Effects of omacor^®on left ventricular remodelling consecutive to post myocardial infarction special issue-myocardial infarction

Ventricular remodelling is the main trigger of the development of heart failure. Therefore, the reduction of structural remodelling is known to prevent the development of heart failure. The aim of the present study was to investigate the effects of OMACOR?, a well known mixture of EPA and DHA in an experimental model of heart failure induced by occlusion of left descending coronary artery and the reperfusion within 2 months. After a long term treatment of 2 months;OMACOR? (100 mg/kg) statistically significantly reduced the expansion of infarcted zone (35% ± 4%, P ± 3% in the vehicle group). The phosphorylation of Cx43 as biomarker of the cardiac remodelling was visualised by immunofluorescence in rat’s heart at the end of the study. In the vehicle-infarcted group, a significant de-phosphorylation of Cx43 was observed (8.2 ± 1.0 u.a, n = 8 compared to 11.8 ± 1.3 u.a in the sham group, n = 9) confirming a remodelling process in the infarcted group. In the group treated with OMACOR?,the de-phosphorylation of Cx43 was no longer observed compared to the sham group (16.4 ± 2.9 u.a, n = 9, NS). The present results demonstrate that a long term treatment with OMA-COR? reduced the infarcted size in experimental models of heart failure and that these anti-remodelling effects are due at least in part by resynchronizing the gap junction activity.

Hypoxia training attenuates left ventricular remodeling in rabbit with myocardial infarction

Objective Previous studies showed that hypoxia preconditioning could protect cardiac function against subsequent myo-cardial infarction injury. However, the effect of hypoxia on left ventricular after myocardial infarction is still unclear. This study therefore aims to investigate the effects of hypoxia training on left ventricular remodeling in rabbits post myocardial infarction. Methods Adult male rabbits were randomly divided into three groups： group SO （sham operated）, group MI （myocardial infarc-tion only） and group MI-HT （myocardial infarction plus hypoxia training）. Myocardial infarction was induced by left ventricular branch ligation. Hypoxia training was performed in a hypobaric chamber （having equivalent condition at an altitude of 4000 m, FiO214.9%） for 1 h/day, 5 days/week for four weeks. At the endpoints, vascular endothelial growth factor （VEGF） in the plasma was measured. Infarct size and capillary density were detected by histology. Left ventricular remodeling and function were as-sessed by echocardiography.Results After the 4-week experiment, compared with the group SO, plasma VEGF levels in groups MI （130.27 ± 18.58 pg/mL,P〈 0.01） and MI-HT （181.93 ± 20.29 pg/mL,P〈 0.01） were significantly increased. Infarct size in Group MI-HT （29.67% ± 7.73%） was deceased remarkably, while its capillary density （816.0 ± 122.2/mm2） was significantly increased. For both groups MI and MI-HT, left ventricular end-diastolic and end-systolic dimensions were increased whereas left ventricular ejection fraction was decreased. However, compared with group MI, group MI-HT diminished left ventricular end-diastolic （15.86 ± 1.09 mm,P〈 0.05） and end-systolic dimensions （12.10 ± 1.20 mm,P〈 0.01） significantly and im-proved left ventricular ejection fraction （54.39 ± 12.74 mm,P〈 0.05）.ConclusionHypoxia training may improve left ven-tricular function and reduce remodeling via angiogenesis in rabbits with MI.

Assessment of Regional Left Ventricular Myocardial Function in Rats after Acute Occlusion of Left Anterior Descending Artery by Two-dimensional Speckle Tracking Imaging

This study evaluated the change in regional left ventricular myocardial function in rats following acute occlusion of the left anterior descending coronary artery （LAD） by using two-dimensional speckle tracking imaging （2D-STI）. Sixty Wistar rats were randomly divided into two groups, a myocardial infarction （MI） group, in which 50 rats were subjected to LAD occlusion for 30–45 min, and a sham-operated （SHAM） group that contained 10 rats serving as control. Echo-cardiography was performed at baseline and 1, 4 and 8 week（s） after the operation. High frequency two-dimensional images of left ventricular short axis at papillary muscle level were recorded. Peak systolic radial strain （PRS） and circumferential strain （PCS） were measured in the mid-ventricle in short-axis view by using EchoPAC workstation. Left ventricular internal diameter at diastole （LVIDd） and systole （LVIDs）, fractional shortening （FS）, ejection fraction （EF） and left ventricular mass （LVM） were measured by anatomical M-model echocardiography. Infarct size was measured using triphenyl tetrazolium chloride （TTC） staining 1 week and 8 weeks after the operation. Fibrosis of left ventricu-lar myocardium was displayed using Van Gieson staining 1 week after the infarction. In terms of the TTC staining results, the left ventricle fell into three categories： infarcted, peri-infarcted and remote myocardial regions. Compared with those at baseline and in the SHAM group, （1） PRS and PCS in the infarcted, peri-infarcted and remote myocardial regions were significantly decreased in the MI group within 1 week after the operation （P〈0.05） and the low levels lasted 8 weeks; （2） Compared with those at baseline, LVIDd, LVIDs, FS, EF and LVM in the MI group showed no significant dif-ference 1 week after the operation （P〉0.05）. However, LVIDd, LVIDs and LVM were increased sig-nificantly 4 and 8 weeks after the operation （P〈0.05）, and FS and EF were decreased substantially （P〈0.05）. Van Gieson staining showed that fibrosis developed in all the three myocardial regions to varying degrees. It is concluded that 2D-STI is non-invasive and can be used to assess regional func-tion of myocardium with different blood supply in rats following acute occlusion of the LAD, and can be used as a sensitive and reliable means to follow up the process of left ventricular remodeling.

Real-time Three-dimensional Echocardiographic Assessment of Left Ventricular Remodeling Index in Patients with Hypertensive Heart Disease and Coronary Artery Disease

Left ventricular remodeling index （LVRI） was assessed in patients with hypertensive heart disease （HHD） and coronary artery disease （CAD） by real-time three-dimensional echocardiography （RT3DE）. RT3DE data of 18 patients with HHD, 20 patients with CAD and 22 normal controis （NC） were acquired. Left ventricular end-diastolic volume （EDV） and left ventricular end-diastolic epicardial volume （EDVepi） were detected by RT3DE and two-dimensional echocardiography Simpson biplane method （2DE）. LVRI （left ventricular mass/EDV） was calculated and compared. The results showed that LVRI measurements detected by RT3DE and 2DE showed significant differences inter-groups （P〈0.01）. There was no significant difference in NC group （P〉0.05）, but significant difference in HHD and CAD intra-group （P〈0.05）. There was good positive correlations between LVRI detected by RT3DE and 2DE in NC and HHD groups （t=0.69, P〈0.01; r=0.68, P〈0.01）, but no significant correlation in CAD group （r=0.30, P〉0.05）. It was concluded that LVRI derived from RT3DE as a new index for evaluating left ventricular remodeling can provide more superiority to LVRI derived from 2DE.

MicroRNA-29a attenuates angiotensin-Ⅱ induced-left ventricular remodeling by inhibiting collagen,TGF-β and SMAD2/3 expression

Background Left ventricular(LV)remodeling is the most common target organ damage in hypertension.Previously,our study found that plasma microRNA-29a(miR-29a)level was associated with the LV remodeling in hypertensive patients.However,the causal relationship between miR-29a and LV remodeling remains unknown.Thus,the aim of this study was to investigate the regulation mechanism of miR-29a in LV remodeling.Methods&Results Overexpression and knockdown miR-29a mice were generated by tail-intravenous injection of miR-29a-mimic and inhibitor lentivirus for one week respectively.Then the mice were subjected to angiotensin-II(AngII)induced LV remodeling by subcutaneous AngII capsule osmotic pumping into AngII for four weeks.AngII-induced LV remodeling mice as the model group(n=9).Age-matched male SPF C57/BL6J mice(6–8 weeks old)were treated with the pumping of saline as a vehicle(n=6).In vivo,overexpression miR-29a ameliorated AngII-induced LV remodeling,while knockdown miR-29a deteriorated LV remodeling.Simultaneously,we observed that overexpression miR-29a mice inhibited but knockdown miR-29a mice increased cardiac cross-sectional area,indicating that miR-29a has an antagonistic effect on cardiac hypertrophy.Further studies found that overexpression miR-29a inhibited the content of the LV collagen including collagen I and III.Moreover,the expression of transforming growth factor-β(TGF-β)and phosphorylated SMAD2/3 decreased with the down-regulation of collagen I and III in overexpression miR-29a mice.Conclusions Our finding indicates that overexpression miR-29a attenuates LV remodeling by inhibiting collagen deposition,TGF-β,and phosphorylated SMAD2/3 expression.Thus,intervention miR-29a may be a therapeutic target for attenuating LV remodeling.

COMPARISON OF THE EFFECTS OF LOSARTAN,ENALAPRIL AND THEIR COMBINATION IN THE PREVENTION OF LEFT VENTRICULAR REMODELING AFTER ACUTE MYOCARDIAL INFARCTION IN THE RAT

Objectives. To compare the effects of losartan, enalapril and their combination in the prevention ofleft ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in the rat. Methods. AMI model was induced in female SD rats by ligating left coronary artery. Forty-eight hours after the procedure, 83 surviving rats were randomized into one of the following 4 groups: 1 ) AMI control group (n =19), 2) losartan group (n= 22, 3 mg @ kg - 1 @ d - 1 ), 3 ) enalapril group (n = 20, 1 mg @ kg - 1 @ d - 1 ), 4) losartan - enalapril combinative group (n = 22, 3 and 1 mg @ kg- 1 @ d - 1 respectively). 5 ) sham-operated group ( n =10) and 6) normal rats group (n = 10) were selected randomly to serve as non-infarction controls. Losartan and enalapril were delivered by direct gastric gavage. After 4 weeks of medical therapy, hemodynamic studies were performed in each group, then the rat hearts were fixed with 10% formalin and pathologic analysis on them was performed. Complete experimental data was obtained in 56 rats, comprising 1 ) AMI controls (n = 11 ), 2) losartan group (n = 10), 3 ) enalapril group (n = 10), 4) the combination of losartan and enalapril group (n = 11 ),5) sham - operated group (n = 6) and 6) normal controls (n=8). Results. There were no significant differences among the 4 AMI groups in MI size (41.7% ～ 43.4%, all P＞ 0.05). Compared with sham group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), long and short axis length (L and D), as well as LV absolute and relative weight (LVAW and LVRW)in AMI group were all significantly increased ( P ＜0.05 ～ 0. 001 ); whereas the maximum left ventricular pressure rising and droping rates ( + dp/dt) and their corrected values by LV systolic pressure ( + dp/dt/LVSP)were significantly reduced (all P ＜0.001 ), indicating LVRM occurred and LV systolic and diastolic function impaired after AMI. Compared with AMI group , LVEDP, LVV, LVAW and LVRW were all significantly decreased (P ＜0.05～0.001 ); while + dp/dt/LVSP were significantly enhanced in all 3 treatment groups (P ＜0.05～0.001 ) except -dp/dt/LVSP in losartan group (P＞ 0. 05 ). There were no significant differences in the above indices among the 3 treatment groups (all P＞ 0.05). Conclusion. Both losartan and enalapril can prevent from LVRM after AMI in the rat and improve LV function with equivalent effects. There seems no additive effect when the 2 drugs are used in combination.

Effect of Astragalus Injection on Left Ventricular Remodeling in Aged Patients with Acute Early-stage Myocardial Infarction

Objective: To observe the effect of Astragalus Injection (AI) on left ventricular remodeling in aged patients with acute myocardial infarction (AMI). Methods: Patients with AMI were randomly divided into the AI group (46 cases) treated with AI and the control group (46 cases) treated conventionally. Left ventricular end-diastolic volume index (LVEDVI), left ventricular end-systolic volume index (LVESVI), anterior endocardial segmental length (ASL) and posterior endocardial segmental length (PSL) were all assessed by echocardiogram after 1 week and 4 weeks treatment. The cardiac systolic and diastolic functions were detected by nuclide gating cardiac blood pool imaging at the 4th week. Results: After four weeks' treatment, no obvious change of LVEDVI, LVESVI and ASL in the AI group was found, but these indexes increased significantly in the control group, with significant difference shown between the two groups (P<0. 05). As compared with the control group, the left ventricular ejection fraction (LVEF), left ventricular peak ejecting rate (LVPER) and left ventricular peak filling rate (LVPFR) were heightened, the time for peak filling rate (LVTPFR) in the left ventricle was shortened in the AI group. Conclusion: AI is one of the effective drugs in reversing left ventricular remodeling in aged patients with AMI.

Comparative Proteomic Analysis in Left Ventricular Remodeling following Myocardial Infarction in Rats

Objective Left ventricular remodeling （LVR） following myocardial infarction （MI） is a key pathophysiological process in which MI develops into heart failure. The exact mechanism of LVR remains unclear. We performed differential proteomic analysis on the myocardia of rats with LVR after MI, to explore the mechanism of ventricular remodeling after MI. Methods In the LVR group （n=12）, after the anterior descending coronary artery was ligated, the rats were fed for four weeks before the LVR models were established. Rats in the sham-operated group （n=11） underwent thread-drawing without ligation. The hemodynamic parameters, pathological findings, and proteomics were compared between the two groups. Results In the LVR group, the left ventricular end-diastolic pressure increased, the maximal left ventricular pressure increase/decrease ratio decreased significantly, and the left ventricular systolic pressure decreased. H-E staining and Masson staining of cardiac muscle tissues of the LVR group showed myocytolysis, disarray, and collagen proliferation. Twenty-one differentially expressed proteins were detected by proteomic analysis. We validated two proteins using western blot analysis. The differentially expressed proteins could be divided into six categories： energy metabolism-related proteins, cytoskeletal proteins, protein synthesis-related proteins, channel proteins, anti-oxidation- related proteins, and immune-related proteins. Conclusion These differentially expressed proteins might play key roles in LVR following M

Effects of Perindopril on Left Ventricular Remodeling and Osteopontin Expression in Rats With Myocardial Infarction

Objectives To observe the effects of perindopril on left ventricular remodeling and myocardial osteopontin expression in rats with myocardial infarction. Methods In this study male adult SD rats were randomly divided into 3 groups: sham-operation group, MI-saline group and MI-perindopril group. Left anterior descending artery was ligated to generate myocardial infarction. Perindopril (2 mg/kg body weight/day) was administered from the next day of MI. Four weeks later, left ventricular diameter (LVEDD and LVESD) and left ventricular ejection fraction was estimated with echocardiography, LVSP, LVEDP and±dp/dtmax was detected with hemodynamic measurement, cardiomyocyte diameter and interstitial fibrosis infiltration were evaluated with histological methods, and myocardium osteopontin protein expression level was detected with western blot. Results ①Compared with the sham-operation group, all rats with MI developed significant systolic and diastolic dysfunction, as was indicated by decreased LVEF, LVSP and±dp/dtmax, as well as increased LVEDP. ②Rats with MI showed significantly dilated left ventricles and higher ventricular weight / body weight ratio, significantly increased cardiomyocyte diameter and marked interstitial fibrosis in the non-infarction area. ③Perindopril treatment partly prevented cardiac dysfunction and left ventricular remodeling as indicated by the parameters mentioned above. ④No osteopontin protein was detected in myocardium of sham-operation rats. In rats with MI, high level osteopontin protein expression was significantly inhibited by perindopril treatment. Conclusions In rats with MI, perindopril treatment significantly prevented left ventricular remodeling and myocardium osteopontin protein expression.

Comparison of Arrhythmias among Different Left Ventricular Geometric Patterns in Essential Hypertension

The differences of arrhythmias among distinct left ventricular geometric patterns in the patients with essential hypertension were studied. 179 patients with essential hypertension received 24 h dynamic ECG recording, ambulatory blood pressure monitoring, echocardiography examination, etc. According to the examinations, left ventricular geometric patterns and arrhythmias were identified. The comparison of morbidity of arrhythmias between the left ventricular remodeling group and the normal geometric pattern group was performed. The multiple stepwise regression analysis was carried out to identify the independent determinants of arrhythmias. After these predictors were controlled or adjusted, the severity of arrhythmias among different left ventricular geometric patterns was compared. It was found that the morbidity of atrial arrhythmia, ventricular arrhythmia and complex ventricular arrhythmias in the left ventricular remodeling group was significantly higher than in the normal geometric pattern group respectively. There were many independent factors influencing on arrhythmias in essential hypertension. Of all these factors, some indices of left ventricular anatomic structure, grade of hypertension, left atrial inner dimension, E/A, diastolic blood pressure load value at night and day average heart rate and so on were very important. After the above mentioned factors were adjusted, the differences of the orders of arrhythmias between partial geometric patterns were reserved, which resulted from the differences of the geometric patterns. Many factors contributed to arrhythmias of essential hypertension, such as grade of hypertension, LVMI, LA, PWT and so on. The severity of arrhythmias was different in different left ventricular geometric patterns.

Effect of carvedilol on cardiac function and left ventricular remodeling in rats after acute myocardial infarction

Objective: To observe the effect of carvedilol injection on left ventricular function and collagen remodeling in rat with myocardial infarction. Methods: Sixty rats with a model of myocardial infarction were randomly divided into nine groups. The rats of therapeutical group were treated with carvedilol injection (2 mg/d intraperitoneal injection) and/or captopil (2 g/L drinking water) . Acute myocardial infarction ( AMI) group did not receive drug treatment. The animals were sacrificed at 4 weeks and 8 weeks after coronary artery ligation. The levels of plasma angiotensin II and plasma aldosterone and left ventricle function were determined at different time. The collagen content and the ratio of type I and III collagen of noninfarcted area were also assessed. Results: Compared with AMI group, the levels of plasma and myocardium angiotensin II and plasma aldosterone in both carvedilol and captopil group decreased at the eighth week (P<0.05). In addition, carvedilol improved systolic and diastolic function (P<0. 05). Compared with sham group, both collagen content and the ratio of type I / III collagen of noninfarcted area increased in AMI4 and AMI8 group (P<0. 05). The hydroxyproline levels and the ratio of type I/III collagen significantly decreased after carvedilol and/or captopil treatment , compared with AMI group at 4 or 8 week (P <0. 05). Conclusion: Carvedilol can improve cardiac function after myocardial infarction and has beneficial effect on left ventricular remodeling.

Left Ventricle Geometry Remolding after Heart Transplantation:A Two-dimensional Ultrasound Study

The function of the transplanted heart will be affected by acute allograft rejection, chronic rejection, high blood pressure and so on, which may induce the reconstruction of the left ventricle and the increase of left ventricular mass （LVM）, and eventually lead to left ventricular hypertrophy that will significantly affect the prognosis of heart transplantation （HT）. The purpose of this study was to dy- namically monitor the changes of left ventricular geometric patterns after HT using two-dimensional echocardiography and to understand the remodeling process and its possible influencing factors. The left ventricular internal diameter, interventricular septal wall thickness, posterior wall thickness at end dias- tole were measured and the relative wall thickness （RWT）, left ventricular mass, left ventricular mass index were calculated respectively in 34 HT patients and 34 healthy volunteers by two-dimensional echocardiography. The type of left ventricular geometry was identified based on the echocardiographic determination of LVM index （LVMI） and RWT. The HT patients were divided into three groups ac- cording to the time length after surgery： A （3 months postoperatively）, B （6 months postoperatively） and C （12 months postoperatively）. We compared the parameters of left ventricle between HT group and normal control group, and explored the risk factors causing the increase of LVM. The results showed that 4 patients （16%） in group A had concentric remodeling. Nine patients （34.62%） in group B had re- construction, including 5 cases of concentric remodeling, 2 cases of concentric hypertrophy and 2 cases of eccentric hypertrophy. The hypertrophy incidence rate was 15.4% in group B. 15 patients （62.5%） had reconstruction in group C, including 9 cases of concentric remodeling, 5 cases of concentric hyper- trophy, and 1 case of eccentric hypertrophy. The prevalence of hypertrophy was 25%. Multivariate analysis showed that hypertension and acute rejection history were the risk factors that resulted in left ventricular hypertrophy. It is concluded that the left ventricular remodeling occurs following cardiac transplantation at an early stage and the incidence of left ventricular hypertrophy increases with survival time. In this study, the one-year prevalence of left ventricular hypertrophy was 25% after surgery. Hy- pertension and acute rejection history are risk factors that can predict the left ventricular hypertrophy.

Cardiovascular magnetic resonance imaging assessment of outcomes in acute myocardial infarction

Cardiovascular magnetic resonance(CMR) imaging uniquely characterizes myocardial and microvascular injury in acute myocardial infarction(AMI), providing powerful surrogate markers of outcomes. The last 10 years have seen an exponential increase in AMI studies utilizing CMR based endpoints. This article provides a contemporary, comprehensive review of the powerful role of CMR imaging in the assessment of outcomes in AMI. The theory, assessment techniques, chronology, importance in predicting left ventricular function and remodelling, and prognostic value of each CMR surrogate marker is described in detail. Major studies illustrating the importance of the markers are summarized, providing an up to date review of the literature base in CMR imaging in AMI.

Surgery for left ventricular aneurysm after myocardial infarction： techniques selection and results assessment

Background The most appropriate surgical approach for patients with post-infarction left ventricular （LV） aneurysm remains undetermined. We compared the efficacy of the linear versus patch repair techniques, and investigated the mid-term changes of LV geometry and cardiac function, for repair of LV aneurysms. Methods We reviewed the records of 194 patients who had surgery for a post-infarction LV aneurysm between 1998 and 2010. Short-term and mid-term outcomes, including complications, cardiac function and mortality, were assessed. LV end-diastolic and systolic dimensions （LVEDD and LVESD）, LV end-diastolic and end-systolic volume indexes （LVEDVI and LVESVI） and LV ejection fraction （LVEF） were measured on pre-operative and follow-up echocardiography. Results Overall in-hospital mortality was 4.12%, and major morbidity showed no significant differences between the two groups. Multivariate analysis identified preoperative left ventricular end diastolic pressure 〉20 mmHg, low cardiac output and aortic clamping time 〉2 hours as risk factors for early mortality. Follow-up revealed that LVEF improved from 37% pre-operation to 45% 12 months post-operation in the patch group （P=0.008）, and from 44% pre-operation to 40% 12 months postoperation in the linear group （P=0.032）. In contrast, the LVEDVI and LVESVI in the linear group were significantly reduced immediately after the operation, and increased again at follow-up. However, in the patch group, the LVEDVI and LVESVI were significantly reduced at follow-up. And there were significant differences in the correct value changes of LVEF and left ventricular remodeling between linear repair and patch groups. Conclusions Persistent reduction of LV dimensions after the patch repair procedure seems to be a procedure-related problem. The choice of the technique should be tailored on an individual basis and surgeon＇s preference. The patch remodeling technique results in a better LVEF improvement, further significant reductions in LV dimensions and volumes than does the linear repair technique. The results suggest that LV patch remodeling is a better surgical choice for patients with post-infarction LV aneurysm.

Protective effect of ghrelin on left ventricular remodeling in spontaneously hypertensive rats is associated with the peroxisome proliferator-activated receptor gamma-dependent pathway

Background Studies suggested that exogenous ghrelin administration could prevent early left ventricular remodeling in rats with myocardial infarction. We investigated herein whether ghrelin attenuated left ventricular remodeling induced by hypertension and whether ghrelin＇s effect was mediated through the peroxisome proliferator-activated receptor gamma （PPAR-y）-dependent pathway. Methods Spontaneously hypertensive rats （8-week-old males） were randomly divided into three groups with 12 rats in each： ghrelin group （received ghrelin 100 IJg/kg subcutaneously （sc） twice daily）; ghrelin＋GW9662 group （received the PPAR-y antagonist GW9662 at 2 mg/kg sc, and then ghrelin as above）; saline controls. Normal male Wistar Kyoto rats （n=-12） served as normal controls. Four weeks later, the effects of ghrelin on cardiac remodeling were evaluated by echocardiographic, hemodynamic, and histopathological examination, and gene expression analysis （PPAR-y protein and mRNA expression）. The serum levels of C-reactive protein （CRP） and tumor necrosis factor （TNF）-a were detected by enzyme linked immunosorbent assay. Results Ghrelin prevented ventricular remodeling, increased PPAR-y expression in the myocardium, suppressed collagen I and collagen Ill mRNA expression, and also decreased the serum levels of TNF-a, but not CRP. All abovementioned effects of ghrelin were inhibited by GW9662. Conclusion Ghrelin inhibited ventricular remodeling induced by hypertension, and the preventive effects of ghrelin may be mediated by the anti-inflammatory actions of the PPAR-y-dependent pathway.

Effect of Different Styles of Coronary Heart Disease and Its Risk Factors on Cardiac Remodeling and Dysfunction

Objectives To evaluate the effect of different styles of coronary heart disease （CHD）, different regions of acute myocardial infarction （AMI）, its risk factors and branches of coronary stenosis on left ventricular remodeling and dysfunction by applying echocardiography. Methods 251 patients with CHD and 96 patients without CHD （NoCHD） were verified by selective coronary angiography. CHD patients were divided into stable angina pectoris （SAP） 26, unstable angina pectoris（UAP） 53, acute myocardial infarction （AMI） 140 and old myocardial infarction （OMI） 30 based on clinical situation, cTnT, cardiac enzyme and ECG. AMI patients were further divided into subgroups including acute anterior myocardial infarct （Aa,n = 53）, acute inferior myocardial infarction （Ai, n=54） and Aa＋Ai （n=33） based on ECG. Cardiac parameters： end-diastolic interventricular septum thickness（IVSd）, end-diastolic left ventricular internal diameter （LVd）, left ventricular mass （LM）, end-diastolic left ventricular volume （EDV）, end-systolic left ventricular volume （ESV） and left ventricular ejection fraction（LVEF） were measured by ACUSON 128XP/10 echocardiography. Multiples linear regression analyses were performed to test statistical associations between LVEF and the involved branches of coronary stenosis, blood pressure, lipids, glucose and etc after onset of myocardial infarction. Results EDV and ESV were increased and LVEF decreased on patients with AMI,OMI and UAP （P〈0.05-0.0001）. LM was mainly increased in patients with OMI （P〈0.01） and LVd was mainly enlarged in patients with AMI. EF was significantly decreased and EDV, ESV, LM and LVd were remarkably increased in AMI patients with Aa and Aa＋Ai. With the multiple linear regression analyses by SPSS software, we found that LVEF was negatively correlated to the involved branches of coronary stenosis as well as to systolic blood pressure after onset of myocardial infarction while there was no significant correlation between LVEF and other factors. LVEF was significantly decreased, and LVd and LM increased in AMI patients with antecedent hypertension, compared to patients without hypertension （P〈0.001）. Conclusions Effects of different styles of CHD and different regions of AMI on left ventricular remodeling and cardiac function are different. Myocardial infarction, especially Aa and Aa＋Ai, is one of the most important causes of left ventricular remodeling and cardiac dysfunction. Multiple vessel stenosis and systolic blood pressure at the onset of myocardial infarction reduce LVEF in AMI patients. Antecedent hypertension may accelerate the effect of AMI on cardiac remodeling and dysfunction. Therefore primary and secondary preventions of CHD are critical for protecting heart from remodeling and dysfunction.

What is the optimal initiation timing of angiotensin converting enzyme inhibitor treatment for maximum benefits in acute myocardial infarction patients？

Randomized clinical trials led to the clinical recommendation that angiotensin-converting enzyme inhibitors （ACEI） should be used as standard therapy in most patients experiencing an acute myocardial infarction （AMI）. However, the optimal initiation timing of treatment, as well as the exact mechanisms, have not been completely resolved, especially with the development of reperfusion strategy after AMI. Earlier initiation of ACEI might be associated with more prompt recovery of left ventricular ejection fraction due to more rapid attenuation of negative remodeling.

Effects of emergency or late PCI therapy on autonomic nervous function in myocardial infarction patients

Background It＇s an effective treatment to achieve percutaneous coronary intervention in AMI patients, which rapidly improves the blood supply of coronary artery. Studies have shown that different modes of PCI therapy have different effects in AMI patients. The aim of this study was to explore the effects and clinical significances of emergency or late PCI therapy on left ventricular remodeling and cardiac autonomic function in acute myocardial infarction （AMI） patients. Methods One hundred and fifty cases of AMI patients were randomly divided into three groups, which all were given the routine medicine. The two therapy groups were the emergency PCI group （n = 60） and the late PCI group （n = 50）. The variations of heart rate turbulence （HRT） and heart rate variability （HRV） parameters were observed after 2 weeks of treatment by 24-hour ambulatory ECG. Results Compared with the control group, after 2 weeks of treatment, the levels of TS, SDNN and SDANN of two PCI-treated group was significantly higher （P 〈 0.01）, TO were lower （P 〈 0.01） than which in the control group. There were significant differences in TS, SDNN, SDANN and TO between the two PCI treatment group （P 〈 0.05）. Conclusion Emergency PCI or late PCI may give coronary effective reperfusion, improve left ventricular function and autonomic nervous function, and prevent malignant arrhythmias to occur. The treatment of primary PCI is superior to delayed PCI.