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1 -expressing mice, even prior to the onset of ventricular failure.
2 e animals that received L-NAME died of right ventricular failure.
3 was used as a molecular phenotypic marker of ventricular failure.
4 ancy with the development of angina and left ventricular failure.
5 ed, in contrast to what is described in left ventricular failure.
6 ascular resistance and, eventually, in right ventricular failure.
7 ling of the pulmonary vasculature, and right ventricular failure.
8 eath contributing to the progression of left ventricular failure.
9 artery pressure, often culminating in right ventricular failure.
10 can progress and result in progressive right ventricular failure.
11 t ventricular dysfunction and nine had right ventricular failure.
12 sfunction, pulmonary hypertension, and right ventricular failure.
13 tive heart failure died from refractory left ventricular failure.
14 ysiology, assessment and management of right ventricular failure.
15 es for the diagnosis and management of right ventricular failure.
16 ublished practice guideline focused on right ventricular failure.
17 to extensive left ventricular infarction and ventricular failure.
18 othoracic surgery, require therapy for right ventricular failure.
19 tients with pulmonary hypertension and right ventricular failure.
20 complicated by cardiogenic shock due to left ventricular failure.
21 death has been questioned as a mechanism of ventricular failure.
22 or beta(1)AR have resulted in phenotypes of ventricular failure.
23 R with 884 patients who had predominant left ventricular failure.
24 and early mortality due to systemic (right) ventricular failure.
25 on results in bradycardia and development of ventricular failure.
26 ction than patients under 60 years with left-ventricular failure.
27 dial infarction, Q wave infarction, and left-ventricular failure.
28 t were not associated with clinical systemic ventricular failure.
31 ry hypertension, which can progress to right ventricular failure, an important cause of morbidity and
33 wave reflections in the pathogenesis of left ventricular failure and cardiovascular disease, but thei
38 trials: the Prospective Randomized study Of Ventricular failure and Efficacy of Digoxin (PROVED) and
39 antially affected by the development of left-ventricular failure and other clinical indices, such tha
47 ely to develop complications related to left ventricular failure, and have improved early and late su
48 sulting in systemic hypertension, acute left ventricular failure, and multiple cardiac arrhythmias al
49 in their practice, but until recently right ventricular failure as a primary clinical entity receive
50 ently elevated in patients with chronic left ventricular failure as a result of dysregulation of vasc
51 pression of Galphaq develop progressive left ventricular failure associated with myocyte contractile
52 eta-blockers in patients with isolated right ventricular failure because of pulmonary arterial hypert
53 rative period were not attributable to right ventricular failure (chronic thromboembolic pulmonary hy
54 se, with higher rates of both for those with ventricular failure, compared with patients who had mech
56 of the Glenn or Fontan procedure, including ventricular failure, cyanosis, protein-losing enteropath
57 hat in atrial myocytes from hearts with left ventricular failure, enhanced CaTs during ECC exert posi
58 reful perioperative attention to avoid right ventricular failure from acutely elevated pulmonary arte
61 Patients aged 70 years or older without left-ventricular failure had significantly better survival at
62 tients who underwent angiography, those with ventricular failure had significantly lower in-hospital
64 es of impaired adrenergic signaling in right ventricular failure/hypertrophy (RVH) are poorly underst
65 ogressive SAVV regurgitation causes systemic ventricular failure in CCTGA patients, who are commonly
66 rious side effects were exacerbation of left ventricular failure in patients with congestive heart fa
67 if patient survival and mechanisms of right ventricular failure in pulmonary hypertension could be p
68 focus on the pathophysiology of acute right ventricular failure in the critical care setting and sum
69 ith low oxygen saturation; treatment of left ventricular failure in those with postcapillary pulmonar
70 ost common serious adverse events were right ventricular failure (in 3% of patients in each group) an
72 n was associated with hemodynamic changes of ventricular failure including lower resting ejection fra
75 ble hemodynamic threshold beyond which right ventricular failure is certain to occur, nor are there v
78 rial Registry patients with predominant left ventricular failure (LVF) were divided into four groups:
80 ics, critical illness, intensive care, right ventricular failure, mitral stenosis, prostacyclin, nitr
81 ased pulmonary vascular resistance and right ventricular failure; morbidity and mortality remain unac
83 cohort died of their disease; however, right ventricular failure or sudden death was the sole cause o
86 e cardiogenic shock is due primarily to left ventricular failure, other causes such as acute mitral r
89 It is usually seen as a consequence of left ventricular failure, pulmonary embolism, pulmonary hyper
90 sing the search words right ventricle, right ventricular failure, pulmonary hypertension, sepsis, sho
92 : age over 65 years, hypertension, diabetes, ventricular failure, rheumatic valvular disease, and pri
93 ratio>0.6) of whom four patients had a right ventricular failure (right ventricular end-diastolic are
94 Critical care specialists encounter right ventricular failure routinely in their practice, but unt
96 OF REVIEW: Pulmonary hypertension and right ventricular failure (RVF) in left ventricular systolic d
98 rowth hormone administered to rats with left ventricular failure starting 1 month after MI was associ
99 al work elucidating the pathobiology of left ventricular failure, there is a paucity of data on the c
100 overall and by shock etiology: left or right ventricular failure versus mechanical complications.
108 tanding of the molecular mechanisms of right ventricular failure will lead to the development of new
109 h sudden cardiovascular collapse, acute left ventricular failure with pulmonary edema, disseminated i
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