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1 rity, and rescue animals from sepsis-induced myocardial failure.
2 ular hypertrophy followed by a transition to myocardial failure.
3 N apoptosis may serve as biologic markers of myocardial failure.
4 ons for the pathophysiology and treatment of myocardial failure.
5 as been implicated in the pathophysiology of myocardial failure.
6 yocytes may contribute to the progression of myocardial failure.
7 were independent risk factors for death and myocardial failure.
8 ons of segmental function that precede overt myocardial failure.
9 significantly increased in individuals with myocardial failure, a condition associated with increase
10 mmunodeficiency virus infection, septicemia, myocardial failure, atherosclerosis, metabolic disorders
11 ase (CAD) who died suddenly, 32% who died of myocardial failure, but in non-CAD patients, they were p
12 a may contribute to ventricular dilation and myocardial failure by promoting the remodeling of inters
14 nts) with SD and 40% (6 of 15 patients) with myocardial failure did not have the MI diagnosed during
15 MI was classified as "sudden unexpected" or "myocardial failure" from clinical information only, the
19 he mechanisms by which interleukin 6 induces myocardial failure in meningococcal sepsis and to identi
22 n from compensatory concentric remodeling to myocardial failure is not completely understood in human
24 e overloading may eventually decompensate to myocardial failure, mechanisms responsible for this tran
25 involved children who died from intractable myocardial failure preceded by a metabolic acidosis, lip
27 AR function contribute to the development of myocardial failure, transgenic mice with cardiac-restric
29 t in the intrinsic defect(s) responsible for myocardial failure will likely translate into important
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