2014•Unpublished venueRequires access

References for Section II

William J. Rea, Kalpana Patel

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Abstract

Until the early 1990s, the prevailing paradigm of heart failure pathophysiology involved impaired contractility, pump failure, and declining hemodynamics. Changes in pressure, volume, and ow were thought to be directly responsible not only for the immediate symptoms but also for the progressive worsening of the disease. However, clinical trials with agents that favorably altered acute hemodynamics by decreasing peripheral vasoconstriction or increasing contractility failed to change the natural history of heart failure. In the authors’ opinion, this is because triggering agents were not removed, including environmental toxins, which, along with the hypoxia, deteriorate the system. In addition, nutrients were not adequately replaced, which, if they had been, would help the individual cope with his or her altered metabolism.

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What this paper is about

Until the early 1990s, the prevailing paradigm of heart failure pathophysiology involved impaired contractility, pump failure, and declining hemodynamics. Changes in pressure, volume, and ow were thought to be directly responsible not only for the immediate symptoms but also for the progressive worsening of the disease. However, clinical trials with agents that favorably altered acute hemodynamics by decreasing peripheral vasoconstriction or increasing contractility failed to change the natural history of heart failure. In the authors’ opinion, this is because triggering agents were not removed, including environmental toxins, which, along with the hypoxia, deteriorate the system. In addition, nutrients were not adequately replaced, which, if they had been, would help the individual cope with his or her altered metabolism.

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Available abstract

Until the early 1990s, the prevailing paradigm of heart failure pathophysiology involved impaired contractility, pump failure, and declining hemodynamics. Changes in pressure, volume, and ow were thought to be directly responsible not only for the immediate symptoms but also for the progressive worsening of the disease. However, clinical trials with agents that favorably altered acute hemodynamics by decreasing peripheral vasoconstriction or increasing contractility failed to change the natural history of heart failure. In the authors’ opinion, this is because triggering agents were not removed, including environmental toxins, which, along with the hypoxia, deteriorate the system. In addition, nutrients were not adequately replaced, which, if they had been, would help the individual cope with his or her altered metabolism.

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