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Circulation. 2003;108:1044-1048
doi: 10.1161/01.CIR.0000085656.57918.B1
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(Circulation. 2003;108:1044.)
© 2003 American Heart Association, Inc.


Clinician Update

Resynchronization Therapy for the Treatment of Heart Failure

Leslie A. Saxon, MD; Kenneth A. Ellenbogen, MD

From the University of Southern California University Hospital, Los Angeles, Calif (L.A.S.), and the Medical College of Virginia, Richmond, Va (K.A.E.).

Correspondence to Kenneth A. Ellenbogen, MD, Medical College of Virginia, PO Box 980053, Richmond, VA 23298-0053. E-mail kellenbogen@pol.net


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


*    Introduction
 
Heart failure remains a major cardiovascular health problem, afflicting 22 million individuals worldwide and approximately 5 million persons in the United States alone. Management of patients with this problem represents the largest single expense to Medicare. A common feature predictive of adverse clinical outcomes in patients with congestive heart failure is prolongation of the QRS duration. Several different types of studies suggested QRS delay was an independent risk factor for adverse outcome, particularly in patients with left ventricular dysfunction.1,2 These data were derived from both longitudinal population studies and retrospective studies performed in heart failure patients with pacemakers and "acquired" left bundle branch block (LBBB).1,2 The significance of QRS delay in heart failure patients is that this common finding may be observed in up to 30% of patients with moderate to severe heart failure.

Acute studies performed with hemodynamic measurements and nuclear imaging phase analysis demonstrate that QRS delay, particularly LBBB, creates electrical and mechanical dyssynchrony in patients with depressed left ventricular function. Delayed and inhomogeneous left ventricular activation reduces stroke volume, left ventricular ejection fraction, and time for aortic ejection. Reductions in left ventricular dP/dT, increased left ventricular end-systolic and diastolic volumes, and abnormal patterns of wall stretch are also seen.3–5 Additionally, ventricular dyssynchrony promotes functional mitral regurgitation. Acutely pacing the right and left ventricle simultaneously or pacing the left ventricle alone results in marked improvements and restoration of a more homogeneous contraction pattern (Figure 1 and Figure 2Down).


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Figure 1. The upper panels represent phase images . . . [Full Text of this Article]




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