CORRESPONDENCE: LETTER TO THE EDITOR
Cardiac Resynchronization Therapy
Ole-A. Breithardt, MD*
* Medizinische Klinik 2, Universitätsklinikum Erlangen, Ulmenweg 18, DE-91054 Erlangen, Germany (Email: olebreithardt{at}gmx.de).
Two recent studies published in JACC (1,2) suggest that the indication for cardiac resynchronization therapy (CRT) may be extended to heart failure patients with normal QRS width (<120 ms) and evidence of mechanical dyssynchrony identified by tissue Doppler imaging.
Cardiac resynchronization therapy is an electrical therapeutic approach to treat an electrical conduction delay that in turn causes mechanical failure, mainly within the left ventricle. This pathophysiologic concept has been elaborated and proven in numerous well-designed and well-controlled animal experiments, in hemodynamic studies in humans, and in mathematical models (3–6) but it is now challenged by a new approach that completely disregards the traditional electrical basis for resynchronization therapy and focuses solely on mechanical dyssynchrony.
Although it seems logical to look closer for the presence of mechanical dyssynchrony, by means of echocardiography or other imaging modalities, before recommending resynchronization therapy, I believe that we cannot completely ignore the electrocardiogram (ECG) at this time. Some important issues have not been addressed by both studies: how to deliver ventricular pacing in patients with normal electrical conduction and how to achieve sufficient ventricular capture to resynchronize ventricular contraction. It would be interesting to learn more about the intrinsic PR interval before pacemaker implantation and how the atrioventricular delays were set to ensure ventricular capture without interruption of atrial filling. How many patients had evidence of complete ventricular capture by the ECG at rest and in how many patients was mechanical resynchronization achieved by fusion between intrinsic activation and the pacing stimuli?
Both trials (1,2) are certainly very intriguing and stimulating, but they are also clearly limited by their design, mainly due to the lack of a control group with inactivated pacing. Thus, the 2 studies can only serve to initiate larger randomized multicenter trials before the ECG can be completely abandoned as a selection criterion for resynchronization therapy.
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References
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1. Yu CM, Chan YS, Zhang Q, et al. Benefits of cardiac resynchronization therapy for heart failure patients with narrow QRS complexes and coexisting systolic asynchrony by echocardiography J Am Coll Cardiol 2006;48:2251-2257.[Abstract/Free Full Text]2. Bleeker GB, Holman ER, Steendijk P, et al. Cardiac resynchronization therapy in patients with a narrow QRS complex J Am Coll Cardiol 2006;48:2243-2250.[Abstract/Free Full Text] 3. Kass DA, Chen CH, Curry C, et al. Improved left ventricular mechanics from acute VDD pacing in patients with dilated cardiomyopathy and ventricular conduction delay Circulation 1999;99:1567-1573.[Abstract/Free Full Text] 4. Auricchio A, Stellbrink C, Block M, et al. Effect of pacing chamber and atrioventricular delay on acute systolic function of paced patients with congestive heart failure Circulation 1999;99:2993-3001.[Abstract/Free Full Text] 5. Blanc JJ, Etienne Y, Gilard M, et al. Evaluation of different ventricular pacing sites in patients with severe heart failure: results of an acute hemodynamic study Circulation 1997;96:3273-3277.[Abstract/Free Full Text] 6. Claus P, Bijnens B, Breithardt OA, Herbots L, Sutherland GR. Why ischemic hearts respond less to cardiac resynchronisation therapyA modeling study. In: Magnin IE, Montagnat J, Clarysse P, Nenonen J, Katila T, editors. Functional Imaging and Modeling of the Heart. Berlin: Springer; 2003. pp. 287-294.
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