miRNA-21 Expression in the Serum of Elderly Patients with Acute Myocardial Infarction.

BACKGROUND The aims of this study were to examine the expression of miRNA-21 in the serum of elderly patients (>65 years) with acute myocardial infarction (AMI) and to investigate the potential role of serum miRNA-21 as a marker of early cardiac myocyte damage. MATERIAL AND METHODS Thirty-eight elderly patients with recent AMI, 27 elderly patients with unstable angina pectoris, and 25 healthy elderly individuals were included in the study. Serum miRNA-21 expression was determined following total RNA extraction and reverse-transcribed into cDNA, followed by reverse transcription-polymerase chain reaction (RT-PCR). Serum creatine kinase MB isoenzyme (CK-MB) and cardiac troponin I (cTnI) levels were analyzed by electrochemiluminescence. Apoptosis of human cardiac myocytes (HCM) was analyzed using fluorescence-activated cell sorting (FACS), and protein expression of caspase-3 was detected using Western blot. RESULTS Expression levels of miRNA-21 in the serum of elderly patients with AMI were positively correlated with serum levels of CK-MB (r=0.3683, P=0.0229) and cTnI (r=0.5128, P=0.009). Following tumor necrosis factor (TNF)-α induction, the apoptosis rates of HCM transfected with the miRNA-21 mimic short hairpin RNA (shRNA) were downregulated by 39.1% compared with control HCM cells, and protein expression of c-Jun N-terminal kinases (JNK) and p38 were unchanged (P>0.05); protein expression of p-JNK, p-p38 and caspase-3 were downregulated by 37.1%, 35.8%, and 36.0%, respectively. CONCLUSIONS Expression of miRNA-21 was upregulated in the serum of elderly patients with AMI, which inhibited TNF-a induced apoptosis in HCM by activating the JNK/p38/caspase-3 signaling pathway.

Recent advances in understanding the biochemical and molecular mechanism of diabetic nephropathy.

Diabetic nephropathy (DN) is a chronic disease characterized by proteinuria, glomerular hypertrophy, decreased glomerular filtration and renal fibrosis with loss of renal function. DN is the leading cause of end-stage renal disease, accounting for millions of deaths worldwide. Hyperglycemia is the driving force for the development of diabetic nephropathy. The exact cause of diabetic nephropathy is unknown, but various postulated mechanisms are: hyperglycemia (causing hyperfiltration and renal injury), advanced glycosylation products, activation of cytokines. In this review article, we have discussed a number of diabetes-induced metabolites such as glucose, advanced glycation end products, protein kinase C and oxidative stress and other related factors that are implicated in the pathophysiology of the DN. An understanding of the biochemical and molecular changes especially early in the DN may lead to new and effective therapies towards prevention and amelioration of DN.

Role of the Na(+)/H(+) exchanger on the development of diabetes mellitus and its chronic complications.

Micro- and macrovascular complications are the main cause of morbidity and mortality in diabetes mellitus. The Na(+)/H(+) exchanger (NHE) is a family of proteins which exchange Na(+) for H(+) according to their concentration gradients in an electroneutral manner. The exchanger also plays a key role in several other cellular functions including proliferation, differentiation, apoptosis, migration, and cytoskeletal organization. Since not much is known on the relationship between NHE and diabetes mellitus, this review outlines the contribution of NHE to chronic complications of diabetes mellitus, such as diabetic nephropathy; diabetic cardiomyopathy.

The effects of selenium supplementation on antibody titres in patients with Hashimoto's thyroiditis.

INTRODUCTION: The objective of this study was to evaluate the effect of selenium supplementation on autoantibody titres, thyroid ultrasonography, and thyroid function in patients with Hashimoto's thyroiditis (autoimmune thyroiditis) and normal thyroid reference range. MATERIAL AND METHODS: A total of 100 patients were given 200 ug/d selenium yeast orally, their thyroid function, levels of serum selenium, thyroid peroxidase antibodies (TPOAb), thyroglobulin antibodies (TGAb), and urine iodine were measured, and thyroid ultrasonography was performed before administration and three and six months afterwards, and the data were statistically analysed. RESULTS: The subjects exhibited a selenium deficiency before the administration of selenium, and the serum levels increased to moderate levels three and six months after the selenium supplementation (p < 0.05). The titres of TGAb decreased significantly in patients after six months of selenium supplementation (p < 0.05). In the high antibody group, TgAb decreased after 6 months compared with baseline (p = p < 0.05), and TPOAb decreased after 3 and 6 months of selenium supplementation compared with baseline (p < 0.05). CONCLUSION: In patients with autoimmune thyroiditis and normal thyroid reference range, there was a general selenium deficiency, but after six months of treatment it was shown that selenium supplementation may be effective in reducing the titres of TGAb and TPOAb.

KB-R7943 inhibits high glucose-induced endothelial ICAM-1 expression and monocyte-endothelial adhesion.

Hyperglycemia is the major cause of diabetic angiopathy. The aim of our study was to evaluate the impact of KB-R7943, an inhibitor of Na+/Ca2+ exchanger (NCX) on cell growth and function of human "diabetic" endothelial cells (EC). Intercellular adhesion molecule-1 (ICAM-1) expression and NCX activity were determined after EC were exposed to high glucose in the absence and presence of KB-R7943. Coincubation of EC with high glucose for 24 h resulted in a significant increase of monocyte-endothelial cell adhesion and the expression of ICAM-1. These effects were abolished by KB-R7943 and KB-R7943 significantly decreased the activation of NCX induced by high glucose. These findings suggested that KB-R7943 may play a role in inhibiting expression of adhesion molecules by inhibiting the reverse activation of NCX.

[Outcome of patients with ST-elevation myocardial infarction complicated by pre-hospital cardiac arrest underwent emergency percutaneous coronary intervention].

OBJECTIVE: To evaluate the outcome of ST-elevation acute myocardial infarction (STEMI) patients complicated pre-hospital cardiac arrest underwent percutaneous coronary intervention (PCI). METHODS: From September 2004 to November 2008, 1446 consecutive patients with acute STEMI underwent PCI in our department. 49 out of 1446 patients complicated by pre-hospital cardiac arrest. Clinical outcome including total mortality, adverse cardiac events, stroke and bleeding events during the hospitalization period and within 1 year after discharge was compared between patients with or without pre-hospital cardiac arrest. RESULTS: PCI success rate was similar (85.7% vs. 88.8%, P = 0.497) while the incidence of in-hospital cardiogenic shock 22.4% vs. 3.0%, P < 0.001 and cardiac arrest (44.9% vs. 5.9%, P < 0.001) and in-hospital mortality (36.7% vs. 2.0%, P < 0.001) were significantly higher in patients with pre-hospital cardiac arrest than patients without pre-hospital cardiac arrest. Time from symptom onset to emergency treatment, asystole as initial rhythm, Glasgow coma scale (GCS ≤ 7) and cardiogenic shock on admission were independent risk factors of in-hospital death in patients with pre-hospital cardiac arrest. During follow up, incidences of overall mortality, re-infarction, revascularization and stroke were similar between the two groups. CONCLUSIONS: STEMI patients with pre-hospital cardiac arrest undergoing emergency PCI are facing higher risk of cardiogenic shock and cardiac arrest and higher in-hospital mortality compared to those without pre-hospital cardiac arrest. However, the post-hospital discharge outcome was similar between the two groups.

Effect of atorvastatin on expression of IL-10 and TNF-alpha mRNA in myocardial ischemia-reperfusion injury in rats.

Myocardial ischemia and reperfusion (MI/R) is associated with an intense inflammatory reaction, which may lead to myocyte injury. Because statins protect the myocardium against ischemia-reperfusion injury via a mechanism unrelated to cholesterol lowering, we hypothesized that the protective effect of statins was related to the expression of TNF-alpha (TNF-alpha) and interleukin-10 (IL-10) mRNA. Seventy-two rats were randomly divided into three groups as follows: sham, I/R and I/R+atorvastatin. Atorvastatin (20 mg kg(-1)day(-1)) treatment was administered daily via oral gavage to rats for 2, 7 or 14 days. Ischemia was induced via a 30-min coronary occlusion. Reperfusion was allowed until 2, 7 or 14 days while atorvastatin treatment continued. We measured infarct size, hemodynamics and the plasma levels and the mRNA expression of TNF-alpha and IL-10 in the three groups. We demonstrated that the up-regulation of expression of both TNF-alpha mRNA and IL-10 mRNA was associated the increased plasma levels of TNF-alpha and IL-10 in the ischemic and reperfused myocardium compared with that in the sham group (P<0.01). Atorvastatin treatment prevented ischemia-reperfusion-induced up-regulation of both TNF-alpha and IL-10 mRNA, and improved left ventricular function (P<0.01). Our findings suggested that atorvastatin may attenuate MI/R and better recovery of left ventricle function following ischemia and reperfusion and IL-10 was not directly likely involved in this protective mechanism.

The 223A>G polymorphism of the leptin receptor gene and lipid-lowering efficacy of simvastatin in Chinese patients with coronary heart disease.

OBJECTIVE: To investigate whether leptin receptor (LEPR) 223A>G polymorphism influences serum lipid levels and whether this polymorphism affects the effectiveness of simvastatin in Chinese patients with coronary heart disease (CHD). METHODS: A total of 312 patients with CHD were treated with simvastatin 20 mg/day. Fasting serum lipids were determined before and after 12 weeks of treatment. RESULTS: Patients with AA genotype had significantly higher total cholesterol (TC) levels and lower high-density lipoprotein cholesterol (HDL-C) levels than those with GG genotype (P < 0.05) before simvastatin treatment. In addition, the ability of simvastatin to increase HDL-C levels was significantly lower in patients with AA genotype than those with GG genotype (P < 0.05). CONCLUSIONS: The 223A>G polymorphism of LEPR significantly modulates the HDL-C response to simvastatin in Chinese patients with CHD.

Early use of omeprazole benefits patients with acute myocardial infarction.

BACKGROUND: Bleeding complications are not uncommon in patients with acute myocardial infarction (AMI) during treatments. How to prevent the occurrence of upper gastrointestinal bleeding in AMI patients has become one of the most intractable problems. And there are conflicting data on the efficacy and complication rate of omeprazole treatment. We conducted an intervention study to determine whether using omeprazole could benefit AMI patients. METHODS: A total of 237 patients with AMI were divided into two groups at random: omeprazole group including 114 patients and control group including 123 patients. Omeprazole 40 mg by intravenous drip was given to the patients in omeprazole group when they were admitted to the hospitals. From the second day they were given omeprazole 20 mg per day by oral administration for 7 days. In contrast, no gastric acid inhibitor was given to the patients in control group. The incidence of upper gastrointestinal bleeding, the recanalization rate and overall mortality in both groups were observed. RESULTS: The incidence of upper gastrointestinal bleeding in omeprazole group was 5.3% (6/114) which was much lower than 14.6% (18/123) in control group (P = 0.017), but the recanalization rate had no significant difference between the two groups (P = 0.681). The overall mortality in omeprazole group was lower than that of control group (3.5% vs. 10.6%, P = 0.035). CONCLUSIONS: Our findings suggest that early use of omeprazole in AMI patients could decrease the incidence of upper gastrointestinal bleeding and the overall mortality, without influencing the recanalization rate. Early use of omeprazole might benefit AMI patients.

Effect of R219K polymorphism of the ABCA1 gene on the lipid-lowering effect of pravastatin in Chinese patients with coronary heart disease.

1. In the present study, we investigated the effects of the R219K polymorphism of the ATP-binding cassette transporter A1 (ABCA1) gene on serum lipid levels and the response to statin therapy in Chinese patients with coronary heart disease (CHD). 2. The study population consisted of 365 patients with CHD and 246 control subjects without signs or symptoms of CHD. Patients with CHD were treated with 20 mg/day pravastatin. Fasting serum lipids were determined before and after 12 weeks of treatment. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). 3. The R219K polymorphism of the ABCA1 gene was not significantly associated with CHD (P > 0.05). Compared with controls, patients with the RR genotype had significantly higher serum triglyceride levels and lower high-density lipoprotein-cholesterol (HDL-C) levels than those with the KK genotype (P < 0.05). In addition, the effects of pravastatin in increasing HDL-C levels were significantly greater in patients with the KK genotype compared with those with the RR genotype (P < 0.05). 4. In conclusion, the R219K polymorphism of ABCA1 was associated with altered lipoprotein levels and the R219K variant significantly modulated the HDL-C response to pravastatin in Chinese patients with CHD.

Influenza virus infection and risk of acute myocardial infarction.

Increasing evidences have shown that pathogens might promote atherosclerosis and trigger acute myocardial infarction (AMI). But the conclusions from various studies on the correlation between previous influenza virus (IV) infection and AMI were inconsistent. We conducted a case-control study to assess the association of previous IV infection and AMI. Questionnaire survey was conducted to collect information about demographic characteristics and heart disease risk factors. Fasting blood sample was obtained to measure IgG antibodies to influenza virus A(IV-A), influenza virus B(IV-B), cytomegalovirus (CMV), herpes simplex virus type-1 (HSV-1) and type-2 (HSV-2), adenovirus (ADV), rubella virus (RV) and Chlamydia pneumoniae (CP) and measure the level of some biochemistry markers. Compared to controls, cases were more likely to have positive IgG antibodies to IV-A and IV-B (IV-A: OR, 3.3; 95%CI, 1.5 to 7.4; IV-B: OR, 17.2; 95%CI, 7.7 to 38.0). After adjustment for potential confounding variables, the risk of AMI was still associated with the presence of IgG antibodies to IV-A (adjusted OR, 7.5; 95%CI, 1.3 to 43.0) and IV-B (adjusted OR, 27.3; 95%CI, 6.6 to 113.8). The study supported the hypothesis that previous IV infection took part in the development of atherosclerosis and trigger the occurrence of AMI.

[Intensive atorvastatin therapy in patients with acute myocardial infarction].

OBJECTIVE: To assess the safety and efficacy of 40 mg daily atorvastatin in patients with acute myocardial infarction. METHODS: A total of 1102 patients with AMI admitted to our hospital from 2003 to 2007 were assigned to atorvastatin 40 mg daily within 24 hours of hospitalization and continued till 3 months post discharge. Patients with LDL-C < 2.0 mmol/L or increased liver enzyme level (3 times higher than normal) at discharge received atorvastatin 20 mg daily. Lipid profiles, high-sensitivity C-reactive protein, liver enzyme level were measured at admission, hospital discharge and 3 months after discharge. RESULTS: (1)The mean hospitalization duration was (10.17 +/- 1.83) days. LDL-C was continuously decreased [(3.24 +/- 1.04) mmol/L at admission, (2.27 +/- 2.00) mmol/L at discharge and (1.48 +/- 0.78) mmol/L at 3 months after discharge, all P < 0.05]. HDL-C decreased from (1.45 +/- 0.38) mmol/L to (1.20 +/- 0.30) mmol/L at hospital discharge, then increased to (1.65 +/- 1.79) mmol/L at 3 months after hospital discharge (all P < 0.05). TC and apoB were also significantly decreased from admission to discharge (all P < 0.05). (2) high-sensitivity C-reactive protein level significantly decreased from admission to hospital discharge and at 1 months after hospital discharge [(49.71 +/- 50.46) mg/L vs. (8.80 +/- 17.66) mg/L vs. (2.61 +/- 2.30) mg/L, all P < 0.05]. (3) Increased ALT > 120 U/L (3 times higher than normal) were found in 127(11.25%), AST > 120 U/L were found in 26(2.40%) patients at discharge. There were still 4 patients with increased ALT (> 120 U/L) at 1 months after discharge and all returned to normal at 3 months after discharge. CONCLUSION: Intensive atorvastatin therapy with a dose of 40 mg daily is safe and effective for patients with AMI.

[Clinical observation of high thoracic epidural anesthesia therapy for patients with congestive heart failure secondary to ischemic cardiomyopathy].

OBJECTIVE: To investigate the effects of high thoracic epidural anesthesia (HTEA) on chronic heart failure (CHF) and its safety. METHODS: 117 patients with ischemic cardiomyopathy (ICM) of NYHA class II - IV and with the LVEF < or = 45%, 90 males and 27 females, aged 45 - 81, were Randomly divided into 2 groups: control group (n = 54, treated with the routine medication) and HTEA group (n = 63, administrated epidurally with 0.5% lidocaine 3 - 5 ml every two hours from 9 a.m. to 11 p.m. everyday via an epidural catheter for one month in addition to the routine treatment). Echocardiography was performed before and after the treatment to examine the cardiac structure and left ventricular systolic function. The plasma brain natriuretic peptide (BNP) was examined before and after the treatment. RESULTS: The clinical symptoms and signs of the HTEA group were improved markedly. The total effective rate was 95.2% in the HTEA group, significantly higher than in the control group (85.2%, P < 0.05). Echocardiographic parameters showed that the diameters of ventricles and atrium decreased by 3 - 5 mm in the HTEA group. The left ventricular end diastolic volume (LVEDV) of the HTEA group reduced from (337 +/- 132) ml before treatment to 274 ml +/- 109 ml after treatment, and the left ventricular end systolic volume (LVESV) of the HTEA group reduced from (215 +/- 99) ml before treatment to (147 +/- 73) ml after treatment (both P < or = 0.001). The regurgitation area of mitral valve of the HTEA group reduced from (6.6 +/- 3.7) cm(2) before treatment to (4.3 +/- 2.7) cm(2) after treatment, and the regurgitation area of tricuspid valve of the HTEA group reduced from (5.4 +/- 3.2) cm(2) before treatment to (3.3 +/- 2.3) cm(2) after treatment (both P < 0.01). No changes were observed in the E/A ratio in both groups. The BNP level fell from (678 +/- 521) ng/L to (237 +/- 225) ng/L in the HTEA group (P < or = 0.05). In the HTEA group, one patient died because of deterioration of cardiac function. HTEA was well tolerated and caused lower incidence of adverse events. CONCLUSIONS: HTEA obviously improves the heart function of the patients with CHS secondary to ICM. Consequently, HTEA is effective and safe in CHF patients with favorable tolerance.

[Efficacy of the thrombectomy on no-reflow in patients with acute myocardial infarction].

OBJECTIVE: To study the efficacy of the percutaneous thrombectomy on no-reflow in the patients with acute myocardial infarction (AMI) with angiographically proven thrombus. METHODS: A total of 68 patients suffering from AMI with coronary thrombus shown by angiography were randomly divided into a group of percutaneous coronary intervention (PCI) therapy (n = 34) and a group of PCI plus percutaneous thrombectomy (n = 34). At 24 hours and 1 week after PCI, real-time imaging was performed by contrast pulse sequencing technology. Contrast score index (CSI), regional wall motion score index (WMSI), endocardial length of contrast defect (CDL) and wall motion abnormality (WML) were calculated. RESULTS: In patients treated with a percutaneous thrombectomy, CSI, WMSI, CDL/left ventricular length (LV), and WML/LV were significantly lower than in PCI group at both time points of observation, and these indexes were markedly decreased at 1 week after PCI compared with 24 hours after PCI (P<0.05 or P<0.01). CONCLUSION: The beneficial effect of the thrombectomy occurs at the microvascular level. Thrombectomy reduces the no-flow phenomenon and the extent of microvascular obstruction, thus it is a feasible therapy in patients with AMI.

[The efficacy of percutaneous coronary intervention combined percutaneous thrombectomy on coronary thrombotic lesions in patients with acute myocardial infarction].

OBJECTIVE: To evaluate the efficacy of percutaneous coronary intervention (PCI) combined percutaneous thrombectomy on coronary thrombotic lesions in patients with acute myocardial infarction (AMI). METHODS: PCI were performed in 56 patients with AMI and positive coronary thrombus shown by angiography and these patients were randomly divided into PCI therapy group (n = 28) and PCI combined percutaneous thrombectomy group (n = 28). Real-time myocardial contrast echocardiography (RT-MCE) was performed at 24h and 1 week after PCI. Contrast score index (CSI), regional wall motion score index (WMSI), endocardial length of contrast defect (CDL), and wall motion abnormality (WML) were calculated. The plasma level of hs-CRP was measured by immunonephelometry. The plasma concentration of N-terminal proB-type natriuretic peptide (NT-proBNP) and matrix metalloproteinase-9 (MMP-9) were detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: CSI, WMSI, CDL and WML at 24 hours and 1 week post procedure as well as the levels of hs-CPR and NT-proBNP at 1 week post procedure [(4.56 +/- 1.98) mg/L vs. (5.96 +/- 2.03) mg/L, P < 0.05; (544.7 +/- 185.3) pmol/L vs. (897.6 +/- 215.9) pmol/L, P < 0.01] were significantly lower in PCI combined percutaneous thrombectomy group than those in PCI group in various time points. There were no differences in the plasma level of MMP-9 between the two groups [(672.7 +/- 175.9) microg/L vs. (609.6 +/- 196.5) microg/L, P > 0.05] at 1 week after PCI. CONCLUSIONS: PCI combined percutaneous thrombectomy can significantly reduce no-reflow phenomenon, improve microcirculation and myocardial dysfunction. Thus PCI combined percutaneous thrombectomy is a feasible therapy in patients with AMI.

Effects of angiotensin converting enzyme inhibitor, angiotensin II type I receptor blocker and their combination on postinfarcted ventricular remodeling in rats.

BACKGROUND: Transforming growth factor (TGF) beta(1)-Smads signal plays an important role in cardiac remodeling following myocardial infarction (MI). In addition, both angiotensin converting enzyme inhibitor (ACEI) and angiotensin II type I receptor blocker (ARB) can effectively prevent left ventricular remodeling. The current study focused on whether the combination of ACEI and ARB is more beneficial for preventing ventricular remodeling and whether Smad proteins mediate this beneficial effect. METHODS: MI was induced by ligating the left anterior descending coronary artery in rats. Twenty-four hours after ligation, the survived rats were randomly divided into five groups and treated for 8 weeks: placebo group, ACEI group (benazepril 10 mg.kg(-1).d(-1)), ARB group (irbesartan 50 mg.kg(-1).d(-1)), ACEI + ARB group (benazepril 10 mg.kg(-1).d(-1) + irbesartan 50 mg.kg(-1).d(-1)) and control group (sham-operated rats). After 8 weeks, we examined the following indexes: the ratio of ventricular weight to body weight (VW/BW), left ventricular end diastolic dimension (LVDd), ejection fraction (EF), fractional shortening (FS), ratio of E-wave to A-wave velocity, collagen of noninfarcted zone, the mRNA expression of TGFbeta(1), Smad 2, and Smad 3 by RT-PCR in noninfarcted zone, the protein expression of Smad 2 and Smad 3 in noninfarcted zone by Western blot. RESULTS: VW/BW significantly increased in the placebo groups compared with that in the control group (P < 0.01). This increase was limited in ACEI, ARB, and combined groups (P < 0.01 compared with placebo group). There was no significant difference among the three actively treated groups. Collagen was increased in placebo group (5.68 +/- 0.5)% compared with that in control group (P < 0.01). ACEI, ARB and combined treatment attenuated this increase of collagen [(4.3 +/- 0.5)%, (3.5 +/- 0.5)%, (3.2 +/- 0.4)%] in comparison with that in placebo group (P < 0.01 respectively). Combined treatment showed more significant effect on collagen deposition. EF and FS significantly decreased, LVDd and E/A significantly increased in placebo group compared with that in control group (P < 0.01 respectively). ACEI, ARB and combined treatment ameliorated these indexes (P < 0.01 compared with placebo group). The mRNA expression of TGFbeta(1), Smad 2, and Smad 3 (0.700 +/- 0.045, 0.959 +/- 0.037 and 0.850 +/- 0.051) increased in placebo group compared with that in control group (P < 0.01). ACEI, ARB and combined treatment normalized the increase (P < 0.01). Furthermore, ARB and combined treatment proved to be more effective in decreasing TGF beta(1) and Smad mRNA expression than ACEI treatment (P < 0.01). The expression of Smad 2 and Smad 3 protein increased in placebo group compared with that in control group (P < 0.01). ACEI, ARB and combined treatment normalized the increase (P < 0.01). Furthermore, ARB and combined treatment proved to be more effective than ACEI alone (P < 0.01). CONCLUSIONS: TGFbeta(1)-Smads signal activation is correlated with ventricular remodeling following MI. ACEI and ARB treatment prevents ventricular remodeling by inhibiting expression of Smad 2 and Smad 3. ARB and combined treatment are more effective than ACEI alone.

[The prognostic value of hyponatremia in patients with acute myocardial infarction].

OBJECTIVE: To evaluate the prognostic significance of hyponatremia in patients with AMI. METHODS: The study population consisted of 670 patients with AMI in coronary care unit in our hospital from January 2003 to December 2004. The patients were designed into three groups according to serum sodium concentration within twenty four to forty eight hours following the onset of AMI: Group A. Na(+) > or = 135 mmol/L; Group B. Na(+) 120-135 mmol/L; Group C. Na(+) < or = 120 mmol/L. The data of myocardial enzymes, myocardial infarction size, heart function and inhospital mortality were analyzed retrospectively. RESULTS: 1. The inhospital mortality of each group: group A was 7.6% (17/225), group B was 8.1% (34/421), group C was 33.3% (8/24). The difference between group C and group B or group A was significant. The P value was little than 0.05. 2. Activities of serum creatine phosphatase kinase and serum creatine phosphatase kinase isoenzymes and myocardial infarction sizes in each group were different (P < 0.05). 3. 59 cases of all died and 611 cases of all recovered in duration of hospital stay. Serum sodium concentrations of the recovered group were (133.00 +/- 5.25) mmol/L, and that of the died group were (122.00 +/- 7.25) mmol/L (P < 0.01). 4. In a multivariate logistic regression analysis, hyponatremia was associated with 30-day mortality in patients with AMI. In analysis of the association between the degree of hyponatremia and outcome, we observed that the risk of 30-day mortality increased with the severity of hyponatremia. CONCLUSION: Hyponatremia may be one of the important markers that predict a worse prognosis in patients with AMI.

[Evaluation of right ventricular function by tissue Doppler echocardiography and Tei index in right ventricular myocardial infarction].

OBJECTIVE: With tissue Doppler imaging and right ventricular Tei index, right ventricular function in patients with right ventricular myocardial infarction (RVMI) was assessed. METHOD: 51 patients admitted to coronary care units and diagnosed as acute inferior myocardial infarction were further studied with the ECG criterion of ST segment elevation >or= 1mm in V(4R) to establish the diagnosis of RVMI. 23 patients were thus diagnosed as RVMI and 28 patients not. 20 healthy subjects served as controls. Clinical and echocardiography index were recorded. Peak systolic and peak early and late diastolic velocities (Sm, Em, Am) and Em/Am were acquired from the apical four-chamber view at the lateralside of tricuspid annulus, the septal side of the tricuspid annulus and the RV free mid-wall using DTI. Interval between tricuspid closing and reopening and ejection time (ET) from parasternal short-axis view were recorded by pulse-wave Doppler. RV Tei index was calculated. RESULTS: Sm and Em at the lateral side of tricuspid annulus and the RV free mid-wall reduced significantly in patients with RVMI as compared with those without RVMI and healthy individuals (Sm at the lateral (7.0 +/- 2.0) cm/s vs (8.7 +/- 1.9) cm/s and (10.6 +/- 2.1) cm/s, P < 0.01; Em at the lateral (6.3 +/- 1.9) cm/s vs (7.9 +/- 1.8) cm/s and (9.6 +/- 1.9) cm/s, P < 0.01; Sm at the RV free mid-wall (6.4 +/- 1.9) cm/s vs (8.0 +/- 1.9) cm/s and (9.4 +/- 2.0) cm/s, P < 0.05; Em at the RV free mid-wall (6.1 +/- 2.0) cm/s vs (7.6 +/- 2.0) cm/s and (9.2 +/- 2.3) cm/s, P < 0.05). RV Tei index in patients with RVMI also increased as compared with that in the other two groups (0.65 +/- 0.19 vs 0.40 +/- 0.15 and 0.26 +/- 0.10; P < 0.01). CONCLUSIONS: The evaluation of velocities at the lateral side of tricuspid annulus and the RV free mid-wall using DTI and RV Tei index provides a noninvasive and rapid method for assessing right ventricular function in patients with RVMI.

[Relationship between expression of Smad and ventricular remodeling after myocardial infarction in rats].

OBJECTIVE: To investigate the relationship between expression of Smad3, Smad7 and ventricular remodeling in rats after myocardial infarction. METHODS: Myocardial infarction was induced by left anterior descending coronary artery ligation in rats (n = 11) and sham-operated rats were used as control (n = 10). The rats were sacrificed 8 weeks later. Heart weight/body weight (HW/BW), mean blood pressure, left ventricular end diastolic pressure (LVEDP), collagen content in the un-infarcted area were examined. The mRNA levels of transforming growth factor (TGF)beta(1), Smad 3, Smad7 were determined by RT-PCR. RESULT: Compared with controls, the level of HW/BW, LVEDP and collagen content were significant increased. The mRNA expression of TGFbeta(1) and Smad3 was significantly increased in areas of myocardial infarction, border of the infarction, interventricular septum and right ventricle. The expression of Smad7 mRNA in these areas was decreased. CONCLUSION: These results indicated that TGFbeta(1)-Smads signaling was correlated to the ventricular remodeling after myocardial infarction. Smad3 might promote the process while Smad7 inhibit the process.

[Relationship between plasma brain natriuretic peptide concentration and clinical prognosis in patients of acute myocardial infarction].

OBJECTIVE: To evaluate the value of brain natriuretic peptide (BNP) in estimating risk stratification in patients with acute myocardial infarction (AMI) and to determine the relationship between BNP and adverse cardiac events after AMI. METHODS: The 135 subjects were selected into the study, including 25 healthy subjects and 110 patients with a first AMI. The plasma concentrations of BNP were measured at two to four days after infarction in patients and healthy controls. Left ventricular function was evaluated by echocardiography with the parameters of left ventricular ejection function (LVEF) after 3 months. Patients were followed up at 12 months. The main outcome measures were heart failure, left remodeling, mortality and other adverse cardiac events at one year. RESULTS: Plasma BNP concentrations in patients with AMI were much higher than those in the health control people (416.7 +/- 208.0 ng/L versus 61.8 +/- 34.1 ng/L, P < 0.01). The BNP count ranged from 5 to 2500 ng/L in AMI patients. There was no association between the BNP count and mortality rate. The development of new congestive heart failure (CHF) was associated with a higher BNP count (P = 0.02). The development of any of the clinical end points (death/CHF/shock) occurred more frequently in patients with a higher BNP count (13.8% for BNP count of < 100 ng/L, 39.1% for BNP count of 100 - 200 ng/L, 43.3% for BNP count of 200 - 400 ng/L, 46.4% for BNP count of > 400 ng/L; P = 0.019). Plasma BNP concentrations remained independently associated with the development of clinical end points in multivariable model that adjusted for potential confounding variables. CONCLUSION: The results of the present study confirm that the elevated BNP count related to the risk stratification and prognosis in patients with AMI. Elevations in BNP count are associated with a higher incidence of new CHF and adverse clinical outcomes after AMI. It could serve as a strong predictor for the subsequent development of poor outcomes in AMI patients.