298 rt Association (NYHA) class III or IV HF and left ventricular dysfunction who were randomized to spir
299 f 362 patients with ischemic cardiomyopathy (left ventricular dysfunction with >70% stenosis in >/=1
300 atients experienced some degree of segmental left ventricular dysfunction, with severity proportional