PMC:2948162 / 9409-16565 JSONTXT

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{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/2948162","sourcedb":"PMC","sourceid":"2948162","source_url":"https://www.ncbi.nlm.nih.gov/pmc/2948162","text":"Results\n\nIMH and MVO\nSignal intensity on the T2W and LGE images within the territory of the IRA was increased in all patients. The AAR and IS were 26 ± 12% and 15 ± 11% of LV mass, respectively. MVO was observed in 49 (54%) and IMH in 39 patients (43%), and both were always located subendocardially within the infarct core. IMH was only observed in patients with MVO. A significant correlation was found between MVO and IMH extent (r = 0.8, p \u003c 0.001, Fig. 1), but absolute MVO extent was larger than that of IMH [3.1 ml (IQR 1.6–5.3) vs. 2.2 ml (IQR 1.6–3.5), p = 0.04].\nFig. 1 Correlation between IMH and MVO. a Original scale values. b Log transformed values. A good linear correlation is seen between MVO and IMH (r = 0.86, p \u003c 0.001). Open circles indicate observed values and stars indicate predicted values in the MVO(+)/IMH(-) group. Note that most of the predicted values are within the lower range of observed values\n\nSubgroups\nBased on the presence or absence of MVO and IMH, patients were classified into three groups: 41 patients with MVO(−)/IMH(−), 10 with MVO(+)/IMH(−) and 39 with MVO(+)/IMH(+) (Fig. 2). For most of the baseline characteristics, there were no significant differences between groups (Table 1), except for pre-PCI TIMI 3 flow, which was only observed in the MVO(−)/IMH(−) group. There was no difference in the use of glycoprotein IIbIIIa inhibitor between groups.\nFig. 2 Magnetic resonance image examples from each patient group. Top row (a, b): MVO(−)/IMH(−) patient; middle row (c, d): MVO(+)/IMH(−) patient; bottom row (e, f): MVO(+)/(IMH(+) patient. T2-weighted images are shown on the left (a, c, e) and corresponding late gadolinium-enhanced images on the right (b, d, f). Oedema and infarct border zones are indicated by arrowheads and IMH and MVO by asterisks\nTable 1 Baseline characteristics\nGroup FDR p value\nMVO(−)/IMH(−) (n = 41) MVO(+)/IMH(−) (n = 10) MVO(+)/IMH(+) (n = 39)\nAge (years) 61 ± 9 59 ± 15 59 ± 12 0.64\nMale (%) 27 (66) 6 (60) 32 (82) 0.29\nDM (%) 4 (10) 1 (10) 1 (3) 0.49\nSmoking (%) 33 (80) 9 (90) 36 (92) 0.38\nHypertension (%) 20 (49) 3 (30) 12 (31) 0.35\nHypercholesterolaemia (%) 11 (27) 3 (30) 11 (28) 0.95\nPositive family history (%) 16 (39) 3 (30) 22 (56) 0.29\nAnterior location (%) 10 (24) 2 (20) 16 (41) 0.30\nPrevious angina (%) 13 (32) 3 (30) 21 (54) 0.20\nGIIbIIIa inhibitor (%) 17 (41) 5 (50) 23 (59) 0.38\nTIMI 3\n Pre-PCI (%) 10 (24) 0 (0) 0 (0) 0.004\n Post-PCI (%) 36 (88) 9 (90) 35 (90) 0.66\nRentrop ≥2 (%) 9 (22) 5 (50) 7 (18) 0.20\nThrombosuction (%) 9 (22) 2 (20) 11 (28) 0.89\nTime to PCI (min) 217 (165–304) 177 (148–248) 201 (160–291) 0.65\nAAR (%) 19 ± 121.2 27 ± 81 33 ± 92 \u003c0.001\nIS (%) 8 ± 83.4 16 ± 73.5 23 ± 94.5 \u003c0.001\nMyocardial salvage (%) 54 ± 326 40 ± 25 28 ± 246 0.004\nMVO (% of LV mass) 0 0.8 (0.4–1.9) 1.7 (1.0–3.3) 0.07\nIMH (% of LV mass) 0 0 1.6 (1.0–2.4)\nValues are presented as mean ± SD or median and IQR; AAR: area at risk; DM: diabetes mellitus; IS: infarct size at baseline; IHM: intramyocardial haemorrhage; MVO: microvascular obstruction; PCI: percutaneous coronary intervention. Superscripts indicate significant post-hoc, pairwise comparisons\nThe AAR and IS were largest in the MVO(+)/IMH(+) group, intermediate in the MVO(+)/IMH(−) group and smallest in the MVO(−)/IMH(−) group (Table 1). Myocardial salvage, defined as the difference between AAR and IS, was lowest in the MVO(+)/IMH(+) group, intermediate in the MVO(+)/IMH(−) group and highest in the MVO(−)/IMH(−) group (28 ± 24%, 40 ± 25% and 54 ± 32%, respectively, p \u003c 0.001, Table 1 and Fig. 3).\nFig. 3 Area at risk (AAR) and infarct size (IS). AAR (grey bars) and IS (white bars) represented as percentages of LV mass for each patient group. The MVO(+)/IMH(−) group represents an intermediate group. Myocardial salvage is the difference between AAR and IS\nThe MVO extent tended to be larger in the MVO(+)/IMH(+) patients compared with the MVO(+)/IMH(−) patients [1.7% (IQR 1.0–3.3%) vs. 0.8% (IQR 0.4–1.9%) of LV mass, respectively, p = 0.07].\n\nPredicted IMH size in patients with MVO but without IMH\nThe IMH in the MVO(+)/IMH(−) patients could have been missed as a result of the limits of spatial resolution of T2W CMR. To investigate this, predicted IMH size values for MVO(+)/IMH(−) were calculated based on the following model derived from the MVO(+)/IMH(+) group data:\nAll predictors in the above model were statistically significant. Observed and predicted IMH values are displayed in Fig. 1a and b. Predicted values are marked as stars. In either case it is evident that only two patients had sufficiently small predicted IMH outside the observed value range in the other patients. Theoretically, these two values could have been missed by T2W CMR. Conversely, several of the predicted values were still of sufficient size, at least comparable to that of the observed counterparts, and as such they could have been detected by CMR.\n\nFunctional parameters and LV remodelling\nThe LVEDVi and LVESVi decreased from baseline to follow-up and were highest in the MVO(+)/MVO(+) group, intermediate in the MVO(+)/IMH(−) group and lowest in the MVO(−)/IMH(−) group at both time points (Table 2). Likewise, LVEF improved in all three groups, but remained lowest in the MVO(+)/MVO(+) group, intermediate in the MVO(+)/IMH(−) group and highest in the MVO(−)/IMH(−) group in the univariate comparisons (Fig. 4).\nTable 2 Functional parameters at baseline and follow-up\nGroup FDR p value\nMVO(−)/IMH(−) (n = 41) MVO(+)/IMH(−) (n = 10) MVO(+)/IMH(+) (n = 39)\nLVEDVi (ml/m2)\nBaseline 81 ± 141 86 ± 15 88 ± 171 0.24\nFollow-up 78 ± 182 76 ± 12 88 ± 202 0.13\nLVESVi (ml/m2)\nBaseline 38 ± 113 43 ± 11 47 ± 133 0.01\nFollow-up 34 ± 124 34 ± 6 45 ± 154 0.01\nLVEF (%)\nBaseline 55 ± 85 51 ± 6 47 ± 75 \u003c0.001\nFollow-up 57 ± 76 55 ± 3 50 ± 76 \u003c0.001\nValues are presented as mean ± SD; IMH: intramyocardial haemorrhage; LVEDVi: left ventricular end diastolic volume index; LVESVi: left ventricular end-systolic volume index; LVEF: left ventricular ejection fraction; MVO: microvascular obstruction. Superscripts indicate significant post-hoc, pairwise comparisons\nFig. 4 Left ventricular ejection fraction (LVEF) at baseline and follow-up. LVEF significantly increased in all three groups from baseline (grey bars) to follow-up CMR (white bars), but remained intermediate in the MVO(+)/IMH(−) group\nTable 3 displays the fixed effect parameter estimates of the random intercept model. Subjects were taken as random effect, whereas time and MVO/IMH groups were taken as fixed effect factors adjusted for IS. LVEF significantly increased over time (for all groups), showing a significant negative association with IS. Note that the presence of IMH or MVO had no significant independent predictive value for LVEF once adjusted for IS.\nTable 3 Fixed effect parameter estimates of the random intercept model. Outcome variable: LVEF\nβ (SE) p value\nIntercept 55.651 (2.086) \u003c0.001\nIS −0.452 (0.071) \u003c0.001\nTime 2.660 (0.623) \u003c0.001\nMVO(−)/IMH(−) −0.023 (1.648) 0.989\nMVO(+)/IMH(−) 0.004 (2.059) 0.998\nMVO(+)/IMH(+) Reference\nIS: infarct size. Error and random intercept variances were 15.762 and 20.571, respectively 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