Left ventricular diastolic dyssynchrony (LVDD), a dyssynchronous relaxation pattern, has been known to develop after myocardial damage. We aimed to evaluate the dynamic changes in LVDD in the early stage of acute myocardial infarction (AMI) by phase analysis of 99mtechnetium methoxyisobutylisonitrile (99mTc-MIBI) single-photon emission computed tomography (SPECT) gated myocardial perfusion imaging (GMPI) and explore its relationship with the progression of left ventricular remodeling (LVR). The left anterior descending coronary arteries of 16 Bama miniature swine were occluded with a balloon to build AMI models. Animals were imaged by SPECT GMPI before AMI and at 1 day, 1 week and 4 weeks after AMI, and quantitative analysis was performed to determine the extent of left ventricle (LV) perfusion defects, left ventricular systolic dyssynchrony (LVSD) and the LVDD parameters: phase histogram bandwidth (PBW) and phase standard deviation (PSD). Echocardiography was simultaneously applied to evaluate left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), and the LVDD parameters: Te-12-diff and Te-12-SD. Myocardial injury markers were measured, and 12-lead ECGs were performed. The degree of LVR progression was defined as ΔLVESV (%) = (LVESVAMI4weeks − LVESVAMI1day)/LVESVAMI1day. Thirteen swine completed the study. LVDD parameters changed dynamically at different time points after AMI. LVDD occurred as early as 1 day after AMI, peaked at 1 week, and trended toward a partial recovery at 4 weeks. Phase analysis on SPECT GMPI showed a significant correlation with tissue Doppler imaging for the assessment of LVDD during the longitudinal evaluation (r = 0.569 to 0.787, both P <0.05). During the univariate and multivariate regression analyses, the LVDD parameters PBW and PSD as of 1 day after AMI were significantly associated with the progression of LVR, respectively (PBW, β = 0.004, 95% CI 0.001 to 0.007, P = 0.024; PSD, β = 0.008, 95% CI 0.000 to 0.017, P = 0.049). Adjusted smooth curve fitting and threshold effect analysis indicated PBW and PSD break-point values of 142° and 60.4°, respectively, to predict the progression of LVR after AMI. Phase analysis of SPECT GMPI can accurately and reliably characterize LVDD. LVDD occurred on the first day after AMI, reached its peak at 1 week, and partially recovered at 4 weeks after AMI. LVDD as evaluated by phase analysis of SPECT GMPI early after AMI was significantly associated with the progression of LVR. The early assessment of LVDD after AMI may provide helpful information for predicting the progression of LVR in the future.

Objective:To evaluate the left ventricular diastolic dyssynchrony (LVDD) and its influencing factors early after acute myocardial infarction (AMI) using phase analysis of SPECT gated myocardial perfusion imaging (GMPI).Methods:Bama miniature swines ( n=16) were subjected to establish AMI models. GMPI was performed before and 1 d after AMI to obtain the extent of myocardial perfusion defect (Extent, %) and left ventricular systolic dyssynchrony (LVSD)/LVDD parameters, namely the phase histogram bandwidth (PBW) and phase standard deviation (PSD). Meanwhile, left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), and the ratio of early to late peak mitral diastolic flow (E/A) were obtained by echocardiography. Independent-sample t test, paired t test and Pearson correlation analysis were used to analyze the data. Results:Sixteen AMI swines were successfully created. Compared to baseline, Extent, LVEDV and LVESV significantly increased on 1 d after AMI ( t values: -11.14, -4.55, -6.12, all P<0.001), while LVEF and E/A significantly decreased ( t values: 10.16, 2.18, P<0.001, P=0.046). GMPI showed that the LVDD parameters PBW and PSD increased significantly on 1 d after AMI when compared to those at baseline((142.25±72.06)° vs (33.06±8.98)°, (56.15±26.71)° vs (12.51±5.13)°; t values: -6.11, -6.60, both P<0.001). There were significant differences between LVSD parameters and LVDD parameters (PBW: (109.06±62.40)° vs (142.25±72.06)°, PSD: (44.40±25.61)° vs (56.15±26.71)°; t values: -2.73, -2.20, P values: 0.016, 0.044). LVDD parameters PBW, PSD were negatively correlated with E/A after AMI ( r values: -0.569, -0.566, P values: 0.021, 0.022), and positively correlated with the Extent ( r values: 0.717, 0.634, P values: 0.002, 0.008). The phase analysis of SPECT GMPI to evaluate LVDD showed good intra-observer and inter-observe reproducibility (intraclass correlation coefficient (ICC): 0.953-0.984, all P<0.001). Conclusions:LVDD occurs early on 1 d after AMI, and can reflect left ventricular diastolic dysfunction. The Extent is correlated with LVDD significantly. Phase analysis of SPECT GMPI is an accurate method to evaluate LVDD and left ventricular diastolic function.

Background Left ventricular mechanical dyssynchrony (LVMD) is closely associated with left ventricular dysfunction and poor prognosis in patients with acute myocardial infarction (AMI). However, whether mechanical dyssynchrony is present in the noninfarcted areas remains controversial. This research aimed to quantitatively evaluate the global and regional mechanical dyssynchrony early after AMI by phase analysis of single-photon emission computed tomography (SPECT) gated myocardial perfusion imaging (GMPI) and to further explore the related influencing factors. Materials and methods Of 11 Bama suckling pigs, eight animals were successfully subjected to left anterior descending artery occlusion by balloon to generate porcine AMI models and completed the study. SPECT GMPI was performed before AMI and at 1 day, 1 week, and 4 weeks after AMI. The global bandwidth (BW), SD, entropy, total perfusion deficit, summed rest score, regional BW, regional summed motion score, and regional summed thickening score were measured by SPECT GMPI. Results The global BW, SD, and entropy values significantly increased after AMI and showed no significant change among the three time points after AMI. The BW in the infarcted area (left anterior descending artery-dominated area) at 1 day, 1 week, and 4 weeks after AMI was significantly higher than that before AMI, as was the BW in the noninfarcted areas (left circumflex artery-dominated and right coronary artery-dominated areas), which revealed that there was less dyssynchrony in the noninfarcted areas than in the infarcted area at the three time points after AMI. The global BW was positively correlated with the scar burden measured by summed rest score (r=0.709–0.832, all P<0.05), whereas the regional BW in the noninfarcted areas after AMI showed moderate to good correlation with regional summed motion score (r=0.733–0.875, all P<0.05) and regional summed thickening score (r=0.713–0.889, all P<0.05). Conclusion LVMD occurs early on the first day after AMI, with no significant worsening over the next 4 weeks. Mechanical dyssynchrony was present in both the infarcted and noninfarcted areas. The global LVMD is mainly influenced by the scar burden, and the regional mechanical dyssynchrony in the noninfarcted areas is closely associated with the abnormal regional wall thickening and motion, which are indicative of reduced myocardial contractility.

Objective To evaluate the left ventricular systolic synchrony and investigate the early diagnostic value of left ventricular systolic dyssynchrony on cardiotoxicity caused by anthracyclines in pa-tients with diffuse large B-cell lymphoma ( DLBCL) . Methods Thirty-two patients ( 22 males, 10 females, age:22-73(54.4±14.2) years) from June 2016 to January 2019 with confirmed DLBCL and normal gated myocardial perfusion imaging (GMPI) before anthracyclines chemotherapy were enrolled prospectively. GMPI was performed after 6 cycles or more of chemotherapy. Changes of myocardial markers, electrocardiogram (ECG) indicators, left ventricular function indicators including left ventricular ejection fraction (LVEF), left ventricular end-diastolic volume ( LVEDV) , left ventricular end-systolic volume ( LVESV) , peak filling rate ( PFR) , summed motion score ( SMS) and summed thickening score ( STS) as well as left ventricular systolic synchrony indicators including phase bandwidth ( BW) , phase standard deviation ( SD) and entropy before and after anthracyclines chemotherapy were analyzed. Paired t test, Wilcoxon signed rank test and χ2 test were used for data analysis. Results Compared with pre-chemotherapy, the left ventricular systolic synchrony indicators were significantly higher than those before chemotherapy (BW: (42.81±11.37)° vs (29.28±8. 68)°;SD:(11.65±4.64)° vs (8.79±3.14)°;entropy:(39.84±5.51)％ vs (36.19±5.94)％;t values: -9.132 to-3.173, all P<0.05) . There were no significant differences in other indicators ( t values:-1.161 to 1.750, z values:-1.633 to-0.096, all P>0.05). Of 32 patients, 13 patients (40.62％) had left ventricular systolic dyssynchrony, and the rate of chemotherapy-induced left ventricular systolic dyssynchro-ny was significantly higher than that of left ventricular dysfunction (15.62％, 5/32;χ2=4.947, P=0.025). All 5 patients with left ventricular dysfunction caused by chemotherapy had left ventricular systolic dyssyn-chrony. The LVEF of the chemotherapy-induced left ventricular systolic dyssynchrony group was significantly lower than that of the left ventricular systolic synchronization group ((54.54±9.25)％ vs (66.79±7.65)％;t=4.087, P<0.01) . Conclusion Left ventricular systolic dyssynchrony can be appeared in DLBCL patients after chemotherapy and is significantly earlier than left ventricular dysfunction, which can be an early indi-cator of cardiotoxicity caused by anthracycline chemotherapy.

Objective To assess left ventricular remodeling (LVRM) after acute myocardial in-farction (AMI) quantitatively by SPECT gated myocardial perfusion imaging (GMPI), and further explore its influencing factors. Methods Twelve Ba-Ma miniature swine were used to establish AMI model. GMPI was performed at the baseline (before AMI), 24 h, 1 and 4 weeks after AMI. Infarct expansion index, left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction ( LVEF) and myocardial perfusion defect were measured. Meanwhile, creatine kinase isozyme MB (CK-MB) and hypersensitive cardiac troponin I (hs-cTn I) were detected. The changes of LVEDV and LVESV before and after AMI (ΔLVEDV and ΔLVESV) were calculated. Repeated measurement analy-sis of variance, the least significant difference t test and Pearson correlation analysis were performed. Re?sults Nine AMI swine were successfully created. LVRM was present 24 h after AMI. LVEDV and LVESV were significantly greater than those before AMI and aggravated within 1 week after AMI, then were down-wards at 4 weeks after AMI. Before AMI, 24 h, 1 and 4 weeks after AMI, the LVEDV was (34.44±7. 90), (47.56±22.66), (71.89±14.90) and (70.33±19.47) ml (F = 28.836, P<0.001), and the LVESV was (10.11±5.49), (25.33±11.62), (40.89±15.88) and (35.44±17.11) ml (F = 22.450, P<0. 001). In-farct expansion index increased progressively within 4 weeks after AMI (F= 16.054, P<0.001). LVEF was significantly lower after AMI than that before AMI (F = 18.267, P<0.001) and improved at 4 weeks after AMI compared to that at 1 week ((52.56±14.96)％ vs (45.11±15.80)％; t= 2.440, P<0. 05). There was a significant correlation between the change in perfusion defect and the ΔLVEDV or ΔLVESV (r values:0. 731 and 0.700, both P<0.05) at 1 week after AMI. In addition, hs-cTn I at 24 h was correlated withΔLVEDV at 24 h and 4 weeks after AMI, respectively (r values: 0.669 and 0.693, both P<0.05). Conclu?sions LVRM and cardiac dysfunction occur in the early period after AMI. LVRM and cardiac dysfunction are most severe at 1 week after AMI, and recover at 4 weeks after AMI, whereas infarct expansion is aggra-vated within 4 weeks. Infarct size and hs-cTn I are closely related to the degree of LVRM.

Objective To investigate the predictive value of preoperative viable myocardium and postoperative left ventricular mechanical dyssynchrony (LVMD) for adverse cardiovascular events(ACE) after coronary artery bypass graft (CABG) in patients with coronary artery disease (CAD) using myocardial perfusion imaging (MPI).Methods From September 2012 to March 2016,49 patients (44 males,5 females,average age:(64±8) years) with CAD were prospectively recruited.All patients underwent 99Tcmmethoxyisobutylisonitrile (MIBI) SPECT gated MPI (GMPI) and 18F-fluorodeoxyglucose (FDG) PET myocardial metabolic imaging to assess myocardial viability preoperatively.GMPI was repeated 4-6 months after CABG to record postoperative LVMD.Phase analysis was used to measure bandwidth (BW) and standard deviation (SD).Regular follow-up was performed,and ACE were taken as the end point.Cox proportional hazard model,Kaplan-Meier method and log-rank test were used to analyze the data.Results The mean duration of follow-up was (3.82±0.80) years,and ACE were present after CABG in 17 CAD patients (34.7％,17/49).Cox multi-analysis revealed that the number of preoperative viable segments (hazard ratio (HR)=0.208,95％ CI:0.068-0.642) and postoperative BW (HR=1.245,95％ CI:1.099-1.411)were independent influencing factors of ACE in CAD patients after CABG (both P＜0.01).Kaplan-Meier survival analysis showed that the incidence of ACE in patients with ＜ 3 viable segments was significantly higher than those with ≥ 3 viable segments (57.1％ (12/21) vs 17.9％ (5/28);x2 =21.023,P＜0.01).The incidence of ACE was significantly higher in the postoperative BW≥98° group than that in the postoperative BW＜98° group (14/19 vs 10％ (3/30);x2 =38.395,P＜0.01).Conclusions Less preoperative viable segments and severe postoperative LVMD are independent risk factors of ACE after CABG in CAD patients.Postoperative LVMD in CAD patients undergoing CABG may have important clinical value in the riskrestratification and prognosis evaluation.