- Email: [email protected]
Left ventricular dyssynchrony predicts benefit of cardiac resynchronization therapy in patients with end-stage heart failure before pacemaker implantation
Left Ventricular Dyssynchrony Predicts Benefit of Cardiac Resynchronization Therapy in Patients With End-Stage Heart Failure Before Pacemaker Implantation Jeroen J. Bax, MD, PhD, Thomas H. Marwick, MD, Sander G. Molhoek, MD, Gabe B. Bleeker, MD, Lieselot van Erven, MD, PhD, Eric Boersma, PhD, Paul Steendijk, MD, PhD, Ernst E. van der Wall, MD, PhD, and Martin J. Schalij, MD, We evaluated patients with end-stage heart failure who have a high likelihood of response to cardiac resynchronization therapy (biventricular pacing). It appears that 20% of patients do not respond to this expensive therapy despite the use of selection criteria (dilated cardiomyopathy, heart failure, New York Heart Association class II or IV, left ventricular ejection fraction <35%, left bundle branch block, and QRS >120 ms). The presence of left ventricular dyssynchrony is needed to result in improvement after cardiac resynchronization therapy. 䊚2003 by Excerpta Medica, Inc. (Am J Cardiol 2003;92:1238 –1240)
he number of patients presenting with heart failure is increasing rapidly. Recently, cardiac resynchroT nization therapy (CRT) has been proposed as treatment in patients with drug-refractory heart failure.1 The clinical benefit of CRT— evidenced by improvement in heart failure symptoms, quality of life, exercise capacity, and left ventricular (LV) systolic performance— has been demonstrated.1–5 However, 20% to 30% of patients do not respond to CRT despite application of established selection criteria.1 Therefore, additional selection criteria are needed. Myocardial tissue Doppler imaging (TDI) is a noninvasive, echocardiographic approach that allows measurement of both the amplitude (peak systolic myocardial velocity) and timing (time from electrical activation to peak velocity) of myocardial function,6 and it is useful in evaluating LV dyssynchrony and resynchronization after CRT.7–12 The degree of LV dyssynchrony could be used to predict the benefit of pacing before implantation of the pulse generator. Accordingly, the aim of the present report was to evaluate whether dyssynchrony assessed from TDI could predict improvement in systolic LV function directly after CRT. •••
Consecutive patients (n ⫽ 25) with end-stage heart From Leiden University Medical Center, Leiden, The Netherlands; University of Queensland, Brisbane, Australia; and Thoraxcenter Rotterdam, Rotterdam, The Netherlands. Dr. Molhoek is supported by grant 2001D015 and Dr. Bleeker is supported by grants 2002B109 and ICIN from the Dutch Heart Foundation, Utrecht, The Netherlands. Dr. Bax’s address is: Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands. E-mail: [email protected]. Manuscript received April 14, 2003; revised manuscript received and accepted June 23, 2003.
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©2003 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 92 November 15, 2003
PhD
failure, scheduled for implantation of a permanent biventricular pacemaker, were included (Table 1) using established selection criteria for CRT:1 New York Heart Association (NYHA) class III or IV, LV ejection fraction (EF) ⱕ35%, QRS with left bundle branch block configuration, and duration ⬎120 ms. Before pacemaker implantation, 2-dimensional echocardiography at rest was performed to measure LVEF and LV volumes. Next, myocardial TDI was performed to quantify maximum systolic velocity of the different walls and assess timing of maximum velocity after the beginning of the QRS complex. The day after implantation, LVEF and TDI parameters were reassessed. A commercially available system (Vingmed system FiV/ vivid-7 GE-Vingmed, Milwaukee, Wisconsin) was used and standard images were obtained (long-axis, 2and 4-chamber) and saved in cine loop format. LV volumes and LVEF were calculated using the biplane Simpson’s rule. Improvement was defined as an increase in LVEF ⱖ5% after CRT. TDI was performed as previously described,11 and parameters were measured from color images by off-line analysis by an independent observer (THM) blinded to the other echocardiographic results and unaware of whether images were acquired before or after CRT. The sample volume was placed in the basal portions of the septal and lateral walls; peak systolic velocities and time to peak systolic velocities were obtained, and the septal to lateral delay in peak velocity was calculated as an indicator of LV dyssynchrony.11 Results are presented as mean ⫾ SD and compared using the unpaired Student’s t test when appropriate; proportions were compared using chi-square analysis with Yates’ correction. Linear regression analysis was performed to evaluate relations between echocardiographic parameters and the change in LVEF. Multivariate analysis was performed to identify predictors of improvement in LVEF after CRT. A p value ⬍0.05 was considered statistically significant. In the entire group of patients, LVEF improved from 22 ⫾ 5% to 31 ⫾ 10% (p ⬍0.05) after pacing; individual data are shown in Figure 1. Notably, significant improvement in LVEF was observed more frequently in patients with idiopathic dilated cardiomyopathy than in patients with ischemic cardiomyopathy (11 of 14 [79%] vs 6 of 11 [66%]). Moreover, the change in LVEF after implantation was larger in patients with idiopathic dilated cardiomyopathy than in patients with ischemic cardiomyopathy (Figure 1). 0002-9149/03/$–see front matter doi:10.1016/j.amjcard.2003.06.016
TABLE 1 Patient Characteristics (n ⫽ 25) Age (yrs) Men/women Previous infarction LVEF (%) LVEDV (ml) LVESV (ml) Heart failure (NYHA class) III IV QRS (ms) Etiology Ischemic Idiopathic Medication Diuretics ACE inhibitors Spironolactone  blockers Amiodarone
62 ⫾ 9 22/3 9 (36%) 22 ⫾ 5 264 ⫾ 57 208 ⫾ 52 19 6 185 ⫾ 31 11 (44%) 14 (56%) 21 21 10 19 7
(84%) (84%) (40%) (76%) (28%)
FIGURE 2. Relation between the change in peak systolic velocity (⌬PSV) after pacing and the change in LVEF (⌬LVEF) after CRT.
ACE ⫽ angiotensin-converting enzyme; LVEDV ⫽ LV end-diastolic volume; LVESV ⫽ LV end-systolic volume.
FIGURE 3. Relation between the septal to lateral delay in peak systolic velocity at baseline and the change in LVEF after CRT.
FIGURE 1. Individual changes in LVEF before (pre) and after (post) CRT. DCM ⴝ idiopathic dilated cardiomyopathy; ISCH ⴝ ischemic cardiomyopathy.
Seventeen patients had ⱖ5% improvement in LVEF after pacing (from 22 ⫾ 5% to 36 ⫾ 9%) and 8 patients had no improvement in LVEF (21 ⫾ 6% vs 21 ⫾ 7%). In the septum and lateral wall, peak systolic velocities improved from 2.2 ⫾ 1.1 to 2.9 ⫾ 1.2 cm/s (p ⬍0.05) and from 2.0 ⫾ 1.0 to 2.9 ⫾ 2.1 cm/s (p ⬍0.05). The septal to lateral delay in peak velocity improved from 71 ⫾ 38 to 36 ⫾ 34 ms (p ⬍0.01) after CRT. There was a significant relation between the change in peak systolic velocity of the septum (y ⫽ 4.7 · x ⫹ 5.1 [p ⬍0.001], r ⫽ 0.71, n ⫽ 25) and the change in LVEF (Figure 2); a similar relation was observed for the lateral wall (y ⫽ 1.8 · x ⫹ 7.2 [p ⫽ 0.02], r ⫽ 0.45). The septal to lateral delay in peak systolic velocity before implantation was also related to the change in LVEF after CRT (Figure 3). Baseline variables (including age, sex, etiology of cardiomyopathy, use of medication, NYHA class, QRS duration at baseline, LVEF, LV volumes, and
peak systolic velocities in the different walls) were not different between patients with or without improvement in LVEF; the only variable that differed between responders and nonresponders was the septal to lateral delay (86 ⫾ 36 vs 39 ⫾ 17 ms, p ⬍0.01). Multivariate analysis confirmed that this parameter was the only predictor of improvement in LVEF. Importantly, 13 of 17 patients (76%) with an improvement in LVEF after CRT had a septal to lateral delay in peak systolic velocity at baseline of ⱖ60 ms, whereas only 1 of 8 patients (12.5%) without improvement in LVEF had a delay of ⱖ60 ms (p ⬍0.05). At 6 months’ follow-up, patients with improved LVEF (responders) exhibited a significant improvement in NYHA class (from 3.4 ⫾ 0.5 to 1.8 ⫾ 0.5, p ⬍0.001). In addition, the Minnesota score decreased from 44.1 ⫾ 10.6 to 25.6 ⫾ 10.2 (p ⬍0.001), and the 6-minute walking distance increased from 246 ⫾ 73 to 401 ⫾ 112 m (p ⬍0.001). Conversely, in patients without improved LVEF (nonresponders), no improvement in NYHA class was observed, the Minnesota score did not improve (50.2 ⫾ 6.9 vs 52.3 ⫾ 10.9, p ⫽ NS), and the 6-minute walking distance remained unchanged (250 ⫾ 68 vs 254 ⫾ 75 m, p ⫽ NS). BRIEF REPORTS
1239
•••
The findings in the present report can be summarized as: (1) Two-thirds of patients had an improvement in LVEF after CRT. (2) Improvement in LVEF is related to LV dyssynchrony at baseline; a cut-off value of 60 ms in septal to lateral delay appears to differentiate between responders and nonresponders. (3) The immediate improvement in LVEF is followed by an improvement at 6 months in NYHA class, exercise capacity, and quality-of-life score. The precise mechanisms of benefit from CRT are not entirely clear but appear to be related to resynchronization of the left ventricle, resulting in improvement in systolic LV function.1 In the present study, TDI showed LV resynchronization after CRT, as evidenced by a significant decrease in septal to lateral delay in peak systolic velocities. Besides the resynchronization, an acute improvement in LVEF was observed, in agreement with previous reports.1,7,9,13 Sogaard et al9 showed an improvement in LVEF from 29 ⫾ 7% to 35 ⫾ 8%, whereas LVEF improved from 28 ⫾ 10% to 40 ⫾ 15% in the study by Yu et al.7 Improvement in LVEF was accompanied by an improvement in peak systolic velocities of the basal walls. However, not all patients had an improvement in LVEF; 32% of patients had no improvement in LVEF despite the use of generally accepted selection criteria for CRT. Comparable numbers of nonresponders are observed in various other studies; in the Multicenter InSync Randomized Clinical Evaluation trial, for exmaple, 30% of the patients did not respond to CRT despite the use of traditional selection criteria.4 These findings suggest that additional criteria are needed to identify potential responders to CRT, in particular, when one considers the substantial costs of the device and the large number of patients with end-stage heart failure.1 The only predictor of improvement in LVEF after CRT was the presence of substantial LV dyssynchrony. With use of a cut-off value of ⱖ60 ms in septal to lateral delay, separation between responders and nonresponders was possible. Patients with a delay ⱖ60 ms had a high likelihood of improvement in LVEF after CRT, followed by an
1240 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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improvement in NYHA class, quality-of-life score, and 6-minute walking distance. 1. Leclercq C, Kass DA. Retiming the failing heart: principles and current clinical status of cardiac resynchronization. J Am Coll Cardiol 2002;39:194 –201. 2. Cazeau S, Leclercq C, Lavergne T, Walker S, Varma C, Linde C, Garrigue S, Kappenberger L, Haywood GA, Santini M, Bailleul C, Daubert JC, the Multisite Stimulation in Cardiomyopathies (MUSTIC) Study Investigators. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med 2001;344:873–880. 3. Jais P, Takahashi A, Garrigue S, Yamane T, Hocini M, Shah DC, Barold SS, Deisenhofer I, Haissaguerre M, Clementy J. Mid-term follow-up of endocardial biventricular pacing. PACE 2000;23:1744 –1747. 4. Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E, Kocovic DZ, Packer M, Clavell AL, Hayes DL, et al, and the MIRACLE Study Group. Multicenter InSync Randomized Clinical Evaluation. Cardiac resynchronization in chronic heart failure. N Engl J Med 2002;346:1845–1853. 5. Auricchio A, Stellbrink C, Sack S, Block M, Vogt J, Bakker P, Huth C, Schondube F, Wolfhard U, Bocker D, Krahnefeld O, Kirkels H, the Pacing Therapies in Congestive Heart Failure (PATH-CHF) Study Group. Long-term clinical effect of hemodynamically optimized cardiac resynchronization therapy in patients with heart failure and ventricular conduction delay. J Am Coll Cardiol 2002;39:2026 –2033. 6. Cain P, Baglin T, Case C, Spicer D, Short L, Marwick TH. Application of tissue Doppler to interpretation of dobutamine echocardiography and comparison with quantitative angiography. Am J Cardiol 2001;87:525–531. 7. Yu CM, Chau E, Sanderson JE, Fan K, Tang MO, Fung WH, Lin H, Kong SL, Lam YM, Hill MR, Lau CP. Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure. Circulation 2002;105:438 –445. 8. Ansalone G, Giannantoni P, Ricci R, Trambaiolo P, Laurenti A, Fedele F, Santini M. Doppler myocardial imaging in patients with heart failure receiving biventricular pacing treatment. Am Heart J 2001;142:881–896. 9. Sogaard P, Egeblad H, Kim WY, Jensen HK, Pedersen AK, Kristensen BO, Mortensen PT. Tissue Doppler imaging predicts improved systolic performance and reversed left ventricular remodeling during long-term resynchronization therapy. J Am Coll Cardiol 2002;40:723–730. 10. Sogaard P, Kim WY, Jensen HK, Mortensen P, Pedersen AK, Kristensen BO, Egeblad H. Impact of acute biventricular pacing on left ventricular performance and volumes in patients with severe heart failure: a tissue Doppler and threedimensional echocardiographic study. Cardiology 2001;95:173–182. 11. Bax JJ, Molhoek SG, van Erven L, Voogd PJ, Somer S, Boersma E, Steendijk P, Schalij MJ, Van der Wall EE. Usefulness of myocardial tissue Doppler echocardiography to evaluate left ventricular dyssynchrony before and after biventricular pacing in patients with idiopathic dilated cardiomyopathy. Am J Cardiol 2003;91:94 –97. 12. Ansalone G, Giannantoni P, Ricci R, Trambaiolo P, Fedele F, Santini M. Doppler myocardial imaging to evaluate the effectiveness of pacing sites in patients receiving biventricular pacing. J Am Coll Cardiol 2002;39:489 –499. 13. Stellbrink C, Breithardt OA, Franke A, Sack S, Bakker P, Auricchio A, Pochet T, Salo R, Kramer A, Spinelli J. Impact of cardiac resynchronization therapy using hemodynamically optimized pacing on left ventricular remodeling in patients with congestive heart failure and ventricular conduction disturbances. J Am Coll Cardiol 2001;38:1957–1965.
NOVEMBER 15, 2003
he number of patients presenting with heart failure is increasing rapidly. Recently, cardiac resynchroT nization therapy (CRT) has been proposed as treatment in patients with drug-refractory heart failure.1 The clinical benefit of CRT— evidenced by improvement in heart failure symptoms, quality of life, exercise capacity, and left ventricular (LV) systolic performance— has been demonstrated.1–5 However, 20% to 30% of patients do not respond to CRT despite application of established selection criteria.1 Therefore, additional selection criteria are needed. Myocardial tissue Doppler imaging (TDI) is a noninvasive, echocardiographic approach that allows measurement of both the amplitude (peak systolic myocardial velocity) and timing (time from electrical activation to peak velocity) of myocardial function,6 and it is useful in evaluating LV dyssynchrony and resynchronization after CRT.7–12 The degree of LV dyssynchrony could be used to predict the benefit of pacing before implantation of the pulse generator. Accordingly, the aim of the present report was to evaluate whether dyssynchrony assessed from TDI could predict improvement in systolic LV function directly after CRT. •••
Consecutive patients (n ⫽ 25) with end-stage heart From Leiden University Medical Center, Leiden, The Netherlands; University of Queensland, Brisbane, Australia; and Thoraxcenter Rotterdam, Rotterdam, The Netherlands. Dr. Molhoek is supported by grant 2001D015 and Dr. Bleeker is supported by grants 2002B109 and ICIN from the Dutch Heart Foundation, Utrecht, The Netherlands. Dr. Bax’s address is: Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands. E-mail: [email protected]. Manuscript received April 14, 2003; revised manuscript received and accepted June 23, 2003.
1238
©2003 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 92 November 15, 2003
PhD
failure, scheduled for implantation of a permanent biventricular pacemaker, were included (Table 1) using established selection criteria for CRT:1 New York Heart Association (NYHA) class III or IV, LV ejection fraction (EF) ⱕ35%, QRS with left bundle branch block configuration, and duration ⬎120 ms. Before pacemaker implantation, 2-dimensional echocardiography at rest was performed to measure LVEF and LV volumes. Next, myocardial TDI was performed to quantify maximum systolic velocity of the different walls and assess timing of maximum velocity after the beginning of the QRS complex. The day after implantation, LVEF and TDI parameters were reassessed. A commercially available system (Vingmed system FiV/ vivid-7 GE-Vingmed, Milwaukee, Wisconsin) was used and standard images were obtained (long-axis, 2and 4-chamber) and saved in cine loop format. LV volumes and LVEF were calculated using the biplane Simpson’s rule. Improvement was defined as an increase in LVEF ⱖ5% after CRT. TDI was performed as previously described,11 and parameters were measured from color images by off-line analysis by an independent observer (THM) blinded to the other echocardiographic results and unaware of whether images were acquired before or after CRT. The sample volume was placed in the basal portions of the septal and lateral walls; peak systolic velocities and time to peak systolic velocities were obtained, and the septal to lateral delay in peak velocity was calculated as an indicator of LV dyssynchrony.11 Results are presented as mean ⫾ SD and compared using the unpaired Student’s t test when appropriate; proportions were compared using chi-square analysis with Yates’ correction. Linear regression analysis was performed to evaluate relations between echocardiographic parameters and the change in LVEF. Multivariate analysis was performed to identify predictors of improvement in LVEF after CRT. A p value ⬍0.05 was considered statistically significant. In the entire group of patients, LVEF improved from 22 ⫾ 5% to 31 ⫾ 10% (p ⬍0.05) after pacing; individual data are shown in Figure 1. Notably, significant improvement in LVEF was observed more frequently in patients with idiopathic dilated cardiomyopathy than in patients with ischemic cardiomyopathy (11 of 14 [79%] vs 6 of 11 [66%]). Moreover, the change in LVEF after implantation was larger in patients with idiopathic dilated cardiomyopathy than in patients with ischemic cardiomyopathy (Figure 1). 0002-9149/03/$–see front matter doi:10.1016/j.amjcard.2003.06.016
TABLE 1 Patient Characteristics (n ⫽ 25) Age (yrs) Men/women Previous infarction LVEF (%) LVEDV (ml) LVESV (ml) Heart failure (NYHA class) III IV QRS (ms) Etiology Ischemic Idiopathic Medication Diuretics ACE inhibitors Spironolactone  blockers Amiodarone
62 ⫾ 9 22/3 9 (36%) 22 ⫾ 5 264 ⫾ 57 208 ⫾ 52 19 6 185 ⫾ 31 11 (44%) 14 (56%) 21 21 10 19 7
(84%) (84%) (40%) (76%) (28%)
FIGURE 2. Relation between the change in peak systolic velocity (⌬PSV) after pacing and the change in LVEF (⌬LVEF) after CRT.
ACE ⫽ angiotensin-converting enzyme; LVEDV ⫽ LV end-diastolic volume; LVESV ⫽ LV end-systolic volume.
FIGURE 3. Relation between the septal to lateral delay in peak systolic velocity at baseline and the change in LVEF after CRT.
FIGURE 1. Individual changes in LVEF before (pre) and after (post) CRT. DCM ⴝ idiopathic dilated cardiomyopathy; ISCH ⴝ ischemic cardiomyopathy.
Seventeen patients had ⱖ5% improvement in LVEF after pacing (from 22 ⫾ 5% to 36 ⫾ 9%) and 8 patients had no improvement in LVEF (21 ⫾ 6% vs 21 ⫾ 7%). In the septum and lateral wall, peak systolic velocities improved from 2.2 ⫾ 1.1 to 2.9 ⫾ 1.2 cm/s (p ⬍0.05) and from 2.0 ⫾ 1.0 to 2.9 ⫾ 2.1 cm/s (p ⬍0.05). The septal to lateral delay in peak velocity improved from 71 ⫾ 38 to 36 ⫾ 34 ms (p ⬍0.01) after CRT. There was a significant relation between the change in peak systolic velocity of the septum (y ⫽ 4.7 · x ⫹ 5.1 [p ⬍0.001], r ⫽ 0.71, n ⫽ 25) and the change in LVEF (Figure 2); a similar relation was observed for the lateral wall (y ⫽ 1.8 · x ⫹ 7.2 [p ⫽ 0.02], r ⫽ 0.45). The septal to lateral delay in peak systolic velocity before implantation was also related to the change in LVEF after CRT (Figure 3). Baseline variables (including age, sex, etiology of cardiomyopathy, use of medication, NYHA class, QRS duration at baseline, LVEF, LV volumes, and
peak systolic velocities in the different walls) were not different between patients with or without improvement in LVEF; the only variable that differed between responders and nonresponders was the septal to lateral delay (86 ⫾ 36 vs 39 ⫾ 17 ms, p ⬍0.01). Multivariate analysis confirmed that this parameter was the only predictor of improvement in LVEF. Importantly, 13 of 17 patients (76%) with an improvement in LVEF after CRT had a septal to lateral delay in peak systolic velocity at baseline of ⱖ60 ms, whereas only 1 of 8 patients (12.5%) without improvement in LVEF had a delay of ⱖ60 ms (p ⬍0.05). At 6 months’ follow-up, patients with improved LVEF (responders) exhibited a significant improvement in NYHA class (from 3.4 ⫾ 0.5 to 1.8 ⫾ 0.5, p ⬍0.001). In addition, the Minnesota score decreased from 44.1 ⫾ 10.6 to 25.6 ⫾ 10.2 (p ⬍0.001), and the 6-minute walking distance increased from 246 ⫾ 73 to 401 ⫾ 112 m (p ⬍0.001). Conversely, in patients without improved LVEF (nonresponders), no improvement in NYHA class was observed, the Minnesota score did not improve (50.2 ⫾ 6.9 vs 52.3 ⫾ 10.9, p ⫽ NS), and the 6-minute walking distance remained unchanged (250 ⫾ 68 vs 254 ⫾ 75 m, p ⫽ NS). BRIEF REPORTS
1239
•••
The findings in the present report can be summarized as: (1) Two-thirds of patients had an improvement in LVEF after CRT. (2) Improvement in LVEF is related to LV dyssynchrony at baseline; a cut-off value of 60 ms in septal to lateral delay appears to differentiate between responders and nonresponders. (3) The immediate improvement in LVEF is followed by an improvement at 6 months in NYHA class, exercise capacity, and quality-of-life score. The precise mechanisms of benefit from CRT are not entirely clear but appear to be related to resynchronization of the left ventricle, resulting in improvement in systolic LV function.1 In the present study, TDI showed LV resynchronization after CRT, as evidenced by a significant decrease in septal to lateral delay in peak systolic velocities. Besides the resynchronization, an acute improvement in LVEF was observed, in agreement with previous reports.1,7,9,13 Sogaard et al9 showed an improvement in LVEF from 29 ⫾ 7% to 35 ⫾ 8%, whereas LVEF improved from 28 ⫾ 10% to 40 ⫾ 15% in the study by Yu et al.7 Improvement in LVEF was accompanied by an improvement in peak systolic velocities of the basal walls. However, not all patients had an improvement in LVEF; 32% of patients had no improvement in LVEF despite the use of generally accepted selection criteria for CRT. Comparable numbers of nonresponders are observed in various other studies; in the Multicenter InSync Randomized Clinical Evaluation trial, for exmaple, 30% of the patients did not respond to CRT despite the use of traditional selection criteria.4 These findings suggest that additional criteria are needed to identify potential responders to CRT, in particular, when one considers the substantial costs of the device and the large number of patients with end-stage heart failure.1 The only predictor of improvement in LVEF after CRT was the presence of substantial LV dyssynchrony. With use of a cut-off value of ⱖ60 ms in septal to lateral delay, separation between responders and nonresponders was possible. Patients with a delay ⱖ60 ms had a high likelihood of improvement in LVEF after CRT, followed by an
1240 THE AMERICAN JOURNAL OF CARDIOLOGY姞
VOL. 92
improvement in NYHA class, quality-of-life score, and 6-minute walking distance. 1. Leclercq C, Kass DA. Retiming the failing heart: principles and current clinical status of cardiac resynchronization. J Am Coll Cardiol 2002;39:194 –201. 2. Cazeau S, Leclercq C, Lavergne T, Walker S, Varma C, Linde C, Garrigue S, Kappenberger L, Haywood GA, Santini M, Bailleul C, Daubert JC, the Multisite Stimulation in Cardiomyopathies (MUSTIC) Study Investigators. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med 2001;344:873–880. 3. Jais P, Takahashi A, Garrigue S, Yamane T, Hocini M, Shah DC, Barold SS, Deisenhofer I, Haissaguerre M, Clementy J. Mid-term follow-up of endocardial biventricular pacing. PACE 2000;23:1744 –1747. 4. Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E, Kocovic DZ, Packer M, Clavell AL, Hayes DL, et al, and the MIRACLE Study Group. Multicenter InSync Randomized Clinical Evaluation. Cardiac resynchronization in chronic heart failure. N Engl J Med 2002;346:1845–1853. 5. Auricchio A, Stellbrink C, Sack S, Block M, Vogt J, Bakker P, Huth C, Schondube F, Wolfhard U, Bocker D, Krahnefeld O, Kirkels H, the Pacing Therapies in Congestive Heart Failure (PATH-CHF) Study Group. Long-term clinical effect of hemodynamically optimized cardiac resynchronization therapy in patients with heart failure and ventricular conduction delay. J Am Coll Cardiol 2002;39:2026 –2033. 6. Cain P, Baglin T, Case C, Spicer D, Short L, Marwick TH. Application of tissue Doppler to interpretation of dobutamine echocardiography and comparison with quantitative angiography. Am J Cardiol 2001;87:525–531. 7. Yu CM, Chau E, Sanderson JE, Fan K, Tang MO, Fung WH, Lin H, Kong SL, Lam YM, Hill MR, Lau CP. Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure. Circulation 2002;105:438 –445. 8. Ansalone G, Giannantoni P, Ricci R, Trambaiolo P, Laurenti A, Fedele F, Santini M. Doppler myocardial imaging in patients with heart failure receiving biventricular pacing treatment. Am Heart J 2001;142:881–896. 9. Sogaard P, Egeblad H, Kim WY, Jensen HK, Pedersen AK, Kristensen BO, Mortensen PT. Tissue Doppler imaging predicts improved systolic performance and reversed left ventricular remodeling during long-term resynchronization therapy. J Am Coll Cardiol 2002;40:723–730. 10. Sogaard P, Kim WY, Jensen HK, Mortensen P, Pedersen AK, Kristensen BO, Egeblad H. Impact of acute biventricular pacing on left ventricular performance and volumes in patients with severe heart failure: a tissue Doppler and threedimensional echocardiographic study. Cardiology 2001;95:173–182. 11. Bax JJ, Molhoek SG, van Erven L, Voogd PJ, Somer S, Boersma E, Steendijk P, Schalij MJ, Van der Wall EE. Usefulness of myocardial tissue Doppler echocardiography to evaluate left ventricular dyssynchrony before and after biventricular pacing in patients with idiopathic dilated cardiomyopathy. Am J Cardiol 2003;91:94 –97. 12. Ansalone G, Giannantoni P, Ricci R, Trambaiolo P, Fedele F, Santini M. Doppler myocardial imaging to evaluate the effectiveness of pacing sites in patients receiving biventricular pacing. J Am Coll Cardiol 2002;39:489 –499. 13. Stellbrink C, Breithardt OA, Franke A, Sack S, Bakker P, Auricchio A, Pochet T, Salo R, Kramer A, Spinelli J. Impact of cardiac resynchronization therapy using hemodynamically optimized pacing on left ventricular remodeling in patients with congestive heart failure and ventricular conduction disturbances. J Am Coll Cardiol 2001;38:1957–1965.
NOVEMBER 15, 2003