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Temporal changes of left ventricular synchronization parameters and outcomes of cardiac resynchronization therapy

Ahmed, Walida,*; Samy, Waelb; Tayeh, Osamab; Behairy, Nohac; el Fattah, Alia Abdb

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The Egyptian Journal of Critical Care Medicine: August 2016 - Volume 4 - Issue 2 - p 105-112
doi: 10.1016/j.ejccm.2016.04.001
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1. Background

Several studies, e.g. MUSTIC, MIRACLE, COMPANION and CARE-HF studies [1–4] have demonstrated benefits of cardiac resynchronization therapy in patients with end-stage heart failure (HF), provided by multisite pacing of right and left ventricles and improving intraventricular and interventricular dyssynchrony.

Accordingly, the American College of Cardiology/American Heart Association (ACCF/AHA) guidelines have incorporated CRT implantation in managing drug-refractory HF patients with prolonged QRS duration [5]. However, applying conventional criteria, 20–40% of patients fail to respond to CRT [6–11]. It was suggested that electrical dyssynchrony represented by prolonged QRS intervals is not necessarily related to mechanical dyssynchrony, which may explain why 2040% of patients who receive CRT do not show an acceptable response [12–14]. For optimal understanding of CRT response, additional information regarding mechanical LV dyssynchrony is probably needed. Several attempts have questioned mechanical LV dyssynchrony and its impact on CRT [15–19], using different modalities e.g. tissue Doppler imaging (TDI), Gated SPECT LV phase analysis, cardiac magnetic resonance (CMR) [18,22,19,23].

Gated SPECT LV phase analysis has been introduced in 2005 to evaluate LV dyssynchronization, which would also allow for the simultaneous assessment of LV perfusion, function, and mechanical dyssynchrony [18].

In our cardiac imaging lab, we utilized this technique to examine temporal changes in LV dyssynchrony parameters across the process of CRT implantation and to explore the role of LV dyssynchrony upon CRT outcome.

2. Methods

2.1. Patient population

Thirty patients participated in this study. Patients were eligible for CRT implantation according to ACCF/AHA guidelines for managing heart failure [5]. All patients had LVEF≤35%, QRS prolongation>120msec, NYHA III/IV. They were maintained on guidelines directed medical therapy (GDMT) [5]. Patients with ischemic cardiomyopathy were revised for revascularization with a period of 3–6months of follow-up. Patients who remained symptomatic i.e. NYHA III/IV, were deemed candidates for CRT implantation. All patients consented to written consent forms for participation.

2.2. Exclusion criteria

Patients with recent myocardial infarction of less than 3months duration or dysrhythmias that could result into gating artifacts e.g. atrial fibrillation and frequents premature complexes.

2.3. Echocardiographic examination

Each patient was examined using Phillips ATL-HDI 5000 colored echocardiograph machine, with a 2.5–3MHz transducer. Two-dimensional (2-D) and M-mode echocardiography was performed to document volumetric LV measurements. Left ventricle contractility was assessed using Simpson's method.

2.4. Rest myocardial perfusion imaging (Gated SPECT)

Patients were intravenously injected with 20–25mCi Tc-99m SestaMIBI. Acquisition of SPECT images was performed within 1h of the injection of the Tc-99m SestaMIBI using dual head Siemens gamma camera (Symbia E) utilizing Cedars-Sinai software 1994–2009, (8 frames per cycle) [20]. Analysis of Gated SPECT images was performed using Syngo MI VA60A workstation (QGS, QPS and phase analysis).

Images were gated to the R-wave of the ECG, and image acquisition was interrupted for one beat if the R–R interval varied by 15% of the preceding R–R interval. Thirty-two views with 20s each, over 180° arc, with the patient in the supine position head in. Then, processing and filtering of the SPECT images were done using back- projection technique to get the trans-axial image, then short axis, vertical long axis, and horizontal long axis slices. Global functions quantified from gated perfusion SPECT images included left ventricular ejection fraction (LVEF), end-diastolic volume (EDV) and end-systolic volume (ESV).

The seventeen segment model was used for quantitative analysis of radioactive tracer uptake. Segments were scored visually according to tracer uptake defect percentage into five categories; ((0) No tracer uptake defect; (1) 0–25% tracer uptake defect; (2) 25–50% tracer uptake defect; (3) 50–75% tracer uptake defect; (4) 75–100% tracer uptake defect). The highest attainable score is 68. Scar burden was calculated by summing all segment scores; summed rest score (SRS) and dividing SRS by 68. All images were interpreted by a consensus of 2 nuclear cardiology readers and controversial issues were judged by a senior nuclear cardiologist.

2.5. Phase analysis of gated SPECT

Throughout the cardiac cycle, amplitude and phase of systolic wall thickening were extracted from the regional LV count changes throughout the cardiac cycle. Imaging was done with ECG-gated SPECT by use of 8 frames per cardiac cycle. The analysis used first-harmonic fast Fourier transform to approximate the wall thickening data to calculate a phase angle for each region, with 0° corresponding to the peak of the R-wave and one R–R interval corresponding to 360° [18]. Histograms of the calculated phase arrays were obtained and the following quantitative indices were calculated from each phase array: Histogram bandwidth (H. BW): includes 95% of the elements of the phase distribution in degrees, Histogram Standard Deviation (H. SD): is the SD of the phase distribution in degrees.

2.6. Pacemaker implantation

CRT-P/D devices were implanted in the left infraclavicular region. The left ventricular lead was inserted via the coronary sinus.

After 6 months, all patients were subjected to transthoracic echocardiography (TTE) and Gated SPECT phase analysis assessment.

Response was stated as a change of at least 15% decrease of LVES from initial baseline measurements (reverse LV remodeling), using TTE. Patients were divided into two groups, i.e. responders versus non-responders.

2.7. Statistical analysis

Numerical variables were described as mean±SD. Categorical variables were described as percentages. Comparisons were done using Student “t” test for numerical variables, paired “t” test for paired comparisons and Chi-square test for categorical variables. Correlations were plotted and r values (correlation coefficients) were stated. ROC curves were plotted to determine cutoff values. P was considered significant if ≤0.05. Statistics were calculated using IBM® SPSS® Statistics version 20 [21].

3. Results

The mean age of studied patients was 58.7±9.0years old (range 37–71). Twenty-four males were included in our study (80.0%). Echocardiographic response was illustrated in 19 patients (63.3%). Table 1 shows baseline characteristics for recruited patients. In our 30 patients, defects in radioactive tracer uptake comprised 31.8% of examined segments. Summed rest score was 13.9±5.1, with a scar burden of 23.8±8.5%.

Table 1
Table 1:
Comparison of demographic data between responders and non-responders.

Comparison between responders and non-responders showed no significant difference between both groups for their baseline LV volumes and contractility. Tables 2 and 3) and Fig. 1 shows pre-CRT and post-CRT volumetric echocardiographic data.

Table 2
Table 2:
Comparison between responders and non-responders, prior to and post CRT implantation (TTE).
Table 3
Table 3:
Comparison between prior to and post CRT implantation by TTE in both responders and non-responders.
Figure 1
Figure 1:
Temporal changes in LV volumes and contractility in both responders and non-responders, (pre- and post-CRT implantation by TTE). The solid line represents LVED, the dashed line represents LVES and the dotted line represents LVEF.

Left ventricular dyssynchrony assessment through LV phase analysis showed significant differences between responders and non-responders; where non-responders showed higher degrees of histogram bandwidth and histogram SD as in Table 4. Left ventricular phase analysis parameters were also correlated to resting perfusion defect i.e. SRS (histogram BW: r .517, P .003 and histogram SD: r .480, P .007).

Table 4
Table 4:
Comparison between pre- and post-implantation cardiac imaging.

Non-responders showed higher scar burden i.e. summed rest score for non-responders was 17.5±4.0 versus 15.6±6.9 for responders and scar burden was 25.4±5.9% for non-responders versus 22.9±9.8% for responders, but this did not reach statistical significance. Rest perfusion defect comparison between responders and non-responders is shown in Table 5.

Table 5
Table 5:
Rest perfusion defect comparison between responders and non-responders.

Temporal changes across LV phase parameters are shown in Table 6 and Fig. 2. All patients showed significant improvement in their dyssynchrony profile but responders and non-responders did not show the same magnitude of improvement as shown in Table 7. Patients with lower magnitudes of reverse LV remodeling tended to show higher degrees of dyssynchrony as shown in Table 8 and Fig. 3. Through further analysis, LV reverse remodeling was correlated to phase analysis parameters; (Histogram bandwidth: r .387–P .034, and for histogram SD: r .379–P .039) and to changes in LV phase analysis parameters; (Histogram bandwidth: r .785−P<.001 and histogram SD: r .793−P<.001).

Table 6
Table 6:
Comparison between pre- and post-implantation cardiac imaging.
Figure 2
Figure 2:
Temporal changes in LV phase analysis parameters for LV dyssynchrony in both responders and non-responders, (pre- and post-CRT implantation). The solid line represents histogram bandwidth and the dotted line represents histogram standard deviation. (* P value was <.001 for all).
Table 7
Table 7:
LV reverse remodeling and delta changes in LV phase analysis parameters.
Table 8
Table 8:
Relation between LV phase analysis and LV reverse remodeling.
Figure 3
Figure 3:
Correlation between LVES delta change (plotted on horizontal axis) and both histogram BW (blue rhomboid) and histogram SD (red circles), plotted on vertical axis.

A multiple regression was run to predict LV remodeling, (from histogram bandwidth, histogram SD, delta change in histogram BW, and delta change in histogram SD). All variables were insignificant predictors, apart from delta change of histogram SD (Beta=.780, P .010) with R2=.767.

ROC curve was also plotted in Fig. 4 to determine possible cutoff for LV histogram bandwidth and SD that could predict potential CRT non-responders, BW:(Cutoff: 152, AUC 72.2%, sensitivity 72.7%, specificity 63.2%, P .045), SD: (Cutoff: 54°, AUC 74.2%, sensitivity 81.8%, specificity 63.2%, P .03). Neither LV volumes nor contractility could predict CRT outcome. Patients were divided according to our proposed histogram SD into those <54° and ≥54°. Comparison between both groups was tabulated into Table 9.

Figure 4
Figure 4:
ROC for LV phase analysis to predict CRT non-responder. The solid line represents histogram bandwidth and the dotted line represents histogram standard deviation.
Table 9
Table 9:
Comparison between patients with histogram SD < 54° and ≥54°.

4. Discussion

This was a prospective non-controlled study recruiting 30 patients who were eligible for CRT implantation according to ACCF/AHA guidelines for managing heart failure [5]. Cardiac resynchronization therapy was performed in Critical Care department (Cairo University). Patients were followed-up for a period of six months duration.

Cardiac resynchronization therapy responders had better LV reverse remodeling response with improvement in contractile properties in our study. This has been in agreement with other studies where potential effects of cardiac resynchronization therapy had been demonstrated upon LV reverse modeling and functional improvement [1–4]. Cardiac resynchronization therapy is an established therapy for patients with advanced heart failure who have prolonged QRS duration and has been incorporated into recent end-stage HF guidelines [5].

Several attempts were done to quantify mechanical LV dyssynchrony and revealed that LV mechanical dyssynchrony is an important predictor of response to CRT. Several techniques were explored e.g. tissue Doppler imaging (TDI), Gated SPECT LV phase analysis, cardiac magnetic resonance – tissue synchronization index (CMR-TSI), circumferential uniformity ratio estimate (CURE) [18,22,19,23]. In a prospective, multicenter setting, the predictors of response to CRT (PROSPECT) study could not provide any echocardiographic parameters to predict CRT response [24]. Cardiac magnetic resonance (CMR) is an expensive modality, requiring expertise and certain precautions. Phase analysis was first introduced with planar gated blood pool ventriculography for evaluating the contraction pattern of the left ventricle. Phase analysis using GSPECT provides comprehensive assessment of multiple parameters (e.g., LV mechanical dyssynchrony, myocardial scar burden and location), with high intraobserver and interobserver agreement [25].

In our study, there were no significant differences between responders and non-responders, regarding their initial baseline clinical characteristics or echocardiographic measurements. However, LV phase parameters showed significant differences between responders and non-responders, (Bandwidth: 150.7±24.8 vs. 174.1±32.2, P .037, SD: 53.8±9.1 vs. 61.9±10.0, P .033). These parameters improved significantly post-CRT implantation for both responders and non-responders.

Inability to discriminate potential responders, based upon baseline clinical or echocardiographic measurements has been emphasized by Reuter et al., who studied 102 patients and compared characteristics between responders and non-responders receiving biventricular pacing for resistant heart failure management and concluded no single clinical baseline characteristics or echocardiographic or Gated SPECT data for LV volumes and contractility could discriminate between responders and non-responders [26].

However, association between LV dyssynchrony and CRT outcome was echoed in several studies, e.g. Bax et al. who documented significant differences in LV dyssynchrony, evaluated by TDI, between CRT responders and non-responders [27]. Also Henneman et al. studied 42 patients with severe HF and observed significant differences in responders compared to non-responders, regarding histogram bandwidth (175±63° vs. 117±51° [P<0.01]) and phase SD (56.3±19.9° vs. 37.1±14.4° [P<0.01]) [28]. This was also observed by Boogers et al. comparing responders versus non-responders for histogram bandwidth (94±23° vs. 68±21°, P<0.01) and phase SD (26±6° vs. 18±5°, P<0.01) [29]. This was also obvious in our experiment, (Histogram bandwidth: 150.7±24.8 for responders versus 174.1±32.2 for non-responders, P 0.034) (Histogram SD: 53.8±9.1 for responders versus 61.9±10.0 for non-responders, P 0.033).

In our study, there was a significant correlation between resting perfusion defect detected by Gated SPECT imaging and dyssynchronous LV parameters. Association between resting perfusion defect and LV dyssynchrony was explored in previous studies; Murrow et al. studied 28 subjects who underwent successful primary percutaneous coronary intervention for STEMI. In his work, baseline histogram bandwidth correlated with resting perfusion defect size (r=0.67, P<.001), ESV (r=0.72, P<.001), EDV (r=0.63, P=.001), and inversely with LVEF (r=−0.74, P<.001), with improvement in histogram bandwidth over 6months follow-up that correlated with a reduction in LV end-systolic volumes (r=0.43, P=.034) [30]. This also goes in line with work by Samad et al. who noted that the severity and extent of myocardial scar on SPECT imaging were independent predictors of mechanical dyssynchrony [31]. This was also confirmed by Ludwig et al. who studied the effect of LV scar upon LV dyssynchrony and proposed that histogram SD values may be increased by the presence of scar [32].

Our patients who were classified ‘non-responders’, had higher global scar distribution and density, but this did not reach statistical significance. This could be attributed to our small sample size with possibility of type II error. However, these findings could partly explain why patients with higher LV dyssynchrony parameters, showed lower degree of reverse LV remodeling. Those patients had higher SRS scores and larger distribution of scarred segments. This was not taken into consideration in Bax, Boogers and Henneman studies. Besides, non-responders showed a lower degree of LV reverse remodeling than responders did, but this did not reach our response criterion.

Our research showed that LV reverse remodeling correlated to phase analysis parameters and temporal changes in LV end-systolic volume correlated to temporal changes in LV dyssynchrony. This is in agreement with Brandão et al. who studied 30 patients with severe HF before and 3months after CRT. Patients, who exhibited improvement in LVEF, showed favorable changes in EDV, ESV, LV dyssynchrony indices, and regional motion [33]. Samad et al. noted that among significant univariate predictors of mechanical dyssynchrony, enlarging left ventricular volume was associated with increasing Phase SD [31].

After applying ROC curve for LV phase analysis data to predict potential CRT non-responders, a cutoff value of 152° for histogram bandwidth had a sensitivity of 72.7% and specificity of 63.2, and also a cutoff value of 54° for histogram SD yielded a sensitivity of 81.8% and specificity of 63.2%.

Previous attempts to utilize LV phase analysis to predict CRT outcome by Boogers et al., identified a cutoff value of 72.5° for histogram bandwidth to predict CRT response. This yielded a sensitivity of 83% and a specificity of 81%. For phase SD, sensitivity and specificity similar to those for histogram bandwidth were obtained at a cutoff 19.6° [29]. Boogers cutoff values for phase analysis were different to those obtained in a study by Henneman et al. who demonstrated an optimal cutoff value of 135° for histogram bandwidth (sensitivity and specificity of 70%) and of 43° for phase SD (sensitivity and specificity of 74%) for the prediction of response to CRT [28]. Boogers attributed differences to different software packages or to differences in study populations.

5. New knowledge gained

Our observations suggested that marked LV dyssynchronous contraction could result in unfavorable response to CRT. However, LV dyssynchrony parameters could serve as an acceptable predictor for CRT non-response status.

6. Conclusion

Dyssynchronous LV contraction had a significant impact on CRT outcome. The presence of mechanical dyssynchrony could predict CRT outcome and help to discriminate non-responders.

Conflict of interest disclosure statement

No conflicts of interest to be disclosed.


[1] Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass D, De Marco T, et al. For the comparison of medical therapy, pacing and defibrillation in heart failure (COMPANION) investigators cardiac resynchronization therapy with or without an implantable defibrillator in advanced heart failure. N Eng J Med 2004;350:2140-2150.
[2] St John Sutton MG, Plappert T, Abraham WT, Smith AL, DeLurgio DB, Leon AR, et al. Effect of cardiac resynchronization therapy on left ventricular size and function in chronic heart failure. Circulation 2003;107:1985-1990.
[3] Wikstrom G, Blomstrom-Lundqvist C, Andren B, Lonnerholm S, Blomstrom P, Freemantle N, et al. The effects of aetiology on outcome in patients treated with cardiac resynchronization therapy in the CARE-HF trial. Eur Heart J 2009;30:782-788.
[4] Duncan A, Wait D, Gibson D, Daubert JC. Left ventricular remodeling and hemodynamic effects of multisite pacing in patients with left ventricular systolic dysfunction and activation disturbances in sinus rhythm: sub-study of the MUSTIC (multisite stimulation in cardiomyopathies) trial. Eur Heart J 2003;24:430-441.
[5] Yancy CW, Jessup M, Bozkurt B, Butler J, Casey Jr DE, Drazner MH, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;62(16):e147-e239, Oct 15.
[6] Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E, et al. MIRACLE study group. Multicenter InSync randomized clinical evaluation: cardiac resynchronization in chronic heart failure. N Engl J Med 2002;346:1845-1853.
[7] Young JB, Abraham WT, Smith AL, Leon AR, Lieberman R, Multicenter Wilkoff B, InSync ICD, et al. Randomized clinical evaluation (MIRACLE ICD) trial investigators. Combined cardiac resynchronization and implantable cardioverter defibrillation in advanced chronic heart failure: the MIRACLE ICD trial. JAMA 2003;289:2685-2694.
[8] Bax JJ, Van der Wall EE, Schalij MJ. Cardiac resynchronization therapy for heart failure. N Engl J Med 2002;347:1803-1804.
[9] Bax JJ, Bleeker GB, Marwick TH, Molhoek SG, Boersma E, Steendijk P, et al. Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol 2004;44:1834-1840.
[10] Yu CM, Fung JW, Zhang Q, Chan CK, Chan YS, Lin H, et al. Tissue doppler imaging is superior to strain rate imaging and postsystolic shortening on the prediction of reverse remodeling in both ischemic and nonischemic heart failure after cardiac resynchronization therapy. Circulation 2004;110:66-73.
[11] Yu CM, Zhang Q, Chan YS, Chan CK, Yip GW, Kum LC, et al. Tissue doppler velocity is superior to displacement and strain mapping in predicting left ventricular reverse remodelling response after cardiac resynchronization therapy. Heart 2006;92:1452-1456.
[12] Leclercq C, Fairs O, Tunin R, Johnson J, Kato R, Evans F, et al. Systolic improvement and mechanical resynchronization does not require electrical synchrony in the dilated failing heart with left bundle branch block. Circulation 2002;106:1760-1763.
[13] Achilli A, Sassara M, Ficili S, Pontillo D, Achilli P, Alessi C, et al. Long-term effectiveness of cardiac resynchronization therapy in patients with refractory heart failure and “narrow” QRS. J Am Coll Cardiol 2003;42:2117-2124.
[14] Mollema SA, Bleeker GB, Van der Wall EE, Schalij MJ, Bax JJ. Usefulness of QRS duration to predict response to cardiac resynchronization therapy in patients with end-stage heart failure. Am J Cardiol 2007;100:1665-1670.
[15] Galderisi M, Cattaneo F, Mondillo S. Doppler echocardiography and myocardial dyssynchrony: a practical update of old and new ultrasound technologies. Cardiovasc Ultrasound 2007;5:28.
[16] Yu CM, Chau E, Sanderson JE, et al. 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.
[17] Fauchier L, Marie O, Casset-Senon D, et al. Interventricular and intraventricular dyssynchrony in idiopathic dilated cardiomyopathy: a prognostic study with Fourier phase analysis of radionuclide angioscintigraphy. J Am Coll Cardiol 2002;40:2022-2030.
[18] Chen J, Garcia EV, Folks RD, Cooke CD, Faber TL, Tauxe EL, et al. Onset of left ventricular mechanical contraction as determined by phase-analysis of ECG gated myocardial perfusion SPECT imaging development of a diagnostic tool for assessment of mechanical dyssynchrony. J Nucl Cardiol 2005;12:687-695.
[19] Chalil S, Stegemann B, Muhyaldeen S, Khadjooi K, Smith R, Jordan P, Leyva F. Intraventricular dyssynchrony predicts mortality and morbidity following cardiac resynchronization therapy: a study using cardiovascular magnetic resonance tissue synchronization imaging. J Am Coll Cardiol 2007;50:243-252.
[20] Hans-Jürgen Biersack, Freeman Leonard M. Clinical Nuclear Medicine. first ed. Springer; 2007. p. 103.
[21] BM Corp. Released. IBM SPSS Statistics for Windows, Version 22.0. Armonk, NY: IBM Corp; 2013.
[22] Bax JJ, Bleeker GB, Marwick TH, Molhoek SG, Boersma E, Steendijk P, Van der Wall EE, Schalij MJ. Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol 2004;44:1834-1840.
[23] Bilchick KC, Dimaano V, Wu KC, Helm RH, Weiss RG, Lima JA, Berger RD, Tomaselli GF, Bluemke DA, Halperin HR, Abraham T, Kass DA, Lardo AC. Magnetic resonance imaging analysis of dyssynchrony and myocardial scar predicts function class improvement following cardiac resynchronization therapy. JACC Cardiovasc Imaging 2008;1:561-568.
[24] Chung ES, Leon AR, Tavazzi L, et al. Results of the predictors of response to CRT (PROSPECT) trial. Circulation 2008;117:2608-2616.
[25] Trimble MA, Velazquez EJ, Adams GL, et al. Repeatability and reproducibility of phase analysis of gated SPECT myocardial perfusion imaging used to quantify cardiac dyssynchrony. Nucl Med Commun 2008;29:374-381.
[26] Reuter S, Garrigue S, Barold S, Jais P, Hocini M, Haissaguerre M, et al. Comparison of characteristics in responders versus nonresponders with biventricular pacing for drug-resistant congestive heart failure. Am J Cardiol 2002;89:346-350.
[27] Bax JJ, Bleeker GB, Marwick TH, Molhoek SG, Boersma E, Steendijk P, et al. Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol 2004 Nov 2;44(9):1834-1840.
[28] Henneman MM, Chen J, Dibbets P, Stokkel M, Bleeker GB, Ypenburg C, et al. Can LV dyssynchrony as assessed with phase analysis on gated myocardial perfusion SPECT predicts response to CRT? J Nucl Med 2007;48:1104-1111.
[29] Boogers MM, Van Kriekinge SD, Henneman MM, Ypenburg C, Van Bommel RJ, Boersma E, et al. Quantitative gated SPECT-derived phase analysis on gated myocardial perfusion SPECT detects left ventriculardyssynchrony and predicts response to cardiac resynchronization therapy. J Nucl Med 2009 May;50(5):718-725.
[30] Murrow J, Esteves F, Galt J, Chen J, Garcia E, Lin J, et al. Characterization of mechanical dyssynchrony measured by gated single photon emission computed tomography phase analysis after acute ST-elevation myocardial infarction. J Nucl Cardiol 2011;18(5):912-919.
[31] Samad Z, Atchley AE, Trimble MA, Sun JL, Shaw LK, Pagnanelli R, et al. Prevalence and predictors of mechanical dyssynchrony as defined by phase analysis in patients with left ventricular dysfunction undergoing gated SPECT myocardial perfusion imaging. J Nucl Cardiol 2011 Feb;18(1):24-30.
[32] Ludwig DR, Friehling M, Schelbert EB, Schwartzman D. Impact of scar on SPECT assay of left ventricular contraction dyssynchrony. Eur J Nucl Med Mol Imaging 2014 Mar;41(3):529-535.
[33] Brandão SC, Nishioka SA, Giorgi MC, Chen J, Abe R, Martinelli Filho M, et al. Cardiac resynchronization therapy evaluated by myocardial scintigraphy with 99mTc-MIBI: changes in left ventricular uptake, dyssynchrony, and function. Eur J Nucl Med Mol Imaging 2009;36(6):986-996.

Cardiac resynchronization therapy; Phase analysis gated SPECT; Left ventricular dyssynchrony

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