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Background Left atrial (LA) volume is an independent prognosticator in various cardiac diseases. The authors assessed the changes of LA volume after successful percutaneous mitral valvuloplasty (PMV) and the impact of LA enlargement on long-term clinical outcome after PMV. Methods and Results From a prospective PMV registry started in 1988, 303 patients (242 women, age: 39.3±10.8 years) who had undergone successful PMV were followed for 4-20 years (median 11 years). Echocardiographic examination including LA volume measurement was performed before PMV and repeated after PMV. LA volume decreased from 92±50 to 69±42 ml (p < 0.001) immediately after PMV and remained stationary until 1 year after PMV. Since then, LA volume subsequently increased exceeding the pre-PMV level by 8 years after PMV. Multivariate analysis showed that LA volume increase at 10 years after PMV was independently related to the post-PMV mitral valve area, the echo score, the presence of atrial fibrillation and post-PMV LA volume. On multiple regression analysis, pre-PMV LA volume and percentage change of LA volume immediately after PMV emerged as independent predictors of event-free survival along with age, pre-PMV tricuspid regurgitation and post-PMV mitral valve area. Ten-year survival rate was 93% in patients with smaller LA before PMV (≤72 ml/m²), whereas it was only 60% in those with larger LA (>72 ml/m²). Conclusions Progressive increase of LA volume was observed even after successful PMV. Larger pre-PMV LA volume was associated with poor prognosis. [ABSTRACT FROM AUTHOR]

Objective: Left ventricular (LV) apical rotation significantly contributes to LV twist, which has been reported to have a vital role in maintaining LV systolic and diastolic function. Apical hypertrophic cardiomyopathy (ApHCM) is a unique disease with pathological LV hypertrophy at the apex. We aimed (1) to evaluate LV twist mechanics in ApHCM and (2) to demonstrate the influence of predominantly local, pathological involvement of the apical myocardium on LV twist mechanics. Methods: 21 patients diagnosed with ApHCM were consecutively enrolled and compared with normal controls. After a standard echocardiographic examination, we scanned parasternal basal and apical short-axis planes to quantify LV rotations and LV twist using the speckle tracking technique. For better understanding of LV twist mechanics in ApHCM, LV radial and biplanar strains and LV twist-volume curve were also evaluated. Results: Compared with the normal controls, apical rotation was markedly decreased in ApHCM patients (p<0.001), but the decreases in basal rotation were not significant. As a consequence, LV twist was significantly lower in ApHCM patients (p = 0.007). Apical radial (p = 0.01) and biplanar (p<0.001) strains in ApHCM were also significantly decreased. Compared to normal controls, LV twist-volume and twist-radial displacement curves clearly showed a decrement in the slope of the linear systolic phase and a loss of an inflection point separating the early from late untwisting phase in ApHCM patients. Conclusion: LV twist in ApHCM was significantly decreased due to a reduction in apical rotation, suggesting that regional myocardial changes in ApHCM can modify the global LV twist mechanics. Given the close interconnection between LV systolic and diastolic function, impairment of LV twist may lead to the loss of early diastolic suction and finally generate diastolic dysfunction in ApHCM. [ABSTRACT FROM AUTHOR]

Objective: Left ventricular (LV) apical rotation significantly contributes to LV twist, which has been reported to have a vital role in maintaining LV systolic and diastolic function. Apical hypertrophic cardiomyopathy (ApHCM) is a unique disease with pathological LV hypertrophy at the apex. We aimed (1) to evaluate LV twist mechanics in ApHCM and (2) to demonstrate the influence of predominantly local, pathological involvement of the apical myocardium on LV twist mechanics. Methods: 21 patients diagnosed with ApHCM were consecutively enrolled and compared with normal controls. After a standard echocardiographic examination, we scanned parasternal basal and apical short-axis planes to quantify LV rotations and LV twist using the speckle tracking technique. For better understanding of LV twist mechanics in ApHCM, LV radial and biplanar strains and LV twist-volume curve were also evaluated. Results: Compared with the normal controls, apical rotation was markedly decreased in ApHCM patients (p<0.001), but the decreases in basal rotation were not significant. As a consequence, LV twist was significantly lower in ApHCM patients (p=0.007). Apical radial (p=0.01) and biplanar (p<0.001) strains in ApHCM were also significantly decreased. Compared to normal controls, LV twist-volume and twist-radial displacement curves clearly showed a decrement in the slope of the linear systolic phase and a loss of an inflection point separating the early from late untwisting phase in ApHCM patients. Conclusion: LV twist in ApHCM was significantly decreased due to a reduction in apical rotation, suggesting that regional myocardial changes in ApHCM can modify the global LV twist mechanics. Given the close interconnection between LV systolic and diastolic function, impairment of LV twist may lead to the loss of early diastolic suction and finally generate diastolic dysfunction in ApHCM. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the effects of stem cell therapy on restoration of the left ventricular (LV) synchronous contraction in patients with acute myocardial infarction (AMI). Methods: 40 patients with AMI who underwent successful coronary revascularisation were randomly allocated to the cell infusion or the control group. Evaluations were performed with echocardiographic tissue synchronisation imaging to determine LV dyssynchrony and with cardiac magnetic resonance imaging to estimate LV ejection fraction (LVEF) at baseline and at 6 months. To quantify the severity of systolic LV dyssynchrony, the standard deviations of time to peak systolic velocity of the 12 LV segments (Ts-SD) were calculated. Results: At 6 months, greater improvements of Ts-SD (ΔTs-SD: -45.0 (40.2) vs 5.0 (39.9) ms, p<0.001) and LVEF (ΔLVEF: 6.8% (9.1%) vs -0.2% (6.9%), p = 0.015) relative to the corresponding baseline values were observed in the cell infusion group than in the control group. By multivariate analysis, ΔTs-SD and baseline LVEF emerged as the independent determinants of LVEF improvement and cell infusion, and baseline Ts-SD as the determinant of ΔTs-SD improvement. Maximal exercise capacity measured by symptom-limited treadmill testing correlated well with Ts-SD but not with LVEF at 6 months of follow-up. Conclusion: Stem cell therapy had a favourable effect on the restoration of LV synchronous contraction in patients with AMI. [ABSTRACT FROM AUTHOR]

Objective: The effects of stem cell therapy on the coronary vasculature were investigated in patients with acute myocardial infarction who underwent peripheral blood stem cell (PBSC) therapy in the MAGIC Cell-3-DES study. Methods: Among 50 patients with acute myocardial infarction who underwent either sirolimus-eluting stent or paclitaxel-eluting stent implantation for the culprit lesion, intravascular ultrasound was analysed in 36 patients (cell infusion: n = 19 and control: n = 17). In the cell infusion group, PBSCs mobilised by granulocyte-colony stimulating factor were delivered via intracoronary infusion into infarcted myocardium. Proximal and distal reference segments, and stented segments, were evaluated with intravascular ultrasound at immediate post-intervention and 6-month follow-up, respectively. Results: In the proximal and distal reference segments, the serial changes of lumen area, vessel area, and plaque plus media area were not significantly different between the cell infusion and the control groups. Within stented segments, mean neointimal area was similar in the two groups (cell infusion: 0.2 (SD 0.5) mm² vs control: 0.3 (SD 0.4) mm², p>0.05). However, there was a significant increase in mean peri-stent area of stented segment in the cell infusion group compared with the control group (0.7 (SD 1.4) mm² vs -0.1 (SD 1.2) mm², p<0.05). This difference mainly came from paclitaxel-eluting stent-implanted patients. Conclusion: Intracoronary infusion of PBSCs mobilised with G-CSF does not aggravate de novo atherosclerotic lesion and neointimal hyperplasia with DES implantation. However, it may induce peri-stent tissue growth at the stented segment, especially in patients receiving PES. Its clinical significance needs to be evaluated with long-term follow-up. [ABSTRACT FROM AUTHOR]

Objective: The effects of granulocyte-colony stimulating factor (G-CSF) on endothelial function are unknown. Therefore, we investigated the effects of G-CSF on endothelial function. Methods: 76 patients participating in the MAGIC-Cell-3-DES trial were enrolled. These were patients with acute myocardial infarction (AMI) or old MI (OMI) who underwent percutaneous coronary intervention (PCI), and were prospectively randomised into a G-CSF group (G-CSF (10 μg/kg/day) injection for 3 days after PCI) or a control group. Additionally, 20 healthy volunteers were also enrolled. These subjects were categorised into five groups: AMI-control (n = 18), AMI-G-CSF (18), OMI-control (20), OMI-G-CSF (20) and healthy-G-CSF (20). Baseline flow-mediated dilation (FMD) of the brachial artery and serum inflammatory biomarkers were performed on day 1, and repeated on day 4 in all groups. G-CSF was injected for 3 days between days 1 and 4 in the AMI-G-CSF, OMI-G-CSF and healthy-G-CSF groups. Results: In both the healthy-G-CSF and OMI-G-CSF groups, G-CSF increased serum high sensitivity C-reactive protein (hsCRP) (0.3 (0.5) mg/l vs 6.1 (3.5) mg/l and 5.6 (3.8) mg/l vs 13.0 (7.7) mg/l, baseline vs post-G-CSF in the healthy and OMI-G-CSF groups, respectively, p<0.001). In the AMI-G-CSF group, G-CSF hindered the decline of hsCRP during the recovery phase, resulting in a relative increase in hsCRP. However, in all three groups, G-CSF did not significantly alter FMD. Conclusion: Despite an associated increase in systemic inflammation, G-CSF treatment does not lead to acute impairment of brachial artery endothelial function in either healthy subjects or patients with MI. [ABSTRACT FROM AUTHOR]