CORRESPONDENCE: LETTER TO THE EDITOR
Role of Septal to Posterior Wall Motion Delay in Cardiac Resynchronization Therapy
Maria Vittoria Pitzalis, MD, PhD*,
Massimo Iacoviello, MD PhD,
Roberta Romito, MD,
Giovanni Luzzi, MD, PhD,
Matteo Anaclerio, MD, PhD and
Cinzia Forleo, MD, PhD
* East Carolina University, The Brody School of Medicine, Internal Medicine—Cardiology, 600 Moye Boulevard, Greenville, North Carolina 27834 (Email: pitzalism{at}ecu.edu).
In a recent issue of the Journal, Marcus et al. (1) report that septal to posterior wall motion delay (SPWMD) fails to predict reverse remodeling or clinical improvement in patients having heart failure and treated with cardiac resynchronization therapy (CRT), and they conclude that SPWMD should not be used to guide the selection of candidates for CRT. Because these findings and recommendations are contrary to our published reports and have significant clinical implications, it is important for your readership to understand that the method used to determine SPWMD in their study is not the one we demonstrated previously to predict both reverse remodeling and prognosis (2,3). Apart from the limitations and biases inherent in retrospective analyses, we will focus on the differences between the two methods, the one we and others (4–6) have successfully used and the present one, and which we believe led to the disparity in outcomes. We believe that the key to the prognostic value of our method is the measuring of the SPWMD in the short axis. The rationale of measuring the SPWMD by using the short axis view at the level of the papillary muscles, and is related to histological and anatomic relationships not shared with the longitudinal axis.
Specifically, the factors determining the measure of the delay between the septum and the posterior wall obtained by using the two methods differ in several ways:
- 1 The direction of the myocardial fibers differs between the basal and midventricular levels. At the level of the midventricle, the fibers have a circular course.
- 2 The sequence of myocardial activation differs between the basal and midventricle levels in the presence of left bundle branch block (7), is variable (8), and cannot be predicted by the electrocardiogram. In particular, the ventricular conduction delay resulting from an area of conduction failure (due to scarred tissue or functional block) or from slow but homogeneous myocardial propagation gives rise to an activation of the basal segments of the left ventricle that is different from that of mid left ventricular level. This different pattern of activation might be responsible for the fragmented mechanical activity that is seen more frequently at the level of the basal septum than at the mid left ventricular level.
- 3 The long axis evaluation of dyssynchrony is limited by the inherent difficulties to define accurately which area (i.e., lateral, posterolateral) is visualized and obtain a perpendicular to the long axis of the ventricle view (this is the case of both images shown in the study by Marcus et al. [1] in which the midseptum is compared to the basal free wall).
- 4 Basal segments being tied to fibrous skeleton of the heart and their movements are strongly influenced but in variable and unpredictable ways by the movements of the aortic root and mitral annulus. These influences could cause an irregular contraction of the septal wall, thus leading to a more difficult calculation of maximum septal displacement and to a less reproducible measure.
We hope that this explanation helps in understanding that taking the measurement in another way cannot a priori be expected to yield equivalent physiological or clinically relevant information; therefore, the parameter used by Marcus et al. (1), although given the same name as ours, is not the same as ours and that the conclusions drawn by their study cannot be applied to the SPWMD parameter we have described.
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1. Marcus GM, Rose E, Viloria EM, et al. Septal to posterior wall motion delay fails to predict reverse remodeling or clinical improvement in patients undergoing cardiac resynchronization therapy J Am Coll Cardiol 2005;46:2208-2214.[Abstract/Free Full Text]2. Pitzalis MV, Iacoviello M, Romito R, et al. Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony J Am Coll Cardiol 2002;40:1615-1622.[Abstract/Free Full Text] 3. Pitzalis MV, Iacoviello M, Romito R, et al. Ventricular asynchrony predicts a better outcome in patients with chronic heart failure receiving cardiac resynchronization therapy J Am Coll Cardiol 2005;45:65-69.[Abstract/Free Full Text] 4. Macias A, Gavira JJ, Alegria E, Azcarate PM, Barba J, Garcia-Bolao I. Effect of the left ventricular pacing site on echocardiographic parameters of ventricular dyssynchrony in patients receiving cardiac resynchronization therapy Rev Esp Cardiol 2004;57:138-145.[CrossRef][Web of Science][Medline] 5. Dohi K, Suffoletto MS, Schwartzman D, Ganz L, Pinsky MR, Gorcsan 3rd J. Utility of echocardiographic radial strain imaging to quantify left ventricular dyssynchrony and predict acute response to cardiac resynchronization therapy Am J Cardiol 2005;96:112-116.[CrossRef][Web of Science][Medline] 6. Bernheim A, Ammann P, Sticherling C, et al. Right atrial pacing impairs cardiac function during resynchronization therapyacute effects of DDD pacing compared to VDD pacing. J Am Coll Cardiol 2005;45:1482-1487.[Abstract/Free Full Text] 7. Auricchio A, Fantoni C, Regoli F, et al. Characterization of left ventricular activation in patients with heart failure and left bundle-branch block Circulation 2004;109:1133-1139.[Abstract/Free Full Text] 8. Fung JW, Yu CM, Yip G, et al. Variable left ventricular activation pattern in patients with heart failure and left bundle branch block Heart 2004;90:17-19.[Abstract/Free Full Text]
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