doi: 10.1161/CIRCULATIONAHA.105.578153
(Circulation. 2005;112:2891-2893.)
© 2005 American Heart Association, Inc.
Editorial |
Heart Failure Research Continues to Reveal the Flaws in Nature’s Unintelligent Design
From Whitaker Cardiovascular Institute and Molecular Stress Response Unit, Department of Medicine, Boston University School of Medicine, Boston, Mass.
Correspondence to Douglas B. Sawyer, MD, PhD, Whitaker Cardiovascular Institute and Molecular Stress Response Unit, Department of Medicine, Boston University School of Medicine, Boston, MA 02118. E-mail douglas.sawyer@bmc.org
Key Words: Editorials • genes • heart failure
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Current therapy of patients with systolic heart failure focuses on protecting the patient from the chronic activation of hemodynamic reflexes that are activated by decreased tissue perfusion. The same renin-angiotensin, aldosterone, and adrenergic agonists that work in concert to dynamically regulate salt and water homeostasis and tissue perfusion throughout life become the cause of tissue edema, cardiac remodeling, and disease progression in the setting of impaired cardiac function. Although these and other regulators of cardiovascular homeostasis are complex and "highly evolved," their pathophysiologic role in heart failure points out a design flaw of nature. From the point of view of an evolutionary biologist, this arguably "unintelligent design" flaw can be recognized as a consequence of natural selection. Survival of individuals with the ability to dynamically regulate cardiac output, regional blood flow, and salt and water homeostasis in a stressful environment favors a robust neurohormonal system. Although less obvious, it seems reasonable to argue that the now clearly recognized deleterious effects of the neurohormonal response to decreased cardiac function would exert significant negative selection pressure. This latter argument is based on the fact that cardiac injury is rare before reproduction. Fortunately, years of inspired research have unraveled these design flaws, and pharmacological agents have been developed for heart failure patients to protect them from this example of "nature gone bad." Thank God!?
Article p 2930
The story of serum response factor (SRF), highlighted in a study by Parlakian et al in this issue of Circulation,1 illustrates how another of nature’s
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