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(Hypertension. 2006;47:830.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

Understanding Diastolic Heart Failure With Preserved Ejection Fraction

Choosing the Right Model

David E. Dostal; Linley E. Watson

From the Division of Molecular Cardiology (D.E.D.), Cardiovascular Research Institute, Texas A&M University System Health Science Center, College of Medicine, Temple, Tex; and Division of Cardiology (L.E.W.), Scott & White Memorial Hospital, Temple, Tex.

Correspondence to David E. Dostal, Division of Molecular Cardiology, 1901 South 1st St, Bldg 205, Central Texas Veterans Health Care System, Temple, TX 76504. E-mail ddostal@medicine.tamhsc.edu

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

	Introduction

 
Congestive heart failure (HF) is a frequent reason for hospital admission. Fifty percent of HF hospitalizations have normal ejection fraction (EF),¹ referred to as diastolic HF (DHF). In contrast, patients with systolic HF (SHF) have reduced EF. The DHF phenotype describes patients with signs and symptoms of HF, normal EF, normal left ventricular (LV) volume, hypertension with increased relative wall thickness, LV diastolic dysfunction, and predominantly elderly women.^1,2

	Etiology of DHF

 
Longstanding hypertension may result in significant myocardial hypertrophy, appearance of a smaller ventricular chamber, increased ventricular stiffness, and delayed relaxation. Increased ventricular stiffness requires increased pressure to maintain normal filling in the presence of normal or reduced chamber volume.³ Although DHF has not been studied as extensively as SHF, limited data obtained from patients hospitalized for DHF suggest that demographic characteristics, comorbidities, and pathology differ from those with SHF. Despite these differences, DHF is similar to SHF with regard to volume overload, reduced exercise capacity, impaired quality of life, and long-term mortality.¹

	Casual Mechanisms

 
Impaired Active Relaxation
Diastole consists of active relaxation and passive filling of the ventricle. Diastolic dysfunction can be caused by mechanisms intrinsic to the cardiac muscle cells. These include changes in calcium homeostasis resulting from abnormalities in calcium extrusion, decreased uptake of cytosolic calcium by the sarcoplasmic reticulum calcium ATPase pump (SERCA), and changes in the phosphorylation state or levels of proteins (eg, phospholamban, calmodulin, and calsequestrin) that modify SERCA.³ Because active relaxation is energy dependent, impaired diastolic filling is the first manifestation of work-induced ischemia, which is reflected by an upward shift . . . [Full Text of this Article]

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