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(Hypertension. 2006;47:343.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

Cardiac Glycosides and Cardiomyopathy

Paolo Manunta; Mara Ferrandi

From the Division of Nephrogy (P.M.), Dialysis and Hypertension, University "Vita-Salute" San Raffaele, Milan, and Prassis Sigma-Tau Research Institute (M.F.), Settimo Milanese, Italy.

Correspondence to Paolo Manunta, MD, Division of Nephrogy, Dialysis and Hypertension, University "Vita-Salute" San Raffaele, Via Olgettina, 60, 20132 Milan, Italy. E-mail manunta.paolo@hsr.it

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Digitalis-like steroids and related agents have been a mainstay in the treatment of congestive heart failure ever since the publication, in 1785, of Withering’s seminal monograph on foxglove. Heart failure refers to the clinical syndrome that results when the heart is unable to pump sufficient blood to keep up with the metabolic demands of the body. Congestive heart failure is characterized by excessive neuronal and hormonal-mediated fluid retention, expanded intravascular volume, high pulmonary and systemic venous pressures with consequent dyspnea (shortness of breath) on exertion, reduced exercise tolerance, and fatigue. Most heart failure patients also have impaired ventricular systolic function and depressed cardiac output; these are the patients most often treated with digitalis glycosides. These drugs are positive inotropic agents and enhance cardiac contraction. The "cardiotonic steroids" cause cardiac muscle to lose K⁺ and gain Na⁺ because they inhibit the Na⁺ pump (Na⁺,K⁺–ATPase), a plasma membrane protein, present in all cells. The Na⁺ pump uses the energy from ATP to extrude Na⁺ and to maintain the large Na⁺ electrochemical gradient across the plasma membrane.

How does inhibition of the Na⁺ pump augment cardiac contraction? The discovery of the Na⁺-Ca²⁺ exchanger and sarcoplasmic reticulum Ca²⁺ ATPase (Serca) has provided the missing link between Na⁺ pump inhibition and delivery of Ca²⁺ to enhance contractility.¹ An increase of Na⁺-Ca²⁺ exchanger at the plasma membrane and/or a reduced Serca activity may contribute to increased intracellular Ca²⁺ concentrations leading to increased contractility. In 1997, the Digitalis Investigative Group reported on a . . . [Full Text of this Article]

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