Impact of cardiac resynchronization therapy using hemodynamically optimized pacing on left ventricular remodeling in patients with congestive heart failure and ventricular conduction disturbances.
OBJECTIVE
We sought to investigate the impact of six months of cardiac resynchronization therapy (CRT) on echocardiographic variables of left ventricular (LV) function.


BACKGROUND
Cardiac resynchronization therapy has recently been introduced as a new therapeutic modality in patients with advanced heart failure (HF) and conduction abnormalities. However, most studies have only investigated the early hemodynamic effects of CRT.


METHODS
Twenty-five patients (12 women and 13 men; 59.8 +/- 5.1 years old) with advanced HF caused by ischemic (n = 7) or idiopathic dilated cardiomyopathy (n = 18) and a prolonged QRS complex were analyzed. All patients underwent early hemodynamic testing with a randomized testing protocol; echocardiographic measurements were compared before implantation and after six months of CRT.


RESULTS
Left ventricular end-diastolic and end-systolic diameters (LVEDD and LVESD, respectively) were significantly reduced after six months (LVEDD from 71 +/- 10 to 68 +/- 11 mm, p = 0.027; LVESD from 63 +/- 11 to 58 +/- 11 mm, p = 0.007), as were LV end-diastolic and end-systolic volumes (LVEDV from 253 +/- 83 to 227 +/- 112 ml, p = 0.017; LVESV from 202 +/- 79 to 174 +/- 101 ml, p = 0.009). Ejection fraction was significantly increased (from 22 +/- 7% to 26 +/- 9%, p = 0.03). "Nonresponders," with regard to LV volume reduction, had significantly higher baseline LVEDV, compared with "responders" (351 +/- 52 vs. 234 +/- 74 ml, p = 0.018). Overall, there was only mild mitral regurgitation at baseline, with a minor reduction by semiquantitative analysis. The results of early hemodynamic testing did not predict the volume response.


CONCLUSIONS
Cardiac resynchronization therapy may lead to a reduction in LV volumes in patients with advanced HF and conduction disturbances. Volume nonresponders have significantly higher baseline LVEDV.
Stellbrink
C
C
Department of Cardiology, RWTH University of Technology, Aachen, Germany. Christoph.Stellbrink@post.rwth-aachen.de
Breithardt
O A
OA
Franke
A
A
Sack
S
S
Bakker
P
P
Auricchio
A
A
Pochet
T
T
Salo
R
R
Kramer
A
A
Spinelli
J
J
D000368:Aged; D002306:Cardiac Volume / Q000502:physiology; D002311:Cardiomyopathy, Dilated / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D006325:Heart Atria / Q000000981:diagnostic imaging / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy*; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008133:Long QT Syndrome / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy*; D010138:Pacemaker, Artificial; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy*