4.7 Article

Persistent Hemodynamic Benefits of Cardiac Resynchronization Therapy With Disease Progression in Advanced Heart Failure

Journal

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 53, Issue 7, Pages 600-607

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2008.08.079

Keywords

heart failure; hemodynamics; pacing; remodeling

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Objectives Our aim was to determine the potential hemodynamic contributions of cardiac resynchronization therapy (CRT) in patients admitted for advanced decompensated heart failure. Background CRT restores synchrony of the heart resulting in hemodynamic support that can facilitate the reversal of left ventricular (LV) remodeling in some patients. Methods A total of 40 consecutive patients with advanced decompensated heart failure and CRT implanted >3 months, admitted due to hemodynamic derangements, underwent simultaneous comprehensive echocardiographic and invasive hemodynamic evaluation under different CRT settings. Results All patients (mean LV ejection fraction 22 +/- 7%, LV end-diastolic volume 323 +/- 140 ml, 40% ischemic) had experienced progressive cardiac remodeling despite adequate LV lead positions and continuous biventricular pacing. A significant worsening of hemodynamics was observed immediately when CRT was programmed OFF in the majority (88%) of patients (systolic blood pressure: 105 +/- 12 mm Hg to 98 +/- 13 mm Hg; pulmonary capillary wedge pressure: 17 +/- 6 mm Hg to 21 +/- 7 mm Hg; cardiac output: 4.6 +/- 1.4 l/min/m(2) to 4.0 +/- 1.1 l/min/m(2); all p < 0.001). Worsening of hemodynamics coincided with reappearance of significant electrical (QRS width 161 +/- 29 ms to 202 +/- 39 ms, p < 0.001) and intraventricular mechanical dyssynchrony (15 +/- 26 ms to 57 +/- 41 ms, p < 0.001), together with a significant reduction in diastolic filling time (377 +/- 138 ms to 300 +/- 118 ms, p < 0.001). Conclusions Despite progressive cardiac remodeling and decompensation, chronic CRT continues to provide hemodynamic augmentation in the failing heart in most patients. Our data suggest that disease progression may not be explained by diminished beneficial hemodynamic contributions of successful resynchronization. (J Am Coll Cardiol 2009; 53: 600-7) (C) 2009 by the American College of Cardiology Foundation

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