Left atrial morpho-functional remodeling in atrial fibrillation assessed by three dimensional speckle tracking echocardiography and its value in atrial fibrillation screening.

BACKGROUND: Three dimensional speckle tracking echocardiography (3D STE) is a novel technique combining 3D echocardiography and speckle tracking analysis. 3D STE software dedicated to the left atrium (LA) was recently available. Our study aimed to assess (1) atrial fibrillation (AF) related LA morpho-functional remodeling using 3D STE and (2) value of LA function parameters in identifying paroxysmal AF (PAF). METHODS: One hundred thirty-nine PAF, 109 persistent AF (Per-AF) and 59 non-AF subjects underwent 3D STE. LA phasic volumes and total LA emptying fraction (LAEF) were obtained and used to calculate passive (pLAEF) and active LA emptying fraction (aLAEF) based on atrial contraction. LA longitudinal and circumferential strain representing reservoir (LASr/LASrc), conduit (LAScd/LAScdc) and pump (LASct/LASctc) function were also assessed. RESULTS: 3D STE was found to have good reproducibility. Increase of LA volumes and decrease of parameters representing LA reservoir and pump function were independently associated with AF as well as AF burden. The correlations between LA emptying fraction and LA circumferential strain representing the same function were always stronger than those with LA longitudinal strain (p < 0.001). Minimal LA volume, LAEF, aLAEF, LASrc and LASctc can be used to accurately differentiate PAF from non-AF subjects (AUC > 0.8) with great sensitivity and specificity. CONCLUSIONS: Assessing LA remodeling in AF using 3D STE was feasible. AF and AF burden were independently associated with LA enlargement and impairment of reservoir and pump function but not conduit function. LA function parameters can indicate underlying PAF and thus can guide AF screening strategy.

Slit guidance ligand 2 promotes the inflammatory response of periodontitis through activation of the NF-κB signaling pathway.

BACKGROUND AND OBJECTIVES: Periodontitis is a chronic multifactorial inflammatory disease associated with dental plaque biofilms. Slit guidance ligand 2 (SLIT2) has been shown to guide neuronal migration, regulate the inflammatory response and cancer progression. However, the role of SLIT2 in periodontitis is poorly understood. In this study, we investigated the expression of SLIT2 in the gingiva of periodontitis and its role in periodontitis progression. METHODS: Gingiva and gingival crevicular fluid (GCF) were collected from healthy people and periodontitis patients. Immunohistochemistry and enzyme-linked immunosorbent assay (ELISA) were used to analyze SLIT2 secretion level. Healthy human gingival fibroblasts (hGFs) were isolated and the expression of SLIT2 in lipopolysaccharide (LPS)-treated hGFs was detected. The effect of SLIT2 on inflammation was analyzed using western blot and immunofluorescence. SLIT2 knockdown (KD) and overexpression assays in hGFs were performed to investigate the role of SLIT2 in the LPS-induced inflammatory response. RESULTS: Gingival tissues and GCF of periodontitis patients displayed higher expression of SLIT2. Similarly, SLIT2 was upregulated in hGFs in an inflammatory environment (LPS treatment). In addition, SLIT2 treatment increased the expression of the inflammatory mediators interleukin-6 (IL-6) and IL-8 in hGFs. Mechanistically, SLIT2 stimulated the activation of nuclear factor-κB (NF-κB) signaling, as well as LPS. Lastly, SLIT2 KD impaired LPS-induced IL-6 production in hGFs, while SLIT2 overexpression amplified the inflammatory response. CONCLUSION: SLIT2 may be involved in the aggravation of periodontitis by activating NF-κB signaling in hGFs.

The lncRNA H19/miR-541-3p/Wnt/ß-catenin axis plays a vital role in melatonin-mediated osteogenic differentiation of bone marrow mesenchymal stem cells.

Implant dentures become the first choice for denture restoration in patients with tooth loss. However, oral implants often fail in osteoporosis (OP) patients. Melatonin (MT) induces osteogenic differentiation of bone mesenchymal stem cells (BMSCs), suggesting its therapeutic potential in OP treatment. Long non-coding RNA H19 induces osteogenic differentiation of BMSCs, while its regulatory mechanism in MT-involved osteogenic and adipogenic differentiation of BMSCs remains elusive. Ovariectomized (OVX) rat was used to construct an OP model, and bone quality was assessed. Meanwhile, the expression of H19, miR-541-3p, MT and adiponectin (APN) was examined by quantitative reverse transcription-PCR (qRT-PCR) or ELISA. The adipogenic and osteogenic differentiation of BMSCs were determined by oil red O staining and alizarin red S staining, respectively. The targeting relationships between H19, miR-541-3p and APN mRNA were predicted by bioinformatics and confirmed by RNA immunoprecipitation and dual-luciferase reporter assay. The results showed that MT, H19 and APN were down-regulated, while miR-541-3p was up-regulated in the OVX rat model. At the cellular level, MT reduced adipogenic differentiation, heightened osteogenic differentiation of BMSCs, and activated Wnt/ß-catenin pathway, which were reversed by the MT2 selective inhibitor 4-P-PDOT. Overexpressing H19 facilitated the osteogenic differentiation and inhibited the adipogenic differentiation of BMSCs mediated by MT, while H19 knockdown or overexpressing miR-541-3p had the opposite effect. Moreover, H19 functioned as a competitive endogenous RNA and sponged miR-541-3p, and miR-541-3p targeted APN. Overall, MT modulates the osteogenic and adipogenic differentiation of BMSCs by mediating H19/miR-541-3p/APN axis, providing a new reference for the targeted therapy of OP.

Simultaneous surgery of mandibular reduction and impacted mandibular third molar extraction: A retrospective study of 65 cases.

A considerable number of patients with prominent mandibular angle have mandibular third molar impaction that needs surgical removal. Mandibular reduction is a popular and effective surgery to correct prominent mandibular angle, but it has been rarely performed simultaneously with impacted third molar extraction. In order to decrease the number of operations and suffering of patients, safely performing these 2 operations together is necessary and important. From January 2016 to June 2018, patients received mandibular reduction and impacted mandibular third molar extraction together were retrospectively reviewed. Forty-seven patients receiving long-curve mandibular reduction (n = 12) or simple mandibular reduction (n = 35) were included in this study. A total of 65 impacted mandibular third molars were extracted during mandibular reduction. One patient had hematoma within facial soft tissue which reabsorbed spontaneously. Seven patients who underwent long-curve mandibular reduction reported transient inferior lip numbness for several weeks. No infection or poor wound healing was reported. No immediate or delayed mandibular fracture occurred. All the patients were satisfied with both the aesthetic result of mandibular reduction and the unnecessity of receiving a secondary surgery to extract the impacted third molar. Simultaneously performing mandibular reduction and impacted mandibular third molar extraction can effectively reduce the number of operations and patients' suffering. It is also safe with adequate pre-op assessment, professional surgical knowledge, proper use of surgical instruments, meticulous surgical procedures, and correct post-op care.

Three-dimensional mitral valve structure in predicting moderate ischemic mitral regurgitation improvement after coronary artery bypass grafting.

OBJECTIVE: Focusing on 3-dimensional mitral valve structure, this study investigated predictors for moderate ischemic mitral regurgitation (IMR) improvement after off-pump coronary artery bypass grafting (OPCAB). METHODS: This study included 143 patients (age 67.6 ± 7.6 years, 32.9% female) with previous myocardial infarction and moderate IMR undergoing OPCAB. Preoperative 3-dimensional echocardiographic data were analyzed, focusing on mitral annular geometry and leaflet tethering model. Patients were grouped according to IMR at 1-year postoperative follow-up into improved (n = 65), with no or mild IMR, and failure (n = 70), with moderate or severe IMR, groups. Groups were compared to identify predictors of IMR improvement after OPCAB. RESULTS: Eight patients died within 1 year. At 1 postoperative year, improved group included 65 patients; failure group included 70. Improved group had less preoperative annular flattening (smaller nonplanar angle) and segmental leaflet tethering (smaller A3, P1, P2, and P3 tethering angles) than failure group. Nonplanar angle (P < .001) and P3 tethering angle (P < .001) were independent predictors of moderate IMR improvement after OPCAB. Receiver operator characteristic curves defined P3 tethering angle of 28.8° (sensitivity of 78.6%, specificity of 84.6%) and nonplanar angle of 158.1° (sensitivity, 64.3% and specificity of 86.2%) as the cutoff values. CONCLUSIONS: Preoperative moderate IMR can be improved by OPCAB in selected patients. Less annular flattening and P3 leaflet tethering may predict improvement of moderate IMR after OPCAB, suggesting that the annular nonplanar saddle shape and less leaflet tethering toward P3 segment are important for the prognosis of moderate IMR.

Left ventricular regional dyssynchrony predicts improvements in moderate ischaemic mitral regurgitation after off-pump coronary artery bypass.

OBJECTIVES: The aim of this study was to explore the predictors of the improvement in moderate ischaemic mitral regurgitation (IMR) after off-pump coronary artery bypass grafting (OPCAB) focusing on left ventricular (LV) dyssynchrony. METHODS: A prospective study was performed among 135 patients (age at surgery, mean ± SD: 67.0 ± 8.2 years, 33.3% women) with prior myocardial infarction and moderate IMR undergoing OPCAB from 2008 to 2015. Preoperative and follow-up clinical and echocardiographic parameters were analysed, focusing on LV global/regional dyssynchrony. Patients were grouped by IMR at 1 year postoperatively: improved group with no or mild IMR (n = 61) and failure group with moderate or severe IMR (n = 67). Data were compared between groups to explore the predictors of IMR improvement after OPCAB. RESULTS: Seven patients who died before the 1-year postoperative assessment were excluded. At the 1-year follow up, there were 61 patients in the improved group and 67 patients in the failure group. Preoperatively, the improved group had smaller LV global dyssynchrony, LV regional dyssynchrony (papillary muscle systolic dyssynchrony; improved group versus failure group: 48.5 ± 4.5 ms vs 57.1 ± 3.9 ms; P < 0.001) and greater LV ejection fraction (improved group versus failure group: 44.7 ± 5.0% vs 36.7 ± 6.7%; P < 0.001) than the failure group. Papillary muscle systolic dyssynchrony (odds ratio 1.556, 95% confidence interval 1.313-1.845; P < 0.001) and preoperative ejection fraction (odds ratio 0.799, 95% confidence interval 0.691-0.924; P = 0.002) were independent predictors of moderate IMR improvement after OPCAB. CONCLUSIONS: In the selected patients, preoperative moderate IMR could be relieved by coronary artery bypass grafting. Greater ejection fraction and absence of LV regional dyssynchrony may predict the improvement in moderate IMR after coronary artery bypass grafting, suggesting that LV dyssynchrony especially regional dyssynchrony and preserved ventricular function would be important to the outcome of patients with moderate IMR.

The comprehensive impact on human body induced by resolution of growth hormone excess.

CONTEXT: Chronic excess of growth hormone (GH) often leads to systemic complications. The reversibility of these complications after GH resolution is not fully understood. OBJECTIVE: To investigate when and to what extent will the comorbidities be ameliorated. DESIGN: We conducted a prospective study comprising 24 patients with acromegaly, who achieved remission after transsphenoidal surgery. The dynamic changes of endocrine, cardiovascular, respiratory, sleep, bone and morphology parameters were evaluated at enrollment and 1 week, 1 month, 3 months, 6 months and 12 months after surgery. RESULTS: Random GH dropped by 98.4% at the first day postoperatively. IGF-I index dropped by 50% and 64% at 1 week and 1 month respectively and remained unchanged onwards. Glucose metabolism improved significantly at 1 week and stabilized at 1 month. Testosterone in male patients recovered to normal range since 1 month. Systolic blood pressures dropped markedly at 3 months while diastolic blood pressures fell mildly at later visits. Abnormal lung function showed no improvement. The decrease of bone formation and resorption markers occurred at 1 week and 3 months, respectively. At 1 month, the tongue area declined while the airway volume increased significantly, accompanied with improved obstructive sleep apnea syndrome. Extremities, lips and nasal ala became smaller since 1 week. Liver, kidney and spleen volumes declined by 6.4, 15.9, 9.2%, respectively at 1 month. The volumes of pancreas and adrenal showed no change. CONCLUSIONS: The rapid resolution of excessive GH led to the reversible changes of systemic comorbidities in a time-dependent and organ-specific manner.

Predictors of moderate ischemic mitral regurgitation improvement after off-pump coronary artery bypass.

OBJECTIVE: The aim of this study was to explore the predictors of improvement of moderate ischemic mitral regurgitation after off-pump coronary artery bypass grafting. METHODS: A prospective study was performed among 109 patients (aged 66.6 ± 8.6 years, 34.6% were female) with prior myocardial infarction and moderate ischemic mitral regurgitation undergoing off-pump coronary artery bypass grafting. Preoperative and follow-up clinical characteristics and echocardiography data were analyzed, focusing on left ventricular global/regional remodeling and function. Patients were grouped by postoperative ischemic mitral regurgitation at 1 year postoperatively: the improved group with no or mild ischemic mitral regurgitation and the failure group with moderate or severe ischemic mitral regurgitation. Data were compared between the 2 groups to explore the predictors of ischemic mitral regurgitation improvement after off-pump coronary artery bypass grafting. RESULTS: Five patients died within 1 year and were excluded. At the 1-year follow-up, there were 55 patients in the improved group and 49 patients in the failure group. Before surgery, the improved group had smaller left ventricular end-systolic volume, greater left ventricular ejection fraction, greater posterior-inferior volume ratio, and earlier operation timing after infarction than the failure group. Posterior-inferior volume ratio (P < .001), ejection fraction (P = .003), and duration between infarction and operation (P < .001) were independent predictors of preoperative moderate ischemic mitral regurgitation improvement. CONCLUSIONS: In selected patients, preoperative moderate ischemic mitral regurgitation was relieved by off-pump coronary artery bypass grafting. Greater ejection fraction, greater posterior-inferior volume ratio, and early operation timing after infarction may predict the improvement of moderate ischemic mitral regurgitation after off-pump coronary artery bypass grafting, suggesting that posterior-inferior regional remodeling, reserved ventricular function, and early revascularization are important to the outcome.

The gene polymorphism of LOX1 predicts the incidence of LVH in patients with essential hypertension.

BACKGROUND: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) has been shown to play an important role in cardiac remodeling under different pathologic conditions. The role of genetic polymorphisms in the LOX1 gene, however, remains unclear in the development of left ventricular hypertrophy (LVH) for patients with hypertension. METHODS: A total of 536 patients diagnosed with essential hypertension (EH) were recruited in this study. Patients were assigned to the LVH+ (n=143) and LVH- (n=393) groups, respectively. The serum LOX1 level was measured and three single nucleotide polymorphisms (SNPs), i.e. intron 4 (G→A), intron 5(T→G), and 3' UTR (T→C) of the LOX1 gene were genotyped. RESULTS: The genotype frequencies of intron 4 G>A and 3'UTR T>C were not significantly different between the LVH+ and LVH- groups (both P>0.05), however, frequencies of 501G>C were significantly different between those two groups (P=0.007). The 501CC genotype carriers had a markedly higher serum LOX1 level and an increased risk to develop LVH (adjusted OR=2.444, adjusted P=0.002). There was a positive correlation between serum LOX1 level and left ventricular mass index (r=0.907, P<0.001); a cutoff value of 1.0 ng/mL for sLOX-1 was applied to significantly differentiate the LVH+ patients from the LVH- patients with 84% sensitivity and 86% specificity. CONCLUSION: Our data suggest that both the 501>C SNP in the LOX1 gene and the serum LOX1 level may be used to predict the development of LVH among EH patients.

Arctigenin promotes cholesterol efflux from THP-1 macrophages through PPAR-γ/LXR-α signaling pathway.

Cholesterol efflux from macrophages is a critical mechanism to prevent the development of atherosclerosis. Here, we sought to investigate the effects of arctigenin, a bioactive component of Arctium lappa, on the cholesterol efflux in oxidized low-density lipoprotein (oxLDL)-loaded THP-1 macrophages. Our data showed that arctigenin significantly accelerated apolipoprotein A-I- and high-density lipoprotein-induced cholesterol efflux in both dose- and time-dependent manners. Moreover, arctigenin treatment enhanced the expression of ATP binding cassette transporter A1 (ABCA1), ABCG1, and apoE, all of which are key molecules in the initial step of cholesterol efflux, at both mRNA and protein levels. Arctigenin also caused a concentration-dependent elevation in the expression of peroxisome proliferator-activated receptor-gamma (PPAR-γ) and liver X receptor-alpha (LXR-α). The arctigenin-mediated induction of ABCA1, ABCG1, and apoE was abolished by specific inhibition of PPAR-γ or LXR-α using small interfering RNA technology. Our results collectively indicate that arctigenin promotes cholesterol efflux in oxLDL-loaded THP-1 macrophages through upregulation of ABCA1, ABCG1 and apoE, which is dependent on the enhanced expression of PPAR-γ and LXR-α.

Rs12218 In SAA1 gene was associated with serum lipid levels.

BACKGROUND: Serum amyloid A (SAA) is a kind of apolipoprotein. Several studies indicated that SAA genetic polymorphism rs12218 was associated with carotid atherosclerosis, peripheral arterial disease, and serum uric acid levels. However, the relation between rs12218 and lipid levels remains unclear. This study assessed the correlation between SAA1 gene rs12218 polymorphism and lipid levels in a Chinese population. METHODS: A total of 823 participants were selected from the subjects for health check in Shanghai Huashan hospital from Jan. 2013 to Mach. 2013. Correlations between rs12218 polymorphism and lipid levels were investigated through the identification of rs12218 genotypes using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: We found that the SNP rs12218 was associated with triglyceride (TG), total cholesterol (TC), and low-density lipoprotein (LDL-C) levels by analyses of a dominant model (P<0.001, P=0.002, P=0.003, respectively), a recessive model (P<0.001, P=0.001, P=0.005, respectively) and an additive model (P<0.001, P=0.001, P=0.002, respectively), and the difference remained significant after the adjustment of sex, age, alcohol intake, and smoking (All P<0.01). CONCLUSION: Our results indicated that the rs12218 in the SAA1gene was associated with lipid levels in a Chinese population.

Left atrial and right atrial deformation in patients with coronary artery disease: a velocity vector imaging-based study.

BACKGROUND: Impaired left ventricular (LV) function has been shown by strain rate (SR) imaging in patients with coronary artery disease (CAD). Our aim was to investigate global and regional, systolic and diastolic left atrial (LA) and right atrial (RA) longitudinal deformation in CAD using velocity vector imaging. METHODS: Echocardiographic and velocity vector imaging studies were performed in 20 patients with mild CAD, 40 patients with severe CAD and 25 controls. Maximal atrial volume, peak atrial longitudinal strain (ε(s)) and SR during LV systole (SRs), SR during early LV filling (SRe) and late LV filling (SRa) were measured. Longitudinal strain during atrial contraction (ε(a)) was obtained at the onset of P-wave on electrocardiography, and ε(a)/ε(s) was calculated. RESULTS: Longitudinal peak ε(s) and SRs of LA showed decreased trend among CAD patients. The global and lateral LA SRe were prominently lower, while RA ε(a), SRa and ε(a)/ε(s) were prominently higher in 2 CAD groups than control group (P value <0.05). As compared with controls and patients with other single-vessel disease, LA SRa and ε(a)/ε(s) ratio were significantly increased among patients with exclusively left anterior descending coronary artery (LAD) stenosis (SRa 1.14±0.38 s(-1), 1.10±0.41 s(-1), 1.45±0.46 s(-1), P value<0.05; ε(a)/ε(s) 0.44±0.11, 0.44±0.20, 0.57±0.12, P value<0.01). CONCLUSIONS: Apparently decreased SRe of LA and increased ε(a), SRa and ε(a)/ε(s) of RA were found in CAD patients with preserved LVEF and E/E' in gray zone. SRa and ε(a)/ε(s) of LA were found to significantly increase in those with LAD stenosis.

Therapeutic effect of intermittent hypobaric hypoxia on myocardial infarction in rats.

Intermittent hypobaric hypoxia (IHH) preconditioning protects the heart against ischemic injuries. However, little is known about the therapeutic effect of IHH on myocardial infarction (MI). The aim of this study was to test whether IHH treatment influences infarct size and cardiac performance after MI. Seven days after sham operation or left anterior descending coronary artery ligation, male Sprague-Dawley rats were randomly exposed to normoxia or one 6-h period each day of IHH (5,000 m) for 14 and 28 days. Echocardiography analysis showed that IHH significantly reduced left ventricular (LV) dilation and improved cardiac performance after 14- or 28-day treatment compared with MI-normoxic groups. The improvement of LV function was further confirmed in isolated perfused MI-IHH hearts. Such protection was associated with attenuated infarct size, myocardial fibrosis, and apoptotic cardiomyocytes. IHH treatment also enhanced coronary flow and phosphorylation of heat shock protein 27 in both sham and MI groups compared with the control groups. In addition, IHH increased the capillary density and vascular endothelial growth factor expression in peri-infarcted zones compared with sham-IHH and MI-normoxic groups. Our data demonstrated for the first time that IHH treatment exerts a therapeutic effect on MI by attenuating progressive myocardial remodeling and improving myocardial contractility. IHH treatment might provide a unique and promising therapeutic approach for ischemic heart diseases.

2D-speckle tracking echocardiography contributes to early identification of impaired left ventricular myocardial function in patients with chronic kidney disease.

BACKGROUND/AIMS: Our aim was to investigate left ventricular (LV) physiology and short-axis and long-axis regional LV myocardial function throughout the cardiac cycle with 2D-speckle tracking echocardiography (2D-STE) in patients with chronic kidney disease. METHODS: The study population consisted of 40 maintenance hemodialysis patients (hemodialysis group), 20 uremic patients hospitalized for creation of primary arteriovenous fistula (nondialysis group), and a control group of 20 healthy volunteers. LV regional longitudinal, circumferential and radial peak systolic velocity (Vs); early diastolic velocity (Ve); and peak systolic strain (ε) were measured with 2D-STE. RESULTS: Increased LV wall thickness and a decreased E/A ratio were found in the nondialysis and hemodialysis groups as compared to the control group, but there was no difference between the 2 study groups. Longitudinal Vs and Ve of the LV basal segment and middle segment in hemodialysis group and nondialysis group were all slower than those in the control group, and Vs in the nondialysis group was slower than that of the hemodialysis group. Circumferential and radial Vs and Ve were not different among the 3 groups, except that the radial Vs of LV basal segment was markedly decreased in the nondialysis group. Longitudinal peak systolic strain in the hemodialysis and nondialysis groups were both decreased as compared to the control group. Circumferential and radial peak systolic strain was decreased only in the nondialysis group. CONCLUSIONS: 2D-STE may be used to identify early abnormalities in patients with chronic kidney disease who have preserved LV ejection fraction. LV regional function appeared to be better in the hemodialysis group than that in the nondialysis group.

Assessment of left ventricular segmental function after autologous bone marrow stem cells transplantation in patients with acute myocardial infarction by tissue tracking and strain imaging.

BACKGROUND: Emerging evidence suggests that stem cells can be used to improve cardiac function in patients after acute myocardial infarction. In this randomized trial, we aimed to use Doppler tissue tracking and strain imaging to assess left ventricular segmental function after intracoronary transfer of autologous bone-marrow stem cells (BMCs) for 6 months' follow up. METHODS: Twenty patients with acute myocardial infarction and anterior descending coronary artery occlusion proven by angiography were [corrected] randomized into intracoronary injection of bone-marrow cell (treated, n = 9) or diluted serum (control, n = 11) groups. GE vivid 7 and Q-analyze software were used to perform echocardiogram in both groups 1 week, 3 months and 6 months after treatment. Three apical views of tissue Doppler imaging were acquired to measure peak systolic displacement (Ds) and peak systolic strain (epsilonpeak) from 12 segments of LV walls. Left ventricular ejection fraction (LVEF), end-diastolic volume (EDV) and end-systolic volume (ESV) were obtained by Simposon's biplane method. RESULTS: (1) 3 months later, Ds and epsilonpeak over the infract-related region clearly increased in the BMCs group [Ds: (4.49 +/- 2.71) mm vs (7.56 +/- 2.95) mm, P < 0.01; epsilonpeak: (-13.40 +/- 6.00)% vs (-17.06 +/- 6.05)%, P < 0.01], but not in the control group [Ds: (4.74 +/- 2.67) mm vs (5.01 +/- 3.23) mm, P > 0.05; epsilonpeak: (-13.84 +/- 6.05)% vs (-15.04 +/- 6.75)%, P > 0.05]. At the same time, Ds over the normal region also increased, but the Ds enhancement was markedly higher in the BMCs group than that in the control group [(3.21 +/- 3.17) mm vs (0.76 +/- 1.94) mm, P < 0.01]. Parameters remained steady from the 3rd to 6th month in either group (P > 0.05). (2) LVEF in treated and control groups were almost the same at baseline (1st week after PCI) [(53.37 +/- 8.92)% vs (53.51 +/- 5.84)%, P > 0.05]. But 6 months later, LVEF in the BMCs group were clearly higher than that in the control group [(59.33 +/- 12.91)% vs (50.30 +/- 8.30)%, P < 0.05]. (3) There were no evident difference in EDV or ESV between two groups at baseline [EDV: (113.74 +/- 23.24) ml vs (129.94 +/- 32.72) ml, P > 0.05; ESV: (57.12 +/- 18.66) ml vs (62.09 +/- 17.68) ml, P > 0.05]. Three months later, EDV and ESV in the control group were markedly greater than those in the BMCs group [EDV: (154.89 +/- 46.34) ml vs (104.85 +/- 33.21) ml, P < 0.05; ESV: (82.91 +/- 35.79) ml vs (49.54 +/- 23.32) ml, P < 0.05]. But EDV and ESV did not change much from 3rd to 6th month in either group (P > 0.05). CONCLUSIONS: Emergency transplantation of autologous BMCs in patients with acute myocardial infarction helps to improve global and regional contractility and attenuate post-infarction left ventricular remodeling. Tissue tracking and strain imaging provide quick, simple and noninvasive methods for quantifying left ventricular segmental function in humans.

Progression of aortic valve sclerosis and aortic valve stenosis: what is the role of statin treatment?

BACKGROUND: It has recently been suggested that statins could slow the progression of aortic stenosis, but this hypothesis has not been validated in large series. Moreover, there is little information about the role of statin treatment in patients with aortic valve sclerosis. METHODS: From our database 1988--2002, we retrospectively identified 1136 consecutive patients with aortic valve sclerosis (peak aortic velocity [Vmax] > 1.5 and < 2 m/s), or mild to moderate aortic stenosis (Vmax 2.0-3.9 m/s) and with > or = 2 echocardiographic studies > or = 6 months apart; 121 (11 %) were treated with statins. As a control group we randomly selected 121 age-gender-matched patients not treated with statins, with similar initial Vmax. RESULTS: The mean follow-up duration was 54+/-34 months in the statin group, and 50+/-33 months in controls (p = 0.35). There were no differences between statin-treated patients and controls with respect to age, gender, and prevalence of hypertension. More patients in the statin group had documented hypercholesterolemia, diabetes, or had proven coronary artery disease. Overall, the rate of change of Vmax was not different between statin-treated patients and controls (0.13+/-0.24 vs 0.14+/-0.19 m/s/year, p = 0.72). However, in the subgroup of patients with aortic valve sclerosis (n = 52, 26 statin-treated, 26 controls), the rate of change of Vmax was significantly lower in statin-treated patients (0.04+/-0.04 vs 0.08+/-0.06 m/s/year, p = 0.007). CONCLUSIONS: The results of our retrospective study show that statins could be beneficial in retarding the progression of valvular aortic sclerosis to aortic stenosis. This suggests that statins retard the progression of aortic valve lesion in its early stage, a finding that may have important implications in the management of this very common disease.

Spontaneous closure of postinfarction ventricular septal rupture. A case report.

Spontaneous closure of a postinfarction ventricular septal rupture is extremely rare. We present such a case in which the postinfarction ventricular septal rupture closed spontaneously during follow-up. We postulate that the spontaneous closure of the ventricular septal rupture was probably due to thrombosis in the apical and septal aneurysm.