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(Hypertension. 2004;44:623.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Fueling the Hypertrophied Heart

From the Albert Einstein College of Medicine, Bronx, NY.

Correspondence to James Scheuer, Division of Cardiology, Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461. E-mail scheuer@aecom.yu.edu

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

Substrate utilization by heart muscle provides the fuel for both maintenance of structure and function of the myocardium and for ample reserve capacity to meet sudden surges in cardiac energy requirements. Many factors influence the balance of substrate uptake by the myocardium, but in general, utilization of lipids versus carbohydrates correlates to their concentration in the arterial blood.

There is evidence in humans that severe cardiomyopathy and heart failure are accompanied by alterations in the balance of substrates used and of energy reserves, and these may limit myocardial function.¹ However, myocardial metabolic changes have not been well described in human hearts with compensated hypertrophy.

Compensated cardiac hypertrophy due to systolic overload in experimental animals is associated with a recapitulation of a fetal genetic pattern.^2,3 This is most dramatically demonstrated in the hearts of rodents in which their contractile proteins switch from a predominance of -myosin to a more energy conserving ß-myosin pattern,⁴ but also involves enzymes in metabolic pathways of energy transfer.² Many of these genetic alterations affect reactions that influence the balance between carbohydrate and lipid use by the heart. GLUT-4 protein, the main insulin sensitive glucose transporter may be normal or its mRNA reduced.^5,6 GLUT-4 deletion leads to hypertrophy and upregulation of GLUT-1, a glucose independent transporter, and to enhanced insulin independent glucose transport.⁷ However, selective GLUT-1upregulation protects heart function, but may also promote cardiac hypertrophy.⁸ On the lipid side, transcription of PPAR- and other genes related to fatty acid oxidation is also reduced.³ If an imbalance between . . . [Full Text of this Article]