European Journal of Echocardiography (2009) 10, 106–111 doi:10.1093/ejechocard/jen184 Ventricular-arterial coupling in patients with heart failure treated with cardiac resynchronization therapy: may we predict the long-term clinical response? Francesco Zanon1*, Silvio Aggio1, Enrico Baracca1, Gianni Pastore1, Giorgio Corbucci2, Graziano Boaretto1, Gabriele Braggion1, Christian Piergentili1, Gianluca Rigatelli1, and Loris Roncon1 1 Division of Cardiology, General Hospital, Rovigo, Italy; and 2Medtronic Italia, Sesto San Giovanni, Italy Received 21 January 2008; accepted after revision 25 May 2008; online publish-ahead-of-print 18 June 2008 KEYWORDS Objective To evaluate the effects of cardiac resynchronization therapy (CRT) on ventricular-arterial coupling (VAC) in patients with refractory congestive heart failure (HF), left bundle brunch block, and sinus rhythm. Background The ratio between arterial elastance (Ea) and left ventricular end-systolic elastance (Ees), the so-called VAC, defines the efficiency of the myocardium in pumping blood. Methods Seventy-eight patients were studied with echocardiography before CRT, and 1 year later. Endsystolic elastance was calculated according to the method of Chen. Arterial elastance (ratio of the systolic pressure to the stroke volume), end-systolic volume (ESV), and quality of life (QoL) (Minnesota Living with Heart Failure Questionnaire) were assessed at the baseline and after 1 year. Patients with a reduction .15% of ESV or a decrease .33% in QoL score were considered responders to CRT. Results QRS duration and interventricular delay were significantly reduced with CRT compared with baseline (156 + 2 vs. 195 + 3 ms, P , 0.001; and 25 + 2 vs. 55 + 3 ms, P , 0.001, respectively). Arterial elastance/Ees decreased significantly on CRT (2.47 + 1.48 vs. 1.41 + 0.87, P , 0.0001). The lowering of Ea/Ees was congruent to a decrease in intraventricular delay (83.1 + 55.7 vs. 28.4 + 49.5 ms, P , 0.0001) and an increase in ejection fraction (26 + 6.3 vs. 36.9 + 8.0%, P , 0.0001). Responders to CRT were 74 and 71% of the overall patient population, considering as endpoint QoL or ESV, respectively. The analysis of VAC showed a baseline cut-off value of 2, above which 88% and 69% of patients responded to CRT, considering as endpoint QoL or ESV, respectively. Conclusions The non-invasive assessment of VAC may be proposed as an immediate, easy, and optimal tool for quantifying the effect of CRT in patients with HF. Introduction The myocardial pump function and the performance of the entire cardiovascular system are determined by preload, afterload, and contractility.1 The best clinical measure of preload is the end-diastolic volume of the heart. From a clinical point of view, afterload can be estimated by measuring arterial blood pressure. In contrast, contractility is the most difficult parameter to estimate in clinical practice, since this would require invasive measurements of left ventricular (LV) pressure–volume (PV) loops. Left ventricular-arterial coupling (VAC) describes the ratio between arterial elastance (Ea) and ventricular end-systolic * Corresponding author. Tel: þ39 0425 394252; fax: þ39 0425 393597. E-mail address: [email protected] elastance (Ees). The mathematical ratio between these two elastances, the so-called VAC, defines the efficiency of the myocardium in pumping blood through the arteries, which is the desired result of heart contraction. From a mechanical point of view, the net flow and pressure output of a pump depend on three interacting factors: the intrinsic properties, such as power and stroke capacity, the mass or inertia of the fluid to be ejected, and the capacitance— the resistance and inertial properties of the system receiving the ejected material.2 In the cardiovascular system, the left ventricle is obviously the pump, the blood is the fluid, and the arteries constitute the system receiving the ejected blood. As blood viscosity is the only constant factor in this energy transfer, the best performance of the cardiovascular system is determined by the best fit Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2008. For permissions please email: [email protected]. Downloaded from by guest on October 15, 2014 Cardiac resynchronization therapy; Ventricular arterial coupling; Quality of life VAC in patients with HF treated with CRT between the factors characterizing the ventricles and the arteries. The intrinsic properties of the myocardium are strictly related to the end-systolic and -diastolic elastances, which is the consequence of maximal and minimal chamber stiffness. The blood per se determines the inertial load, depending on the mass in the myocardium at the end of the diastole. The arterial load depends on the dimensions of the proximal vessels, the mean vascular resistance, and the pulsatile components related to compliance and wave reflections. The result of the complex interactions among these factors is expressed by the relationship between Ees and Ea, which describes the mechanical pumping function. As the standard methods of evaluating Ees formerly involved invasive techniques, the assessment of VAC was not feasible in clinical practice. Efforts have been made to assess VAC non-invasively,3–5 and a method has recently been developed and validated to estimate LV Ees in humans from noninvasive single-beat parameters.6 The method described by Chen et al. requires five parameters obtained from noninvasive arm-cuff blood pressure, echo-Doppler echocardiography and ECG, thus making VAC assessment feasible in clinical practice (see Appendix). 107 Lead implantation and device programming The target veins for LV pacing were the basal posterior–lateral, basal lateral, middle posterior–lateral, middle lateral, and lateral-apical vein. The RV lead was placed in the apex of the right ventricle, in accordance with standard procedure. A bipolar atrial lead was implanted in the right atrial appendage, and the programmed mode was DDD with AV interval set at 130 ms to guarantee constant capture of the ventricles. No additional procedure for AV delay optimization was carried out and biventricular stimulation was performed simultaneously in both ventricles. Inclusion criteria We considered eligible for enrolment all consecutive patients who fulfilled the following inclusion criteria: (i) cardiomyopathy of any aetiology; (ii) end-stage HF refractory to drugs, including ACEinhibitors, b-blockers, and spironolactone; (iii) NYHA class III or IV; (iv) sinus rhythm; (v) intraventricular delay with QRS duration .0.15 s and left bundle branch block (LBBB) on ECG; (vi) ejection fraction 35%; (vii) end-diastolic diameter 65 mm. Aim of the study Methods The study had the approval of the Ethics Committee and informed consent to participate in the investigation was obtained from each patient before enrolment. All patients underwent a clinical examination and echocardiographic evaluation before CRT and after 1 year of follow-up (FU). Echocardiography was performed by means of a commercially available imaging system (General Electric VIVID Five GE Medical System, Milwaukee, WI, USA) equipped with a 2.5–3.6 MHz probe, with the patient in the left lateral position. The LV volumes and ejection fraction were measured by the biplane Simpson’s method.7,8 Left ventricular Ees was calculated according to the method proposed by Chen et al.6 Arterial elastance was measured as the ratio of the systolic pressure to the stroke volume (SV). The latter was obtained by subtracting the LV end-systolic volume (ESV) from the LV end-diastolic volume.9 The cardiac output was calculated by multiplying the - by the heart rate as measured during echocardiography. QRS duration was also collected. Quality of life (QoL) was assessed by the Minnesota Living with Heart Failure Questionnaire.10 To avoid any influence on the patients, the questionnaire was selfadministered by them at enrolment and after 1 year of FU to identify responders to CRT. A patient was considered to be responder to CRT if the following parameters significantly changed after 1 year of FU, compared with their basal values: (i) 33% decrease in QoL and (ii) 15% decrease in ESV.11 The decrease in QoL was considered a marker to identify clinically responder patients. The decrease in ESV was considered a marker of LV remodelling. A subanalysis of ischaemic and non-ischaemic patients was also performed. Ischaemic CHF was defined as LV systolic dysfunction associated with at least 75% narrowing of at least one of the three major coronary arteries (marked stenosis) or a documented history of a myocardial infarction. Non-ischaemic CHF was defined as LV systolic dysfunction without marked stenosis.12 Echo-Doppler parameters The following echo-Doppler parameters were measured at any FU (enrolment and after 1 year): (i) End-diastolic volume index, measured at the onset of the QRS complex.13 (ii) End-systolic volume index, referred to the smallest LV cavity.13 (iii) Left ventricular ejection fraction (EF).13 (iv) Stroke volume, measured from proximal aorta pulse-wave Doppler-flow and aortic cross-sectional area. (v) Arterial elastance.14 (vi) Left ventricular Ees.6 (vii) VAC expressed as the Ea/Ees ratio (viii) Intraventricular delay: Colour tissue Doppler imaging was acquired in 2D mode from the apical four-chamber and twochamber views to assess myocardial regional function. The mean velocity profile was determined for the interventricular septum and the lateral, inferior, and anterior walls at the level of the basal and medial segments. The regional preejection period was measured for all segments from the onset of QRS to the beginning of the positive component of the regional systolic velocity, defined by zero-crossing or, when this was not possible, as the beginning of the upstroke of the velocity curve after the isovolumic contraction phase.13 (ix) Interventricular delay: the difference between the aortic and pulmonary pre-ejection time. The pre-ejection time is calculated as the interval from the onset of QRS to the beginning of the aortic or pulmonary flow velocity curve recorded by pulsed-wave Doppler in the apical five-chamber view.13 In the first 20 patients, the inter-observer and intra-observer variability of EDV, ESV, EF, and SV was tested to evaluate reproducibility of the data. The inter-observer variability was ,4.2% and the intra-observer variability ,3.4%. Each patient was kept at rest for at least half an hour before measuring any echo parameter. Downloaded from by guest on October 15, 2014 The aim of the study was to prospectively evaluate the longterm effects of cardiac resynchronization therapy (CRT) on VAC, in patients with refractory congestive heart failure (HF), left bundle branch block, and sinus rhythm. 108 F. Zanon et al. Statistical analysis All data are expressed as mean + SD. An intra-patient analysis was performed, and the data were compared by means of paired Student’s t-test. A P-value of 0.05 was regarded as significant. according to the QoL criterion (Figure 3A). When ESV is the endpoint, responders are 50% if VAC , 4, rising up to 100% when VAC . 4 (Figure 3B). Discussion Results Table 1. The echo-Doppler parameters and indexes 1 year after CRT End-diastolic volume index (mL/mq) End-systolic volume index (mL/mq) EF (%) Stroke volume (mL/b) Ea (mmHg/mL) Ees (mmHg/mL/mq) Ea/Ees Intrav.Delay (ms) QoL score Before CRT_Baseline CRT on_1 Year P 1 Year vs. baseline 157.76 + 47.88 118.21 + 41.82 25.96 + 6.30 49.71 + 19.23 2.74 + 1.11 1.25 + 0.47 2.47 + 1.48 83.09 + 55.72 58 + 13 139.90 + 51.44 88.95 + 40.43 38.15 + 8.20 66.09 + 19.37 2.02 + 0.59 1.97 + 1.09 1.31 + 0.71 23.00 + 46.58 34 + 8 0.0002 ,0.0001 ,0.0001 ,0.0001 ,0.0001 ,0.0001 ,0.0001 ,0.0001 ,0.0001 Downloaded from by guest on October 15, 2014 Seventy-eight patients (61 male) entered the study. The mean age was 72 + 9 years (range 44–88): 42% were affected by ischaemic cardiomyopathy. The mean NYHA class was 3.1 + 0.6, the Minnesota quality life score was 62 + 12, and the mean EF was 26 + 7%. Ninety-five per cent of patients were on treatment with ACE-inhibitors, 61% with b-blockers and 67% with spironolactone. At the end of the study, 94 and 63% of the patients were treated with ACE-inhibitors and beta-blockers, respectively. All patients were successfully implanted with CRT devices, defibrillators (34 patients, 44%) or pacemakers depending on the indication. The target veins into which the LV lead was implanted were: basal posterior–lateral in 6 patients (8%), basal lateral in 8 (10%), middle posterior–lateral in 5 (6%), middle lateral in 45 (58%), and lateral-apical in 14 (18%). The mean time of the procedure was 85 + 34 min, of which 9 + 10 min were required for LV lead positioning and 17 + 12 min for fluoroscopy. QRS duration and interventricular delay were significantly reduced with CRT: 195 + 32 vs. 156 + 17 ms, P , 0.001, and 55 + 33 vs. 25 + 19 ms, P , 0.001, respectively. Table 1 summarizes the echo-Doppler parameters and indexes 1 year after CRT, in comparison with the baseline. On CRT, all values significantly improved. According to the improvement of the QoL score, 74% of the overall patient population responded to CRT. According to the improvement of ESV, 71% of patients were classified as responders. The analysis of VAC showed a baseline cut-off value of 2, above which at least 88 and 69% of patients responded to CRT, considering as endpoint QoL or ESV, respectively (Figure 1A and B). A subanalysis of ischaemic and non-ischaemic patients is showed in Figures 2 and 3. At least 75% of all non-ischaemic patients (Figure 2A) are responders to CRT independently of VAC and the percentage becomes very high when VAC 1.5. When the endpoint is ESV (Figure 2B) responders range around 50% if VAC 2, but they rise to 81 and 100% with higher values of VAC. In the case of ischaemic patients, on average 75% responded to CRT when VAC was .2 (range 69–100%), Our study, for the first time, evaluated the long-term effects of CRT on VAC in patients with HF and sinus rhythm. The main result is the positive effect that CRT has on VAC and, moreover, the potential of VAC for identifying patients responder to this therapy. Ea/Ees ratio in normal subjects is generally between 0.7 and 1.0: the range of optimal function.15,16 In patients with congestive HF, this ratio typically rises to as high as 4.0, owing to the relative decline in ventricular contractile function (lower Ees) and concomitant rise in Ea.17–19 Such coupling is detrimental from the standpoint of ventricular performance and metabolic efficiency. In their non-invasive analysis, Chen et al. demonstrated the feasibility of using a single PV point, timed at the onset of ejection (end of the isovolumic period). This method requires five accurately measured parameters obtained from non-invasive arm-cuff blood pressures, echoDoppler, and the electrocardiogram. Correlations between measured and estimated VAC, both at rest and with acute contractility change(s), were generally good, and the reproducibility of measurements over time proved reasonable, making this method applicable in clinical practice.6 The proposed method offers a new tool for a complete estimation of the cardiac network with regard to the final result of the heart: the efficiency of the mechanical pumping function. This method is relatively fast, requiring the evaluation of few parameters and is based on the standard parameters evaluated by echocardiography, plus blood pressure. Ventricular-arterial coupling is calculated immediately by means of a software formula, and the result is a single index that summarizes the mechanical efficiency of the myocardium in pumping blood. Cardiac resynchronization therapy has recently been introduced to improve haemodynamics and symptoms in patients with advanced HF.20–23 Much of the information regarding the clinical benefits of CRT derives from clinical trials,20,24 which together demonstrate that CRT improves symptoms and exercise tolerance in medically treated patients with persistent, moderate-to-severe symptoms of HF, poor LV function, and intraventricular conduction delay.25 Nevertheless, the identification of responders to CRT is still matter of debate. The measurement of VAC VAC in patients with HF treated with CRT 109 Figure 1 Patients responding to CRT in the overall population, as a function of the basal value of VAC: a cut-off value of 2 may identify 88% of responders to CRT as evaluated through the QoL and 69% of responders as defined through ESV. Figure 3 Patients responding to CRT in the ischaemic group, as a function of the basal value of VAC: a cut-off value of 2 may identify 69% of patients responders to CRT as evaluated through the QoL and a cut-off value of 4 may identify 100% of responders defined through ESV. Responders range to 50% when VAC , 4, if ESV is considered the endpoint. not only may allow to estimate the baseline condition and the improvement of the patient submitted to therapeutic actions, but it probably may be of help in the selection of responders. Of course a larger scale, prospective and long-term trial should be designed for this purpose. To define responders and non-responders, we assumed both a clinical criterion based on QoL and a functional parameter of remodelling based on ESV. This is in accordance with the objectives of standard clinical practice. Although different approaches have been proposed to select patients for CRT, there is no unifying definition of responders.26–29 Our proposal is not only coherent with clinical practice, but also coherent with the results of large-scale trials like MUSTIC21 and MIRACLE,20 which first validated CRT on the basis of clinical response. In these two trials, CRT failed to improve clinical status in up to 30% of patients, with a corresponding success rate of 70%. Similarly, we obtained a 74% response with the QoL criterion and 71% with ESV. When ESV Downloaded from by guest on October 15, 2014 Figure 2 Patients responding to CRT in the non-ischaemic group, as a function of the basal value of VAC: a cut-off value of 1.5 may identify 89% of responders to CRT as evaluated through the QoL and a cut-off value of 2 may identify 81% of responders defined through ESV. 110 Study limitations We only used non-invasive methods to estimate all cardiovascular parameters used in the study. Conclusions Cardiac resynchronization therapy increases Ees, which is a main determinant of LV systolic performance, reduces Ea, and improves VAC. The improvement in VAC may suggest an improved mechanical efficiency of the myocardium in pumping blood. The selection of responders to CRT on the basis of the basal value of VAC is promising, but it should be further investigated in a prospective, large-scale, and long-term trial. Acknowledgements We would like to acknowledge the contributions of Paola Raffagnato RN and Antonella Tiribello RN, who provided valuable support for implantation and data collection, and Mrs Giovanna Zucchi, who provided secretarial support. Conflict of interest: In connection with the submitted article, there are no financial associations that might pose a conflict of interest. Appendix The formula proposed and validated by Chen for the estimation of Ees is reported below: Ees ¼ ½Pd ðENdPs0:9Þ=½SVEnd where Pd is the brachial diastolic pressure, Ps the brachial systolic pressure, SV the stroke volume, and ENd the predicted normalized LV elastance at the onset of ejection. The estimate is described by the following formula: ENd ¼ 0:0275 0:165EF þ 0:3656ðPd=PesÞ þ 0:515ENdðavgÞ where Pes=Ps 0.9 and EF is the basal ejection fraction. ENdðavgÞ ¼ 0:35695 7:2266tNd þ 74:249tNd2 307:39tNd3 þ 684:54tNd4 856:92tNd5 þ 571:95tNd6 159:1tNd7 where tNd was determined by the ratio of pre-ejection period (R-wave!flow-onset) to total systolic period (R-wave!end-flow), with the time at onset and termination of flow defined noninvasively from the aortic-Doppler waveform. Once these formulas are implemented on an automatic algorithm, the determination of non-invasive parameters like Ps, Pd, SV, EF, and tNd allows the immediate calculation. References 1. Spiegel von T, Wietasch G, Hoeft A. Basics of myocardial pump function. Thorac Cardiovasc Surg 1998;46:237–41. 2. Kass DA. Age-related changes in ventricular-Arterial coupling: pathophysiologic implications. Heart Fail Rev 2002;7:51–62. 3. Senzaki H, Chen CH, Kass DA. Single-beat estimation of end-systolic pressure-volume relation in humans: a new method with the potential for noninvasive application. Circulation 1996;94:2497–506. 4. Takeuchi M, Igarash Y, Tomimoto S, Odake M, Hayashi T, Tsukamoto T et al. Single-beat estimation of the slope of the end-systolic pressurevolume relation in the human left ventricle. Circulation 1991;83:202–12. 5. Shishido T, Hayashi K, Shigemi K, Sato T, Sugimachi M, Sunagawa K. Single-beat estimation of end-systolic elastance using bilinearly approximated time-varying elastance curve. Circulation 2000;102:1983–9. 6. Chen HC, Fetics B, Nevo E, Rochitte CE, Chiou KR, Ding PY et al. Noninvasive single-beat determination of left ventricular end-systolic elastance in humans. J Am Coll Cardiol 2001;38:2028–34. 7. Gudmundsson P, Rydberg E, Winter R, Willenheimer R. Visually estimated left ventricular ejection fraction by echocardiography is closely correlated with formal quantitative methods. Int J Cardiol 2005;101:209–12. 8. Otterstad JE, Sutton MJ, Frøland G, Skjærpe T, Graving B, Holmes I. Are changes in left ventricular volume as measured with the biplane Simpson’s method predominantly related to changes in its area or long axis in the prognostic evaluation of remodelling following a myocardial infarction?. Eur J Echocardiogr 2001;2:118–25. 9. Razzolini R, Tarantini G, Boffa GM, Orlando S, Iliceto S. Effects of carvedilol on ventriculo-arterial coupling in patients with heart failure. Ital Heart J 2004;5:517–22. 10. Rector TS, Kubo SH, Cohn JN. Patients’ self-assessment of their congestive heart failure. Part II: content, reliability and validity of a new measure, the Minnesota Living with Heart Failure Questionnaire. Heart Fail 1987;3:198–209. 11. Soliman OII, Geleijnse ML, Theuns DAMJ, Nemes A, Vletter WB, van Dalen BM et al. Reverse of left ventricular volumetric and structural remodeling in heart failure patients treated with cardiac resynchronization therapy. Am J Cardiol 2008;101:651–7. 12. Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R et al., for the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) Investigators. Amiodarone or an implantable cardioverter–defibrillator for congestive heart failure. N Engl J Med 2005;352:225–37. 13. American Society of Echocardiography, Committee on Standards. Recommendations for quantification of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr 1989;2:338–67. Downloaded from by guest on October 15, 2014 is considered the reference parameter to evaluate responders, fewer patients reach the cut-off value of 15% improvement. This may suggest that some HF patients can be clinically responders even if there is no cardiac remodelling as evaluated through ESV. Differences are also evident between ischaemic and nonischaemic patients. Probably, ischaemic patients have nonhomogeneous myocardial tissue, and pacing may result in a different effectiveness in each patient. Non-ischaemic patients have a dilated, but homogeneous tissue and we may expect a higher and more reproducible effectiveness of pacing for resynchronization of the LV wall. The recently published study of Steendijk et al.30 shows improved VAC and improved mechanical efficiency with CRT: these haemodynamic findings are consistent with the observed improvements in clinical and functional status. Our study for the first time showed the long-term improvements of VAC with CRT. In addition, we underlined the potential of this parameter to select responders to this electrical therapy and to assess the cardiac performance over the time. It could be undertaken in any institution without additional costs and time, since echocardiography must be performed in each patient before and after implantation of a CRT device. Echocardiography plays an evolving and important role in the care of HF patients treated with biventricular pacing, or CRT. However, no ideal approach has yet been found so we advise that the dyssynchrony reporting should not include a recommendation whether a patient should undergo CRT, as this should be a clinical decision on a case-by-case basis for these borderline or challenging cases.31 Therefore, we think that VAC itself may represent a reliable index of the complex effects of pumping blood. F. Zanon et al. VAC in patients with HF treated with CRT 14. Kelly RP, Ting CT, Yang TM, Liu CP, Maughan WL, Chang MS et al. Effective arterial elastance as index of arterial vascular load in humans. Circulation 1992;86:513–21. 15. van den Horn GJ, Westerhof N, Elzinga G. Interaction of heart and arterial system. Ann Biomed Eng 1984;12:151–62. 16. Starling MR. Left ventricular-arterial coupling relations in the normal human heart. Am Heart J 1993;125:1659–66. 17. Asanoi H, Sasayama S, Kameyama T. Ventriculoarterial coupling in normal and failing heart in humans. Circ Res 1989;65:483–93. 18. Feldman MD, Pak PH, Wu CC, Haber HL, Heesch CM, Bergin JD et al. Acute cardiovascular effects of OPC-18790 in patients with congestive heart failure. Circulation 1996;96:474–83. 19. Ishihara H, Yokota M, Sobue T, Saito H. Relation between ventriculoarterial coupling and myocardial energetics in patients with idiopathic dilated cardiomyopathy. J Am Coll Cardiol 1994;23:406–16. 20. Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E et al. Cardiac resynchronization in chronic heart failure. N Engl J Med 2002; 346:1845–53. 21. Cazeau S, Leclercq C, Lavergne T, Walker S, Varma C, Linde C et al. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med 2001;344:873–80. 22. Linde C, Leclercq C, Rex S, Garrigue S, Lavergne T, Cazeau S et al. Longterm benefits of biventricular pacing in congestive heart failure: results from the MUltisite Stimulation in cardiomyopathy (MUSTIC) study. J Am Coll Cardiol 2002;40:111–8. 23. Auricchio A, Stellbrink C, Sack S. Long-term clinical effect of hemodynamically optimized cardiac resynchronization therapy in patients with heart failure and ventricular conduction delay. J Am Coll Cardiol 2002; 39:2026–33. 111 24. Kass DA, Chen CH, Curry C, Talbot M, Berger R, Fetics B et al. Improved left ventricular mechanics from acute VDD pacing in patients with dilated cardiomyopathy and ventricular conduction delay. Circulation 1999;22: 1567–73. 25. Leclercq C, Hare JM. Ventricular resynchronization. Current state of the art. Circulation 2004;109:296–9. 26. Penicka M, Bartunek J, de Bruyne B, Vanderheyden M, Goethals M, De Zutter M et al. Improvement of left ventricular function after cardiac resynchronization therapy is predicted by tissue Doppler imaging echocardiography. Circulation 2004;109:978–83. 27. Yu CM, Zhang Q, Fung JW, Chan HC, Chan YS, Yip GW et al. A novel tool to assess systolic dyssynchrony and identify responders of cardiac resynchronization therapy by tissue synchronization imaging. J Am Coll Cardiol 2005;45:677–84. 28. Yu CM, Fung JW, Zhang Y, Sanderson JE. Understanding nonresponders of cardiac resynchronization therapy—current and future perspectives. J Cardiovasc Electrophysiol 2005;16:1117–24. 29. Tse H, Lee KLF, Wan S, Yu Y, Hoersch W, Pastore J et al. Area of left ventricular regional conduction delay and preserved myocardium predict responses to cardiac resynchronization therapy. J Cardiovasc Electrophysiol 2005;16:690–5. 30. Steendijk P, Tulner SA, Bax JJ, Oemrawsingh PV, Bleeker GB, van Erven L et al. Hemodynamic effects of long-term cardiac resynchronization therapy. Analysis by pressure–volume loops. Circulation 2006;113: 1295–304. 31. Gorcsan J, Abraham T, Agler DA, Bax JJ, Derumeaux G, Grimm RA et al. Echocardiography for cardiac resynchronization therapy: recommendations for performance and reporting–a report from the American Society of Echocardiography Dyssynchrony Writing Group endorsed by the Heart Rhythm Society. J Am Soc Echocardiogr 2008;21:191–213. Downloaded from by guest on October 15, 2014
© Copyright 2024