Longitudinal evaluation of diastolic dyssynchrony by SPECT gated myocardial perfusion imaging early after acute myocardial infarction and the relationship with left ventricular remodeling progression in a swine model.

BACKGROUND: 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). METHODS: 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. RESULTS: 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, ß = 0.004, 95% CI 0.001 to 0.007, P = 0.024; PSD, ß = 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. CONCLUSIONS: 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.

Mechanical contraction to guide CRT left-ventricular lead placement instead of electrical activation in myocardial infarction with left ventricular dysfunction: An experimental study based on non-invasive gated myocardial perfusion imaging and invasive electroanatomic mapping.

BACKGROUND: Whether the region of the latest electrical activation (LEA) corresponds with the segment of the latest mechanical contraction (LMC) in ischemic cardiomyopathy (ICM) is uncertain. We aimed to investigate the relationship between the left-ventricular (LV) viable segments with LEA and with LMC after myocardial infarction (MI) and analyze the acute hemodynamic responses (dP/dtmax) after cardiac resynchronization therapy (CRT) pacing at different LV sites. METHODS AND RESULTS: Bama suckling pigs (n = 6) were subjected to create MI models. Both gated myocardial perfusion imaging (GMPI) and electroanatomic mapping (EAM) were performed successfully before MI and 4 weeks after MI. LMC was assessed by phase analysis of GMPI, while LEA was evaluated by EAM. The dP/dtmax was measured before CRT and when the CRT LV electrode was implanted in viable segments of LMC, viable segments of lateral wall and scar, respectively. The viable segments of LEA were consistent with the sites of LMC for five in six cases. The dP/dtmax increased significantly compared with that before CRT when the CRT LV electrode was implanted in viable segments of LMC (1103.33 ± 195.76 vs 717.83 ± 80.74 mmHg·s-1, P = .001), which was also significantly higher than in viable segments of lateral wall (751.17 ± 105.62 mmHg·s-1, P = .000) and scar (679.50 ± 60.87 mmHg·s-1, P = .001). CONCLUSIONS: Non-invasive GMPI may be a better option than invasive EAM for guiding LV electrode implantation for CRT in ICM.

Myocardial perfusion imaging detects mechanical dyssynchrony in left ventricular infarcted and noninfarcted areas early after acute myocardial infarction in a porcine model.

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.

Role of Gated Myocardial Glucose Metabolic Imaging in Assessing Left Ventricular Systolic Dyssynchrony after Myocardial Infarction and the Influential Factors.

In this study, we investigated the role of gated myocardial glucose metabolic imaging in assessing left ventricular (LV) systolic dyssynchrony after myocardial infarction (MI) and explored the influencing factors. Bama mini-pigs were divided into normal group and MI group and subjected to gated myocardial metabolic imaging (GMMI) and gated myocardial perfusion imaging (GMPI). The phase bandwidth (BW), standard deviation (SD) and the latest activation site of left ventricle were obtained using program Cedars QGS. The results showed that (1) BW and SD obtained in GMMI and GMPI showed significant correlation in pigs with MI, but not in the normal pigs, (2) BW and SD obtained in GMMI and GMPI had good consistency in both normal pigs and MI pigs, (3) GMMI and GMPI had a 66.7% identity in determining the latest activation site of left ventricle in the normal pigs and 77.8% identity in determining the latest activation site of left ventricle in pigs with MI. Multivariate stepwise regression analysis showed that total perfusion deficit and summed motion score were independent factors affecting BW and SD in GMMI. In conclusion, phase analysis of GMMI images could objectively reflect LV systolic dyssynchrony resulted from interactions of multiple factors.

Protective Effects of Sinomenine on CFA-Induced Inflammatory Pain in Rats.

BACKGROUND The purpose of this study was to investigate the effects of sinomenine (SIN) on CFA-induced inflammatory pain in rats, and to explore the underlying molecular mechanisms. MATERIAL AND METHODS To determine the potential influences of SIN in the pathogenesis of inflammatory pain, an inflammatory pain (IP) mouse model was established and rats were treated with SIN (30 mg/kg). Behavioral tests were used to assess the MWT and TWL of the rats. ELISA assay was used to detect the level of inflammation cytokines. Western blotting and qRT-PCR were carried out to measure the related protein and mRNA expression level, respectively. RESULTS We found that the MWT and TWL of the CFA-treated rats were markedly lower than that of the control rats, and they were significantly increased by SIN administration. The results suggest that IP rats had higher levels of TNF-α, IL-1ß and IL-6 compared with the control rats. SIN administration decreased the levels of TNF-α, IL-1ß, and IL-6. In addition, we found that p-p65 and p-p38 expression notably decreased after SIN treatment in IP rats. Moreover, the results showed that SIN inhibited Cox-2 and PGE2 expression in IP rats. CONCLUSIONS The data indicate that SIN had a protective role in inflammatory pain through repressing inflammatory mediators via preventing the p38MAPK-NF-κB pathway.