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(Circulation. 2004;109:1694-1696.)
© 2004 American Heart Association, Inc.

Focused Perspective

Single Site Left Ventricular Pacing for Cardiac Resynchronization

William G. Stevenson, MD; Michael O. Sweeney, MD

From the Cardiovascular Division, Department of Internal Medicine, Brigham and Women’s Hospital, Boston, Mass.

Correspondence to William G. Stevenson, MD, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail wstevenson{at}partners.org

Key Words: Focused Perspectives • pacing • heart failure • ventricles

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

Chronic, dilated heart failure is often accompanied by delayed ventricular electrical activation manifested as prolonged QRS duration, most commonly in the form of left bundle branch block (LBBB). Exploration of the link between the sequence of cardiac electrical activation and mechanical function is one of the most exciting contemporary areas of research in heart failure, but recognition of the importance of normal ventricular activation patterns for optimal myocardial mechanical performance dates back 75 years. Wiggers¹ observed that asynchronous delayed activation of the ventricular musculature induced by electrical stimulation had adverse hemodynamic consequences in mammals, and he proposed that the more muscle activated before excitation of the Purkinje system, the greater the asynchrony and the weaker the resulting contraction. Forty years later, Schlant² concluded that asynchronous ventricular activation imposed by LBBB was hemodynamically disadvantageous and coined the term "idioventricular kick" to describe the benefit imparted by coordinated activation. Subsequent studies demonstrated that when one segment of the ventricle, such as the septum, contracts earlier than another segment, such as the lateral wall, the second segment stretches, absorbing some of the initial force, and then begins its late contraction, stretching the first segment.^3,4 The resulting contraction is mechanically inefficient, with diminished ejection at an increased metabolic cost. Reductions of myocardial blood flow and wall thickness occur in the region of early activation, a remodeling effect that could theoretically contribute to progression of heart failure.^5,6

See p 1741

In 1984, de Teresa et al⁷ demonstrated that changing the sequence of ventricular activation by . . . [Full Text of this Article]

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Circulation 2004 109: 1741-1744. [Abstract] [Full Text]

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