Reliability of transthoracic echocardiography in estimating the size of Amplatzer septal occluder and guiding percutaneous closure of atrial septal defects / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>In China, transthoracic echocardiography (TTE) is popularly used for pre-intervention examination for atrial septal defect (ASD) and for guiding ASD closure. However, the ability to determine ASD size and the safety and efficacy of TTE for guiding ASD closure still has not been widely accepted. This study aimed to evaluate the efficacy and safety of TTE used before, during and after transcatheter ASD closure with Amplatzer septal occluders (ASO).</p><p><b>METHODS</b>Sixty-eight subjects (15 men and 53 women; mean age (33.7 +/- 17.3) years) were enrolled. TTE was used to measure the diameters and guide transcatheter closure of ASD. The ASD was examined by long-axis view, basal short-axis view, apical four-chamber view and the subcostal view to observe position, diameter and relation with neighbouring structures. The largest diameter was selected as the reference diameter. Patients were divided into 3 groups according to the ASD reference diameter: 22 subjects with ASD diameter 4 - 14 mm (group A); 21 subjects with ASD diameter 15 - 20 mm (group B); and 25 subjects with ASD diameter 21 - 33 mm (group C).</p><p><b>RESULTS</b>ASD was occluded successfully in groups A and B. In group C, occlusion failed in 2 cases; 1 case remained with a 3-mm residual shunt sustained until 6-month follow-up. However, at 6-month follow-up, no case of thromboembolism, ASO dislocation or death occurred in the three groups. The diameter of ASD measured by TTE could accurately predict the ASO size that could successfully occlude the ASD, especially in patients with ASD < 20 mm. The ASD diameter measured by TTE correlated well with ASO size (r = 0.925, P < 0.001; r = 0.976, P < 0.001; r = 0.929, P < 0.001 respectively).</p><p><b>CONCLUSIONS</b>ASD diameter measured by TTE can accurately estimate the size of the ASO needed for successful closure of ASD. The larger the ASD, the much larger the ASO needed. TTE is a satisfactory guiding imaging tool for ASD closure.</p>

The role of atherosclerotic plaque stability and inflammation in the pathogenesis of acute coronary syndrome / 中华心血管病杂志

<p><b>OBJECTIVE</b>To elucidate the effect of inflammation and coronary atherosclerotic plaque destabilization in the pathogenesis of acute coronary syndromes (ACS).</p><p><b>METHODS</b>Twenty-eight patients with ACS and 13 patients with stable angina pectoris (SA) were examined by intravascular ultrasound (IVUS). Coronary plaque morphology and areas in culprit lesions were analyzed. The serum levels of hs-CRP, MMP-9, TIMP-1, sCD40L were also measured.</p><p><b>RESULTS</b>Soft plaques were dominant in culprit lesions of ACS patients (71.4%, 20/28), and hard plaques were dominant in culprit lesions of SA patients [76.9% (10/13), P = 0.004]. At the culprit site, plaque area, plaque burden and remodeling index were all significantly larger in culprit lesions of ACS patients than those of SA patients (all P < 0.05). Positive remodeling was more frequent in ACS patients than in SA patients, whereas negative remodeling was more frequent in SA patients (P < 0.05). The serum levels of hs-CRP, MMP-9, sCD40L were higher in ACS group compared with SA group (P < 0.05, respectively). Moreover, hs-CRP level was positively correlated with MMP-9 (r = 0.671, P = 0.000) and sCD40L (r = 0.494, P = 0.008), respectively, in ACS patients. There was no difference in TIMP-1 between two groups (P = 0.234).</p><p><b>CONCLUSIONS</b>These results suggest that structurally vulnerable plaques are essential element in the pathogenesis of ACS and inflammation might play an important role in plaque vulnerability.</p>

Changes of neutrophil myeloperoxidase in coronary circulation among patients with acute coronary syndrome / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the changes of neutrophil myeloperoxidase (MPO) blood concentration gradient between the systemic circulation and the coronary circulation among patients with acute coronary syndrome and its clinical value.</p><p><b>METHODS</b>Fifty patients underwent coronary angiography, which including 10 patients in AMI group, 20 patients in UA group, 10 patients in SA group and 10 subjects served as control. The levels of MPO and hs-CRP were measured in the serum of blood collected from femoral vein, aortic artery root and coronary sinus.</p><p><b>RESULTS</b>Compared with the control, concentrations of LDL in the AMI, UA and SA groups were significantly increased, while the latter three groups did not differ from each other. In the UA patients, the in-gate percentage of MPO decreased in the coronary sinus compared with that in the root of aortic artery (P < 0.01); the in-gate percentage of MPO decreased through coronary circulation more than through systemic circulation (P < 0.001); the average fluorescent intensity of MPO and the concentrations of hs-CRP showed no difference between samples from the coronary sinus and that from the root of aortic artery. In the AMI patients, the average fluorescent intensity of MPO in the coronary sinus was weakened compared with that in the root of aortic artery (P < 0.05); it decreased through coronary circulation more than through systemic circulation (P < 0.001); neither the in-gate percentage of MPO nor the concentrations of hs-CRP showed significant difference between samples from the coronary sinus and that from the root of aortic artery. In the control and SA groups, samples from the femoral vein, the root of aortic artery, and the coronary sinus did not show differences at the serum level of MPO and hs-CRP. In the UA group, the in-gate percentage of MPO correlated positively with the concentration of hs-CRP (r = 0.78, P < 0.01), and with the level of LDL as well (r = 0.52, P < 0.05); In the AMI group, the average fluorescent intensity of MPO correlated negatively with the concentration of hs-CRP (r = -0.80, P < 0.01), and showed no correlation with the level of LDL (r = 0.22, P > 0.05).</p><p><b>CONCLUSIONS</b>MPO is a better marker for inflammation of the local plaques. It may be one of the mechanisms that MPO induces the transforming from LDL to ox-LDL in plaques vulnerability.</p>