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1 an presented with palpitations and decreased exercise tolerance.
2 Patients with HOCM have reduced exercise tolerance.
3 tion of iron might improve both symptoms and exercise tolerance.
4 or did it decrease cardiomyopathy or restore exercise tolerance.
5 eceptor antagonists abolished differences in exercise tolerance.
6 urthermore, it reduces symptoms and improves exercise tolerance.
7 ansport and utilization of O(2), diminishing exercise tolerance.
8 > or =10 have objective evidence of reduced exercise tolerance.
9 low relaxation and E/Ea > or =10 had reduced exercise tolerance.
10 ostcontraction vasodilatation may compromise exercise tolerance.
11 k of death or MI, but it improved angina and exercise tolerance.
12 y disease (CAD), more severe CAD and a lower exercise tolerance.
13 implications for novel therapies to improve exercise tolerance.
14 ant of exercise hyperventilation and reduced exercise tolerance.
15 f (VE/VCO(2)) in CHF patients with preserved exercise tolerance.
16 atients with known or suspected CAD and high exercise tolerance.
17 le, objective, and physiologic expression of exercise tolerance.
18 fore and after the operation showed improved exercise tolerance.
19 lower V(E); this is associated with improved exercise tolerance.
20 on for Ebstein's anomaly results in improved exercise tolerance.
21 subgroup with symptomatic ischemia and poor exercise tolerance.
22 ronic diabetic neuropathic pain and improves exercise tolerance.
23 ing to short-term improvement in dyspnea and exercise tolerance.
24 acco history developed a cough and decreased exercise tolerance.
25 nt in left ventricular ejection fraction and exercise tolerance.
26 ked sarcolemmal fragility and reduced muscle exercise tolerance.
27 at rest occur in conjunction with excellent exercise tolerance.
28 ible benefits to reduce symptoms and improve exercise tolerance.
29 contribution to ATP synthesis, and increased exercise tolerance.
30 rgement, impaired lung function, and reduced exercise tolerance.
31 ificant improvements in angina frequency and exercise tolerance.
32 duced muscle oxidative function and impaired exercise tolerance.
33 pact on ventricular volume and function, and exercise tolerance.
34 h and nine studies examining their effect on exercise tolerance.
35 a deficit in AMPK activity markedly impairs exercise tolerance.
36 pulmonary neutrophilia and the reduction in exercise tolerance.
37 nd leads to an improvement in LV filling and exercise tolerance.
38 oxidative myofibers, muscle vasculature, and exercise tolerance (33%) are decreased in mdx vs. wild-t
40 ion group than in the medical-therapy group (exercise tolerance, 5.0 MET [metabolic equivalent] vs. 3
47 nexplained exertional dyspnea and diminished exercise tolerance after deployment, an analysis of biop
49 substantial relief of symptoms and improved exercise tolerance and also showed reduced or abolished
50 ults highlight a critical role for TBC1D1 in exercise tolerance and contraction-mediated translocatio
51 tors responsible for development of impaired exercise tolerance and disease progression are incomplet
53 ues to show promise as a method of improving exercise tolerance and enhancing oxidative capacity.
55 horacic radiation therapy (RT) have impaired exercise tolerance and increased cardiovascular mortalit
56 llbeing, but molecular mechanisms underlying exercise tolerance and its plasticity are only partially
57 -dose nitrate therapy significantly improves exercise tolerance and left ventricular size and systoli
58 ble long-term benefit was a trend for better exercise tolerance and less depression of quality of lif
61 tion during exercise in hypoxia and restored exercise tolerance and oxidative function to values obse
64 lated lipid metabolism, leading to increased exercise tolerance and protection against diet-induced o
66 f intravenous iron found improved short-term exercise tolerance and quality of life in patients with
71 tricular resection, including reduced animal exercise tolerance and sudden death in the setting of st
72 hese observations may play a role in reduced exercise tolerance and tachycardia-induced diastolic dys
73 dine produces dose-dependent improvements in exercise tolerance and time to development of ischemia d
74 rease in QRS duration and a deterioration of exercise tolerance and ventricular dysfunction did not p
77 e abnormalities are associated with impaired exercise tolerance, and abnormal HRR predicts increased
78 anadian Cardiovascular Society angina class, exercise tolerance, and antianginal medications), myocar
79 pathy (MM) associated with varying levels of exercise tolerance, and compared responses with those in
80 put, and resulted in weight loss, diminished exercise tolerance, and enhanced susceptibility to induc
82 uced left ventricular hypertrophy, increased exercise tolerance, and improved quality of life, the op
83 lated with poor functional status, decreased exercise tolerance, and invasive hemodynamics variables.
84 ed with less pulmonary regurgitation, better exercise tolerance, and less QRS prolongation and sympto
85 sociated with improved ventricular function, exercise tolerance, and long-term survival in patients w
86 reduction in anginal symptoms, increases in exercise tolerance, and objective improvements in myocar
89 progression, as reflected by lung function, exercise tolerance, and progression-free survival, in pa
90 ostacyclin, PGI2) improves haemodynamics and exercise tolerance, and prolongs survival in severe PPH
91 aningful benefits in lung function, dyspnea, exercise tolerance, and quality of life, with an accepta
94 blood analyses, pulmonary function testing, exercise tolerance, and quality-of-life assessment at 0,
95 in skeletal muscle mitochondrial biogenesis, exercise tolerance, and response to exercise training.
96 rovements in heart failure-related symptoms, exercise tolerance, and reversal of ventricular remodeli
97 m bacterial densities, inflammatory markers, exercise tolerance, and subjective well-being did not ch
98 nduced modest improvements in lung function, exercise tolerance, and symptoms at the cost of more fre
99 s lung tissue and may improve lung function, exercise tolerance, and symptoms in patients with emphys
100 exacerbations, weight gain, quality of life, exercise tolerance, and the total costs of hospital and
101 ysfunction are associated with impairment in exercise tolerance as assessed by peak oxygen consumptio
102 ttle Angina Questionnaire and improvement in exercise tolerance as assessed by treadmill exercise tes
103 s outpatients for assessment of symptoms and exercise tolerance as measured by change in the NYHA cla
104 that lung volume reduction surgery improves exercise tolerance as measured by the 6-min walk distanc
109 hanges in lung function, quality of life, or exercise tolerance between roflumilast- and placebo-trea
110 umber of clinical parameters, lung function, exercise tolerance, biomarkers, and amount of emphysema
111 d QRS duration were univariate predictors of exercise tolerance, but only t-IVT and CAD were independ
113 ure, and blood flow (by 33-66%) and improved exercise tolerance (by 75%) in the dystrophic mice.
115 included functional class and improvement in exercise tolerance, cardiac index, and mean pulmonary ar
117 ores for a given work rate leading to poorer exercise tolerance compared with their counterparts (P <
118 nts with ERVSP > or = 40 mm Hg had decreased exercise tolerance compared with those with ERVSP <40 mm
120 roved collateral vessel function and enhance exercise tolerance during routine physical activity.
121 d desaturation, we evaluated improvements in exercise tolerance facilitated by a wearable, 1-lb, noni
122 m to be required for body weight regulation, exercise tolerance, fatty acid oxidation, or cold-induce
123 r patients have had sustained improvement in exercise tolerance, from 3.5 mo to 4.5 yr after stent pl
124 Baseline predictors of survival included exercise tolerance, functional class, right atrial press
129 he hypothesis that intravenous iron improves exercise tolerance in anemic and nonanemic patients with
130 both TKO and TXNIP(SKM-/-) mice had reduced exercise tolerance in association with muscle-specific i
131 ACE DD genotype is associated with decreased exercise tolerance in CHF, possibly mediated by altered
133 n vivo, which has important implications for exercise tolerance in health and certain disease states
134 hether chronotropic incompetence and reduced exercise tolerance in HF are attributable to beta-blocka
138 (The Influence of Heart Rate Limitation on Exercise Tolerance in Pacemaker Patients [TREPPE]; NCT02
141 giotensin II (Ang II) blockade would improve exercise tolerance in patients with diastolic dysfunctio
142 is study was to identify the determinants of exercise tolerance in patients with Ebstein's anomaly.
143 fferent rate or rhythm control strategies on exercise tolerance in patients with HFpEF and AF is warr
144 e mechanisms linking dynamic obstruction and exercise tolerance in patients with hypertrophic obstruc
145 e that may thereby improve lung function and exercise tolerance in patients with pulmonary hyperinfla
146 ernal counterpulsation improves symptoms and exercise tolerance in patients with symptomatic coronary
147 eintroduced to alleviate dyspnea and improve exercise tolerance in selected patients with emphysema.
149 supplementation on endothelial function and exercise tolerance in stable coronary artery disease (CA
151 ting demonstrated significant improvement in exercise tolerance in TAC/DOCA mice that expressed N2BAs
154 ated and comparable to enalapril in terms of exercise tolerance in this short-term (12-week) study of
155 in immunofluorescence assays (P < 0.05) and exercise tolerance in treadmill tests (P < 0.05), wherea
156 g allograft dysfunction can be subdivided by exercise tolerance in two groups, and quality of life (Q
158 s been independently associated with reduced exercise tolerance, increased heart failure hospitalizat
160 in GLUT4(-/-)HK(Tg) show that HK II improves exercise tolerance, independent of its effects on MGU.
163 ay, therefore, dictate intensities for which exercise tolerance is determined by the magnitude of fat
166 he age of 3-4 mo, and maximal stress-induced exercise tolerance is reduced, indicating impaired physi
168 therapy, improves symptoms, quality of life, exercise tolerance, left ventricular function, and the s
171 dvanced lung allograft dysfunction regarding exercise tolerance might result from altered IC and impa
176 Losmapimod did not cause an improvement in exercise tolerance or lung function, despite being well-
177 acoronary infusion of rFGF2 does not improve exercise tolerance or myocardial perfusion but does show
178 ng: an improvement of at least 25 percent in exercise tolerance or pulmonary-function tests or resolu
180 ed with a greater improvement in symptoms or exercise tolerance or with a reduction in the rate of de
181 erance, such as advanced age, diabetes, poor exercise tolerance, or history of myocardial infarctions
182 oxygen saturation is the major predictor of exercise tolerance, oxygen saturation at peak exercise a
183 ith reduced muscle mass, abnormal indexes of exercise tolerance (peak V(O2), V(E)/V(CO2) slope), ejec
184 ymptomatic state (NYHA class, P<0.05), lower exercise tolerance (peak VO(2), P<0.05), and pronounced
186 costs of chronic inflammation and to foster exercise tolerance provide a rationale for therapeutic u
187 rtant clinical implications, such as reduced exercise tolerance, quality of life, and even survival.
188 domized, single-blinded study, EECP improved exercise tolerance, quality of life, and NYHA functional
189 he placebo group, P=.01) but did not improve exercise tolerance, quality of life, or the need for hos
190 ideline included mortality; hospitalization; exercise tolerance; quality of life; and cardiovascular
191 patients with otherwise unexplained impaired exercise tolerance; recurrent lower airways infection; a
193 Baseline assessments were angina class, exercise tolerance, Seattle angina questionnaire for qua
195 y class (MD, -0.58; 95% CI, -1.00 to -0.16), exercise tolerance (standardized MD, 0.331; 95% CI, 0.08
196 in brachial artery endothelial function and exercise tolerance, suggesting a potential mechanism by
197 py use from baseline for pulmonary function, exercise tolerance, survival, hospital admission, and ad
199 Case series have shown that EECP can improve exercise tolerance, symptoms and myocardial perfusion in
200 a and enhances functional capacity during an exercise tolerance test (ETT) in patients with coronary
201 on or myocardial infarction (MI), with a pre-exercise tolerance test (ETT) likelihood of CAD > or =0.
202 postinfarction angina or a strongly positive exercise tolerance test (ETT) typically had cost-effecti
203 , exercise, and nuclear models by use of pre-exercise tolerance test (ETT), post-ETT, and nuclear inf
206 s were similar in the 2 approaches, with the exercise tolerance test result exerting the greatest lev
207 cumented coronary artery disease, a positive exercise tolerance test, and stable chronic angina pecto
208 Efficacy was evaluated at 90 and 180 days by exercise tolerance test, myocardial nuclear perfusion im
209 depression > or =1 mm from baseline) during exercise tolerance testing (ETT) was examined in patient
211 principally in middle-aged men, suggest that exercise tolerance testing can provide independent progn
214 le cohort studies demonstrate that screening exercise tolerance testing identifies a small proportion
215 ta-blocker therapy underwent cardiopulmonary exercise tolerance testing under 2 conditions in random
217 nsional echocardiography, Holter monitoring, exercise tolerance testing, and ajmaline provocation.
218 to limiting angina during bicycle exercise (exercise tolerance tests), performed at trough of drug a
219 musclin secretion in mice results in reduced exercise tolerance that can be rescued by treatment with
220 al care resulted in an improvement in median exercise tolerance that was modest and of uncertain clin
221 th chronic heart failure (CHF) and preserved exercise tolerance, the value of cardiopulmonary exercis
222 - 0.8 mo) showed significant improvements in exercise tolerance: The distance covered over a 6 min wa
223 to guide management of patients with limited exercise tolerance, those at highest risk for perioperat
226 stress allows an assessment of the patient's exercise tolerance, to be performed while adequately str
227 ly associated with decreased muscle mass and exercise tolerance; untreated LH/FSHD was associated wit
231 f patients were relieved of angina symptoms, exercise tolerance was improved, complications were mini
238 nflammation, lung mechanical properties, and exercise tolerance were determined at different time poi
242 ng patients in the assessment of symptoms or exercise tolerance while expanding the range of patients
243 often performed in stable patients with good exercise tolerance who have not been treated with proven
244 ion) and 60 patients with stage B HF (normal exercise tolerance with left ventricular hypertrophy, an
245 s with elevated HDGF had significantly lower exercise tolerance, worse New York Heart Association fun
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