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1  (92 with HFNEF and 230 with asymptomatic LV diastolic dysfunction).
2 /or reduced global longitudinal strain, with diastolic dysfunction).
3 g, sympatho-vagal imbalance, arrhythmias and diastolic dysfunction.
4 , and 7 patients (29%) met the definition of diastolic dysfunction.
5 asis and cellular remodeling, which leads to diastolic dysfunction.
6 ciated with left ventricular hypertrophy and diastolic dysfunction.
7 lthough MS seems to be associated with worse diastolic dysfunction.
8 chanical mechanism which may partly underlie diastolic dysfunction.
9 r hypertrophy, left ventricular systolic and diastolic dysfunction.
10 iated with cardiac hypertrophy, fibrosis and diastolic dysfunction.
11             It appears to be associated with diastolic dysfunction.
12 r impaired fluid dynamics may be a source of diastolic dysfunction.
13 on in thin-filament HCM, reflecting profound diastolic dysfunction.
14 ats (SHAM) and aortic-banded rats exhibiting diastolic dysfunction.
15 associated with echocardiographic indexes of diastolic dysfunction.
16 s, such as increased myocardial stiffness or diastolic dysfunction.
17 herefore likely to be a major contributor to diastolic dysfunction.
18 RDN reduces BP, HR, and LV mass and improves diastolic dysfunction.
19 d by nondilated left or right ventricle with diastolic dysfunction.
20 entricular ejection fraction and evidence of diastolic dysfunction.
21  Ca(2+) sensitivity, severe hypertrophy, and diastolic dysfunction.
22  significantly lower values in patients with diastolic dysfunction.
23 r pressure overload, leading to fibrosis and diastolic dysfunction.
24 ertension, left ventricular hypertrophy, and diastolic dysfunction.
25                   SCM and LAD MI show severe diastolic dysfunction.
26 from mice with metabolic syndrome-associated diastolic dysfunction.
27 tolerance, a phenotype often associated with diastolic dysfunction.
28  post ASO and are likely to contribute to LV diastolic dysfunction.
29 s is related to changes in right ventricular diastolic dysfunction.
30 ar heart disease often have left ventricular diastolic dysfunction.
31  in post-myocardial infarction patients with diastolic dysfunction.
32 pporting a titin-based mechanism for in vivo diastolic dysfunction.
33  mechanisms underlying arrhythmogenicity and diastolic dysfunction.
34  mice developed fibrotic cardiomyopathy with diastolic dysfunction.
35 ular hypertrophy, interstitial fibrosis, and diastolic dysfunction.
36 lyphenols prevent myocardial hypertrophy and diastolic dysfunction.
37 left ventricular hypertrophy, and associated diastolic dysfunction.
38 l prevented left ventricular hypertrophy and diastolic dysfunction.
39 CE2KO hearts and are likely mediators of the diastolic dysfunction.
40 cterized by left ventricular hypertrophy and diastolic dysfunction.
41 be a valuable target for the treatment of LV diastolic dysfunction.
42 nary hypertension (PH), and left ventricular diastolic dysfunction.
43 ing and an increase in Tei index, suggesting diastolic dysfunction.
44 tropic stress, in association with continued diastolic dysfunction.
45 tion between diffuse myocardial fibrosis and diastolic dysfunction.
46 osolic calcium reuptake kinetics, indicating diastolic dysfunction.
47 ion and contribution to cardiac fibrosis and diastolic dysfunction.
48  frequently associated with left ventricular diastolic dysfunction.
49 rated rats and aortic-banded rats exhibiting diastolic dysfunction.
50  in both normal animals and a pig model with diastolic dysfunction.
51 patients with AD present with an anticipated diastolic dysfunction.
52 reasing the compliance of titin in mice with diastolic dysfunction.
53 l or unrecognized, with a high prevalence of diastolic dysfunction.
54 239.9 vs. 576.7 +/- 472.9 events h(-1) ) and diastolic dysfunction (0.008 +/- 0.004 vs. 0.027 +/- 0.0
55 , and mitral inflow patterns consistent with diastolic dysfunction (1.95 +/- 0.05 FA versus 1.52 +/-
56  prevalent (29.7%) form of cTOD, followed by diastolic dysfunction (21.3%), left atrial enlargement (
57 s(-1)) than in patients with asymptomatic LV diastolic dysfunction (25.33+/-6.06% and 1.37+/-0.33 s(-
58 nd E/e' ratios; 2) their roles in diagnosing diastolic dysfunction; 3) prognostic implications of abn
59  hypertrophy (61% and 39%, respectively) and diastolic dysfunction (35% and 36%, respectively) than h
60                  Nontransgenic TAC developed diastolic dysfunction (65% increase in E/A ratio), where
61 nt and high prevalence of LV hypertrophy and diastolic dysfunction; a subclinical systolic dysfunctio
62 ng pressure during exercise in patients with diastolic dysfunction after myocardial infarction.
63 and fibrosis biomarkers, and the severity of diastolic dysfunction all increased with severity of RVD
64  ventricular arrhythmic burden, and systolic/diastolic dysfunction (all p < 0.05).
65 ation, cardiac hypertrophy, and systolic and diastolic dysfunction, although the pathogenesis of thes
66  model may increase late I(Na), resulting in diastolic dysfunction amenable to treatment with ranolaz
67 e odds ratios (95% confidence intervals) for diastolic dysfunction among individuals with prediabetes
68 tivariable echocardiographic Cox model, only diastolic dysfunction and 2D-GLS remained as independent
69 h are resistant to PKGIalpha oxidation, have diastolic dysfunction and a diminished ability to couple
70 ial volume (LAV) increase is an indicator of diastolic dysfunction and a surrogate marker of signific
71 re at year 0 was associated with both severe diastolic dysfunction and abnormal relaxation 5 years la
72 mposite endpoint in participants with severe diastolic dysfunction and abnormal relaxation were 4.3 (
73 tic cardiomyopathy is characterized by early diastolic dysfunction and adverse left ventricular (LV)
74 y play a central role in the pathogenesis of diastolic dysfunction and arrhythmia.
75                        Finally, Myr improved diastolic dysfunction and attenuated histological abnorm
76  independent of blood pressure, by improving diastolic dysfunction and by modulating cardiac hypertro
77 dings may contribute to the left ventricular diastolic dysfunction and cardiac reserve function impai
78 04, and December 31, 2005, and had grade 2-4 diastolic dysfunction and ejection fraction >/=50% were
79 r filling ratio (E/A), indicative of grade 1 diastolic dysfunction and emphasizing the importance of
80 ertension, left ventricular hypertrophy, and diastolic dysfunction and had higher myocardial natriure
81 )-related cardiomyopathy is characterized by diastolic dysfunction and hyperdynamic features.
82  which may play a role in the development of diastolic dysfunction and inappropriate shortness of bre
83 lood transfusions; P<0.05 for both), whereas diastolic dysfunction and increased filling pressures we
84                                              Diastolic dysfunction and left ventricular remodeling ar
85                        Seventy patients with diastolic dysfunction and near normal left ventricular e
86 cular chamber levels showed that this causes diastolic dysfunction and other symptoms of heart failur
87 on, whereas deficient phosphorylation causes diastolic dysfunction and phenotypes resembling HFpEF.
88 ks of a high-salt diet, 31 of 38 rats showed diastolic dysfunction and preserved ejection fraction al
89     The aging myopathy manifests itself with diastolic dysfunction and preserved ejection fraction.
90 ctions, which are linked to left ventricular diastolic dysfunction and remodeling.
91                             Left ventricular diastolic dysfunction and right ventricular dilatation a
92 ing LV GLS is associated with more severe LV diastolic dysfunction and RV systolic and diastolic dysf
93 sm in experimental models of hypertrophy and diastolic dysfunction and the role of the Ang II type 1
94  Recurrent AF, was associated with increased diastolic dysfunction and vasopressor use and a greater
95 sociations of these arterial parameters with diastolic dysfunction and ventricular-arterial coupling
96 orubicin-injected fish developed ventricular diastolic dysfunction and worsening global cardiac funct
97 left ventricular ejection fraction >50%, and diastolic dysfunction) and 60 patients with stage B HF (
98 ontributes to the development of age-related diastolic dysfunction, and (2) initiation of late-life e
99 ce) develop progressive myocardial fibrosis, diastolic dysfunction, and adverse cardiac remodeling.
100 c hypertrophy, left ventricular systolic and diastolic dysfunction, and autophagy in mice.
101 layed decreased ventricular dimensions, mild diastolic dysfunction, and enhanced systolic function, w
102 II, left ventricular ejection fraction >50%, diastolic dysfunction, and exertional E/e' >13), excludi
103 ioration of Ang-induced cardiac hypertrophy, diastolic dysfunction, and fibrosis, despite the absence
104 e combined rates of LV systolic dysfunction, diastolic dysfunction, and heart failure.
105 EF exacerbates left ventricular hypertrophy, diastolic dysfunction, and HF.
106  ventricular abnormalities, such as low GLS, diastolic dysfunction, and hypertrophy (log-rank P<0.000
107  of myocardial substrate selection, reversed diastolic dysfunction, and normalized blood glucose leve
108 ardial fibrosis, abnormal perfusion reserve, diastolic dysfunction, and only rarely myocardial iron o
109 LV diastolic dysfunction and RV systolic and diastolic dysfunction, and provides incremental prognost
110 iated feature of SCA that is associated with diastolic dysfunction, anemia, and high NT-proBNP.
111     Increased left ventricular (LV) mass and diastolic dysfunction are associated with cardiovascular
112                                      LVH and diastolic dysfunction are associated with elevated sympa
113                                  Both PH and diastolic dysfunction are associated with marked abnorma
114  echocardiography disclosed left ventricular diastolic dysfunction as unexpected cardiogenic cause of
115 ressive development of left ventricular (LV) diastolic dysfunction, as assessed by markers of LV dias
116 tors of mortality or major morbidity: severe diastolic dysfunction, as evidenced by restrictive filli
117 pertrophy and fibrosis with normalization of diastolic dysfunction assessed by pressure-volume loop a
118 tive physician be alerted to the presence of diastolic dysfunction, be knowledgeable of the diastolic
119 mal Doppler E-wave filling patterns indicate diastolic dysfunction but are indistinguishable from the
120 therapy can be of value for the treatment of diastolic dysfunction, but there is a paucity of data ev
121 function (via echocardiography) demonstrated diastolic dysfunction by 2 weeks (20% increase in E/E'),
122 ial energy reserve is limited, contribute to diastolic dysfunction by recruiting cross-bridges, even
123 (b) elevate diastolic [Ca]i, contributing to diastolic dysfunction; (c) cause triggered arrhythmias;
124 3 loss did not affect survival, systolic and diastolic dysfunction, cardiac fibrosis, and cardiomyocy
125 r afterload leads to myocardial hypertrophy, diastolic dysfunction, cellular remodelling and compromi
126 ncreased TAG accumulation, lipotoxicity, and diastolic dysfunction comparable to wild-type mice.
127 D increment) had a stronger association with diastolic dysfunction compared with SBP.
128 ated with more global LV thickening and with diastolic dysfunction, compared to WES feeding alone.
129  of prospective risk markers associated with diastolic dysfunction could allow for targeted primary p
130                                              Diastolic dysfunction could be reversed by ranolazine, p
131 normalities result in progressive and severe diastolic dysfunction, culminating in heart failure.
132  10) compared with patients with isolated LV diastolic dysfunction (DD) (n = 10) and control subjects
133                             Left ventricular diastolic dysfunction (DD) is a key determinant of outco
134                                              Diastolic dysfunction (DD) is an independent predictor o
135                             Left ventricular diastolic dysfunction (DD) is common after myocardial in
136                They contribute to myocardial diastolic dysfunction (DD) through collagen deposition o
137 eft ventricular systolic dysfunction (LVSD), diastolic dysfunction (DD), pulmonary arterial hypertens
138 erved ejection fraction is often preceded by diastolic dysfunction (DD).
139 associated with echocardiographic markers of diastolic dysfunction (DD).
140 oke volume (2.0%, P=0.002), left ventricular diastolic dysfunction (deceleration time [0.9%, P=0.03]
141 hic and clinical variables, left ventricular diastolic dysfunction defined as increased mitral E-to-s
142  corrected abnormal myocardial relaxation in diastolic dysfunction disease models in vitro and in viv
143 ps, patients with mild, moderate, and severe diastolic dysfunction displayed significantly reduced no
144 nt mechanism underlying cardiac fibrosis and diastolic dysfunction during increased renin-angiotensin
145 This study suggests that elevated markers of diastolic dysfunction during pre-LTx echocardiographic e
146 mal levels (0.018 +/- 0.002 s(-1)), reversed diastolic dysfunction (E/E' 14 +/- 1), and normalized bl
147         Twenty-three of them correlated with diastolic dysfunction (E/e') and 5 with left atrial volu
148  deformation indices with Doppler indices of diastolic dysfunction, functional capacity, biomarkers,
149 d ejection fraction and their correlation to diastolic dysfunction, functional class, pathophysiologi
150 astolic dysfunction, be knowledgeable of the diastolic dysfunction grading system and understand the
151                            Participants with diastolic dysfunction had higher ECV (0.49 +/- 0.07 vs 0
152  cardiomyopathy with severe left ventricular diastolic dysfunction has been associated with marked ex
153                      Heart failure (HF) with diastolic dysfunction has been attributed to increased m
154 ar exercise training ameliorates age-related diastolic dysfunction; however, the underlying mechanism
155 - and sex-matched hypertensive patients with diastolic dysfunction (hypertensive heart disease) but n
156 NCA) limits cardiomyocyte hypertrophy and LV diastolic dysfunction in a mouse model of diabetes melli
157  coronary perfusion are likely mechanisms of diastolic dysfunction in aged rats.
158   Late systolic load has been shown to cause diastolic dysfunction in animal models.
159 t ventricular hypertrophy (LVH) and systolic/diastolic dysfunction in asymptomatic patients with HF r
160 emporary measures of longitudinal strain and diastolic dysfunction in defining HF stages is unclear.
161  cardiomyopathy with severe left ventricular diastolic dysfunction in end-stage disease.
162 tex generation is an unreported mechanism of diastolic dysfunction in HCM and probably other causes o
163                                              Diastolic dysfunction in heart failure patients is evide
164         Although macitentan did not modulate diastolic dysfunction in HFpEF, it significantly reduced
165 rdial fibrosis in SCA mice, but the cause of diastolic dysfunction in humans with SCA is unknown.
166        Echocardiography detected evidence of diastolic dysfunction in hypertensive mice that improved
167 is associated with incipient LV systolic and diastolic dysfunction in middle age.
168 of RV remodeling exist in obesity and (2) LV diastolic dysfunction in obesity is related to RV hypert
169 ar mass index or improve certain measures of diastolic dysfunction in patients with chronic kidney di
170 known whether the myofilament contributes to diastolic dysfunction in patients with concentric remode
171 iew summarizes the underlying mechanisms for diastolic dysfunction in patients with mitral and aortic
172              However, it could contribute to diastolic dysfunction in patients with sepsis.
173                                              Diastolic dysfunction in response to hypertrophy is a ma
174 s a novel mechanism that appears to underlie diastolic dysfunction in SCA.
175 ess promotes fibrosis and contributes to the diastolic dysfunction in the aging heart.
176  risk markers, and prognosis associated with diastolic dysfunction in the Coronary Artery Risk Develo
177               Ang 1-7 completely rescued the diastolic dysfunction in the db/db model.
178 ew focuses on recent findings on the role of diastolic dysfunction in the perioperative period and on
179                  The precise mechanism of LV diastolic dysfunction in the presence of myocardial fibr
180 have added value to assess right ventricular diastolic dysfunction in this population.
181 fusion) resulted in more severe systolic and diastolic dysfunction in TIMP4(-/-) mice with enhanced i
182  hypertrophy and remodeling and systolic and diastolic dysfunction in transverse aortic constriction
183                 Exogenous sFLT1 alone caused diastolic dysfunction in wild-type mice, and profound sy
184 ay contribute to increased susceptibility to diastolic dysfunction in women.
185                                              Diastolic dysfunction in young adults is associated with
186                  Risk factors for persistent diastolic dysfunction include higher pre-BAVP LV mass z-
187 correlated with echocardiographic indexes of diastolic dysfunction including a higher mitral E-wave z
188 cus on what is known concerning pre-clinical diastolic dysfunction, including definitions, staging, e
189 lvement, those with NAFLD had features of LV diastolic dysfunction, including higher E-to-e' ratio an
190                       ABSTRACT: The risk for diastolic dysfunction increases with advancing age.
191                            Right ventricular diastolic dysfunction influences outcomes in pulmonary a
192     Incorporation of longitudinal strain and diastolic dysfunction into the Stage B definition reclas
193                                  Age-related diastolic dysfunction is a major factor in the epidemic
194                                              Diastolic dysfunction is a poorly understood but clinica
195                             Left ventricular diastolic dysfunction is an asymptomatic condition assoc
196                                              Diastolic dysfunction is an independent predictor of mor
197                             Left ventricular diastolic dysfunction is an underestimated disease with
198                                              Diastolic dysfunction is associated with microscopic myo
199       Ang II- and PE-induced hypertrophy and diastolic dysfunction is associated with reduced glucose
200                                              Diastolic dysfunction is frequently seen after myocardia
201                                              Diastolic dysfunction is general to all idiopathic dilat
202 usion requirements, whereas left ventricular diastolic dysfunction is predominantly correlated with i
203                                     Although diastolic dysfunction is widely considered a key pathoph
204 mean 6 cm/s [SD 1.2] versus FGR 5.3 [1]) and diastolic dysfunction (isovolumic relaxation time: contr
205 SAM-WD had developed HFpEF, characterized by diastolic dysfunction, left ventricular hypertrophy, lef
206 uction, left ventricular hypercontractility, diastolic dysfunction, left-atrial enlargement and left
207 normalities, including left ventricular (LV) diastolic dysfunction, longitudinal LV systolic dysfunct
208 Z value, +0.45 +/- 0.49, P < 0.001) and more diastolic dysfunction (lower E', Z value, -0.7 +/- 1.02,
209 er left ventricular ejection fraction, worse diastolic dysfunction, lower blood pressure and cardiac
210 ce ameliorated left ventricular hypertrophy, diastolic dysfunction, lung congestion, and myocardial o
211             We investigated left ventricular diastolic dysfunction (LVDD) and its relationship with c
212 olic dysfunction (LVSD) and left ventricular diastolic dysfunction (LVDD).
213 nary venous pressure due to left ventricular diastolic dysfunction may contribute by exacerbating cap
214 and stroke volume (77 mL) were normal, while diastolic dysfunction (medial E/e', 16; deceleration tim
215             Pediatric PH patients exhibit LV diastolic dysfunction most consistent with impaired rela
216               PH patients had evidence of LV diastolic dysfunction, most consistent with impaired LV
217 s confirmed that the abnormalities including diastolic dysfunctions, myocardial fibrosis and metaboli
218 graphically proved mild, moderate, or severe diastolic dysfunction (n = 30, 44-73 years).
219 ortening this segment is sufficient to cause diastolic dysfunction need to be established.
220                                              Diastolic dysfunction occurred in both affected males an
221           Decline in FVC was associated with diastolic dysfunction (odds ratio, 3.39; 95% confidence
222 with E/A ratio (beta +/- SE: 0.12 +/- 0.04), diastolic dysfunction (odds ratio: 0.33; 95% confidence
223 low E/A ratio (beta +/- SE: -0.17 +/- 0.07), diastolic dysfunction (odds ratio: 7.8; 95% confidence i
224  consisting of asymptomatic subjects with LV diastolic dysfunction of similar age, sex, and LV ejecti
225 erstitium, triggering fibrosis, systolic and diastolic dysfunction of stressed hearts.
226 ted, and the impact of left ventricular (LV) diastolic dysfunction on RV hypertrophy is unknown, we a
227      The influence of arterial afterload and diastolic dysfunction on the hemodynamic presentation of
228 lar resistance index was not associated with diastolic dysfunction or Ea/Ees.
229       Whether this miRNA might contribute to diastolic dysfunction or other forms of heart disease is
230 ricular dilation or hypertrophy, systolic or diastolic dysfunction, or both, or various forms of cong
231 ntricular hypertrophy, systolic dysfunction, diastolic dysfunction, or left atrial enlargement).
232 ensive clinical models, 2D-GLS (p < 0.0001), diastolic dysfunction (p < 0.01), the pathologic free li
233 is and evidence of isolated left ventricular diastolic dysfunction (p < 0.05).
234 IPCAR was positively associated with grade I diastolic dysfunction (P < 0.050 for all logistic models
235 CV values (>/=0.40) were more likely to have diastolic dysfunction (P = .003) and increased left atri
236 rial volume (P = .002) and with the grade of diastolic dysfunction (P = .016).
237 o <55% and were more likely to have advanced diastolic dysfunction (P=0.002).
238                          This improvement in diastolic dysfunction parameters in aldosterone-infused
239 e effect may be partially mediated through a diastolic dysfunction pathway that includes left ventric
240                                 Pre-clinical diastolic dysfunction (PDD) has been broadly defined as
241                                  Preclinical diastolic dysfunction (PDD) has been broadly defined as
242  effects in the heart in vivo that lead to a diastolic dysfunction phenotype.
243                                              Diastolic dysfunction portends early mortality in SCA.
244 e sleep apnea, high-level physical training, diastolic dysfunction, predisposing gene variants, hyper
245 SD, 0.3) years between examinations 1 and 2, diastolic dysfunction prevalence increased from 23.8% (9
246 x and includes left ventricular systolic and diastolic dysfunction, pulmonary vascular disease, endot
247  was inversely correlated to the severity of diastolic dysfunction (R = -0.61, P < .001).
248 th LV E/e' as an echocardiographic marker of diastolic dysfunction (r = 0.54, P < 0.05).
249 othesized that pediatric PH patients have LV diastolic dysfunction, related to adverse pulmonary hemo
250                                              Diastolic dysfunction represents a combination of impair
251 d end-systolic chamber elastance, as well as diastolic dysfunction seen at the level of the whole hea
252 lation, pathological myocyte remodeling, and diastolic dysfunction, starting from prediabetes.
253 ad lower LS, greater dyssynchrony, and early diastolic dysfunction, supporting the notion that obesit
254 -deficient mice, however, showed exacerbated diastolic dysfunction, sustained elevation of membrane-t
255 y, smaller left atria, and less systolic and diastolic dysfunction than FG+ probands with HCM.
256 ure, seems to contribute to the systolic and diastolic dysfunction that characterizes the disease.
257 his is often accompanied by left ventricular diastolic dysfunction that has also been a strong indepe
258 lar thickening at 4 weeks of age, as well as diastolic dysfunction that progressed with age, in Hyal2
259 ng that cardiac oxidative stress may mediate diastolic dysfunction through altering the contractile a
260          The latter affects left ventricular diastolic dysfunction through macrophage infiltration, r
261  expression contributes mainly to myocardial diastolic dysfunction through mitochondrial apoptosis, L
262                                              Diastolic dysfunction underlies HFpEF; therefore, elucid
263                            More importantly, diastolic dysfunction usually improves with timely surgi
264                                              Diastolic dysfunction was associated with development of
265                                              Diastolic dysfunction was associated with incident heart
266                              Furthermore, LV diastolic dysfunction was associated with increased LV f
267                                              Diastolic dysfunction was defined using Doppler and tiss
268                 Diabetes mellitus-induced LV diastolic dysfunction was evident on echocardiography-de
269  diameter and left ventricular mass although diastolic dysfunction was more pronounced in OB/MS+ than
270 95% CI 2.07-10.9); however, left-ventricular diastolic dysfunction was not (P>0.05).
271 nts included in the primary analysis, severe diastolic dysfunction was present in 1.1% and abnormal r
272                                              Diastolic dysfunction was present in 26% of patients wit
273                                              Diastolic dysfunction was present in 66% of gradable par
274                                     Baseline diastolic dysfunction was present in 770 patients (72.3%
275                                              Diastolic dysfunction was present in WES+DHA rats compar
276                                  The risk of diastolic dysfunction was significantly higher in overwe
277 ial volume index (an indicator of chronic LV diastolic dysfunction) was significantly increased at 2
278 rdial stiffness, consistent with upheld(101) diastolic dysfunction, was confirmed by an atomic force
279 ry capillary wedge pressure, consistent with diastolic dysfunction, was present in 15 patients (75%).
280 more, parameters reflecting left ventricular diastolic dysfunction were more pronounced in advanced N
281                                      Age and diastolic dysfunction were positively and statin use was
282 left atrial dimension (19%; indicative of LV diastolic dysfunction) when compared with WT.
283 excess left ventricular (LV) hypertrophy and diastolic dysfunction; whether this occurs also in secon
284  (left ventricular hypertrophy, fibrosis and diastolic dysfunction), while the phenotype of vascular
285 in db/db mice, but protected from myocardial diastolic dysfunction, while causing left ventricular ch
286  diabetic cardiac hypertrophy, fibrosis, and diastolic dysfunction, while preserving normal cardiac g
287 xpressing alpha-TM-D137L showed systolic and diastolic dysfunction with decreased myofilament Ca(2+)
288 sed passive stiffness is sufficient to cause diastolic dysfunction with exercise intolerance.
289 eas deficient cMyBP-C phosphorylation causes diastolic dysfunction with HFpEF in cMyBP-C(t3SA) mice.
290 t-HT demonstrated biventricular systolic and diastolic dysfunction with most prominent impairment in
291 progressive left ventricular hypertrophy and diastolic dysfunction with preservation of systolic func
292 ial (LA) enlargement and dysfunction, and LV diastolic dysfunction with preserved systolic function,
293 d by progressive left atrial enlargement and diastolic dysfunction with preserved systolic function.
294 rdiography showed concentric hypertrophy and diastolic dysfunction, with preserved systolic function
295 mpaired transmitral flow indicative of early diastolic dysfunction within 5 weeks.
296 tinguish patients with HFpEF from those with diastolic dysfunction without heart failure.
297 has been broadly defined as left ventricular diastolic dysfunction without the diagnosis of congestiv
298 ly defined as subjects with left ventricular diastolic dysfunction, without the diagnosis of congesti
299 ral chemoreflex pathway in HFpEF exacerbates diastolic dysfunction, worsens sympatho-vagal imbalance
300 ter, mean limb lead QRS voltage, and grade 3 diastolic dysfunction yielded excellent discriminatory c

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