Impact of anemia on long-term outcome in elderly patients with acute coronary syndrome undergoing percutaneous coronary interventions / 中华心血管病杂志

<p><b>OBJECTIVE</b>To assess the impact of pre-procedure anemia on the long-term mortality in elderly patients with acute coronary syndrome (ACS) after percutaneous coronary interventions.</p><p><b>METHODS</b>A total of 1014 ACS patients (≥ 60 years of age) with hemoglobin data and without previous treatment with thrombolytic agents and without end-stage renal failure before the interventional procedure were included. Patients were classified as anemia using the definition of World Health Organization: hemoglobin < 130 g/L in men, and < 120 g/L in women. A total of 253 patients were anemia. The clinical features of patients with and without anemia and association of pre-procedure anemia with long-term mortality were analyzed.</p><p><b>RESULTS</b>Incidence of diabetes and serum creatinine level were significantly higher in anemia patients than in non-anemia patients while systolic blood pressure and low-density lipoprotein cholesterol were significantly lower in anemia patients than in non-anemia patients (P < 0.05 or P < 0.01). The patients were followed up for 528 (178 - 675) days. After adjustment for potential co-variants in Cox regression analysis, pre-procedure anemia was associated with a significantly higher long-term mortality (RR: 3.293, 95%CI: 1.431 - 7.578, P < 0.01).</p><p><b>CONCLUSION</b>Pre-procedure anemia is an independent predictor of long-term mortality in elderly patients with acute coronary syndrome after percutaneous coronary interventions.</p>

Coronary stenting versus bypass surgery in heart failure patients with preserved ejection fraction / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The optimal revascularization strategy in patients with heart failure with preserved ejection fraction (HFPEF) remains unclear. The aim of the present study was to compare the effects of percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) in patients with HFPEF.</p><p><b>METHODS</b>From July 2003 through September 2005, a total of 920 patients with coronary artery disease (CAD) and HFPEF (ejection fraction ≥ 50%) underwent PCI (n = 350) or CABG (n = 570). We compared the groups with respect to the primary outcome of mortality, and the secondary outcomes of main adverse cardiac and cerebral vascular events (MACCE), including death, myocardial infarction, stroke and repeat revascularization, at a median follow-up of 543 days.</p><p><b>RESULTS</b>In-hospital mortality was significantly lower in the PCI group than in the CABG group (0.3% vs. 2.5%, adjusted P = 0.016). During follow-up, there was no significant difference in the two groups with regard to mortality rates (2.3% vs. 3.5%, adjusted P = 0.423). Patients receiving PCI had higher MACCE rates as compared with patients receiving CABG (13.4% vs. 4.0%, adjusted P < 0.001), mainly due to higher rate of repeat revascularization (adjusted P < 0.001). Independent predictors of mortality were age, New York Heart Association (NYHA) class and chronic total occlusion.</p><p><b>CONCLUSION</b>Among patients with CAD and HFPEF, PCI was shown to be as good as CABG with respect to the mortality rate, although there was a higher rate of repeat revascularization in patients undergoing PCI.</p>

Neuregulin-1 attenuates mitochondrial dysfunction in a rat model of heart failure / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Mitochondrial dysfunction plays a pivotal role in the progression of left ventricular (LV) remodeling and heart failure (HF). Recombinant human neuregulin-1 (rhNRG-1) improves cardiac function in models of experimental HF and in clinical trials; however, its impact on mitochondrial function during chronic HF remains largely unknown. The purpose of this study was to investigate whether rhNRG-1 could attenuate the functional and structural changes that occur in cardiac mitochondria in a rat model of HF induced by myocardial infarction.</p><p><b>METHODS</b>Sixty adult rats underwent sham or coronary ligation to induce HF. Four weeks after ligation, 29 animals with LV ejective fraction ≤ 50% were randomized to receive either vehicle or rhNRG-1 (10 µg×kg(-1)×d(-1), I.V.) for 10 days, another 12 sham-operated animals were given no treatment. Echocardiography was used to determine physiological changes. Mitochondrial membrane potential (MMP), respiratory function and tissue adenosine triphosphate (ATP) production were analyzed. Cytochrome c expression and cardiomyocyte apoptosis were determined. Oxidative stress was evaluated by reactive oxygen species production using fluorescence assays and gene expression of glutathione peroxidase measured by real-time quantitative PCR.</p><p><b>RESULTS</b>Compared with sham-operated animals, vehicle treated HF rats exhibited severe LV remodeling and dysfunction, significant mitochondrial dysfunction, increased mitochondrial cytochrome c release, increased myocyte apoptosis and enhanced oxidative stress. Short-term treatment with rhNRG-1 significantly attenuated LV remodeling and cardiac function. Concomitant with this change, mitochondrial dysfunction was significantly attenuated; with ATP production, MMP and respiratory function restored, cytochrome c release and apoptosis inhibited, and oxidative stress reduced.</p><p><b>CONCLUSION</b>The present study demonstrated that rhNRG-1 can significantly improve LV remodeling and cardiac function in the failing heart, this beneficial effect is related to reducing mitochondrial dysfunction, myocyte apoptosis and oxidative stress.</p>

Optimal pharmacotherapy according to guideline improved prognosis of outpatients with chronic heart failure / 中华心血管病杂志

<p><b>OBJECTIVE</b>To evaluate the effects of optimal pharmacotherapy according to guideline on treating chronic heart failure(CHF) in real world clinical practice.</p><p><b>METHODS</b>A total of 231 consecutive outpatients with reduced left ventricular ejection fraction (LVEF ≤ 40%) and enlarged left ventricular end diastolic diameter (male > 55 mm, female > 60 mm) were recruited from January 2001 to June 2009. All patients were treated with optimal pharmacotherapy according to guideline recommendations and followed up to December 31, 2009. Mortality, rehospitalization and changes of heart size and cardiac function at baseline and at the end of follow-up period were analyzed.</p><p><b>RESULTS</b>(1) 14 patients were lost during follow-up (6.1%), and follow-up was complete in 217 patients (93.9%). 97.2% and 98.2% patients were prescribed angiotensin converting enzyme (ACE) inhibitors and β-blockers (βB). Combined of ACE inhibitors and BB use was applied in 95.3% patients. The target dose of ACE inhibitors and βB were reached in 50.7% and 37.3% patients. (2) Lower mortality and re-hospitalization rates were observed in this cohort: all-cause morality, average annual mortality was 11.5% and 3.9% respectively. Re-hospitalization rate was 27.6%. (3) Left ventricular end-diastolic diameter (LVEDD) decreased from (68.2 ± 7.2) mm to (62.2 ± 9.6) mm. LVEDD value was normal or near normal (male ≤ 60 mm, female ≤ 55 mm) in 43.2% patients. LVEF improved form (29.8 ± 7.5)% to (43.3 ± 11.8)%, LVEF was > 40% in 60.4% patients, LVEF was ≤ 40% but increased ≥ 10% after treatment in 22.9% patients.</p><p><b>CONCLUSION</b>Optimal pharmacotherapy according to guideline can improve prognosis of outpatients with CHF.</p>

Factors influencing recovery of left ventricular structure in patients with chronic heart failure / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Angiotensin converting enzyme (ACE) inhibitors and β-blockers (βB) have beneficial effects on left ventricular (LV) remodeling, alleviate symptoms and reduce morbidity and mortality in patients with chronic heart failure (CHF). However the correlation between the d osages of ACE inhibitors, βB, and recovery of LV structure remains controversial. Clinical factors associated with recovery of normal ventricular structure in CHF patients receiving medical therapy are poorly defined. Here we aimed to identify variables associated with recovery of normal or near-normal structure in patients with CHF.</p><p><b>METHODS</b>We recruited 231 consecutive CHF outpatients, left ventricular ejection fraction (LVEF) ≤ 40% and left ventricular end diastolic diameter (LVEDD) > 55/50 mm (male/female), who were receiving optimal pharmacotherapy between January 2001 and June 2009, and followed them until December 31, 2009. They were divided into three groups according to LVEDD and whether they were still alive at final follow-up: group A, LVEDD ≤ 60/55 mm (male/female); group B, LVEDD > 60/55 mm (male/female); and group C, those who died before final follow-up. Apart from group C, univariate analysis was performed followed by Logistic multivariate analysis to determine the predictors of recovery of LV structure.</p><p><b>RESULTS</b>A total of 217 patients completed follow-up, and median follow-up time was 35 months (range 6 - 108). Twenty-five patients died during that period; the all-cause mortality rate was 11.5%. Group A showed clinical characteristics as follows: the shortest duration of disease and shortest QRS width, the lowest N-terminal brain natriuretic peptide (NT-proBNP) at baseline, the highest dose of βB usage, the highest systolic blood pressure (SBP), diastolic blood pressure (DBP) and the lowest New York Heart Association (NYHA) classification, serum creatinine, uric acid, total bilirubin and NT-proBNP after treatment. Logistic multivariate analysis was performed according to recovery or no recovery of LV structure. Data showed that LVEF at follow-up (P = 0.013), mitral regurgitation at baseline (P = 0.020), LVEDD at baseline (P = 0.031), and βB dosage (P = 0.041) were independently associated with recovery of LV diameter.</p><p><b>CONCLUSION</b>Our study suggests that four clinical variables may predict recovery of LV structure to normal or near-normal values with optimal drug therapy alone, and may be used to discriminate between patients who should receive optimal pharmacotherapy and those who require more aggressive therapeutic interventions.</p>

Prognostic value of baseline C-reactive protein levels in patients undergoing coronary revascularization / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>C-reactive protein (CRP) is a lowly expressed marker for inflammatory response. This study aimed to evaluate the prognostic value of baseline CRP levels in patients undergoing coronary revascularization in the context of modern medical treatment.</p><p><b>METHODS</b>This was a retrospective study in a single center. Four hundred and fourteen patients were enrolled, who underwent coronary revascularization and received adequate medication for secondary prevention of coronary heart disease. The study compared the follow-up clinical outcomes between high level CRP group (CRP > 5 mg/L) and low level one. The median follow-up time was 551 days.</p><p><b>RESULTS</b>Compared with low CRP group, the relative risk (RR) of the major adverse cardiovascular and cerebral events (MACCE) in high CRP group was 5.131 (95%CI: 1.864-14.123, P = 0.002). There were no significant differences in death, myocardial infarction and stroke during the follow-up between two groups, but a higher risk of re-revascularization was found in high CRP group (RR 6.008, 95%CI: 1.667-21.665, P = 0.006). Cox regression analysis showed that only CRP level could contribute to MACCE during the follow-up. MACCE-free rate was much lower in high CRP group (Kaplan-Meier log-rank P < 0.001).</p><p><b>CONCLUSION</b>In the context of modern medical treatment, the baseline level of CRP is an independent predictor for long-term prognosis in patients with coronary revascularization.</p>

Neuregulin-1 preconditioning protects the heart against ischemia/reperfusion injury through a PI3K/Akt-dependent mechanism / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Neuregulin-1 (NRG-1), the ligand of the myocardial ErbB receptor, is a protein mediator with regulatory actions in the heart. This study investigated whether NRG-1 preconditioning has protective effects on myocardial ischemia/reperfusion (I/R) injury and its potential mechanism.</p><p><b>METHODS</b>We worked with an in vivo rat model with induced myocardial ischemia (45 minutes) followed by reperfusion (3 hours). NRG-1 message was detected in the heart using RT-PCR and the protein levels of NRG-1 and ErbB4 were detected by Western blotting analysis. Infarct size was assessed using the staining agent triphenyltetrazolium chloride and cardiac function was continuously monitored. The levels of creatine kinase and lactate dehydrogenase in plasma were analyzed to assess the degree of cardiac injury. The extent of cardiac apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and by Western blotting analysis of cleaved caspase-3. We examined the phosphorylation of Akt in the myocardium and the effect of PI3K/Akt inhibition on NRG-1-induced cardioprotection.</p><p><b>RESULTS</b>Transcription and expression of NRG-1 and phosphorylation of its ErbB4 receptor were significantly upregulated in the I/R hearts. NRG-1 pretreatment reduced the infarct size following cardiac I/R in a concentration-dependent manner with an optimal concentration of 4 µg/kg in vivo. NRG-1 pretreatment with 4 µg/kg, i.v. markedly reduced the plasma creatine kinase and lactate dehydrogenase levels. Pretreatment with NRG-1 also significantly reduced the percentage of TUNEL positive myocytes and the level of cleaved caspase-3 in the I/R hearts. Pretreatment with NRG-1 significantly increased phosphorylation of Akt following I/R. Furthermore, the cardioprotective effect limiting the infarct size that was induced by NRG-1 was abolished by co-administration of the PI3K inhibitor LY294002.</p><p><b>CONCLUSIONS</b>The concentration of NRG-1, a new autacoid, was rapidly upregulated after myocardial I/R. NRG-1 preconditioning has cardioprotective effects against I/R injury through a PI3K/Akt-dependent mechanism in vivo.</p>

Myocardial autophagy variation during acute myocardial infarction in rats: the effects of carvedilol / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The loss of cardiac myocytes is one of the mechanisms involved in acute myocardial infarction (AMI)-related heart failure. Autophagy is a common biological process in eukaryote cells. The relationship between cardiac myocyte loss and autophagy after AMI is still unclear. Carvedilol, a non-selective alpha1- and beta-receptor blocker, also suppresses cardiac myocyte necrosis and apoptosis induced by ischemia. However, the association between the therapeutic effects of carvedilol and autophagy is still not well understood. The aim of the present study was to establish a rat model of AMI and observe changes in autophagy in different zones of the myocardium and the effects of carvedilol on autophagy in AMI rats.</p><p><b>METHODS</b>The animals were randomly assigned to a sham group, an AMI group, a chloroquine intervention group and a carvedilol group. The AMI rat model was established by ligating the left anterior descending coronary artery. The hearts were harvested at 40 minutes, 2 hours, 24 hours and 2 weeks after ligation in the AMI group, at 40 minutes in the chloroquine intervention group and at 2 weeks in other groups. Presence of autophagic vacuoles (AV) in the myocytes was observed by electron microscopy. The expression of autophagy-, anti-apoptotic- and apoptotic-related proteins, MAPLC-3, Beclin-1, Bcl-xl and Bax, were detected by immunohistochemical staining and Western blotting.</p><p><b>RESULTS</b>AVs were not observed in necrotic regions of the myocardium 40 minutes after ligation of the coronary artery. A large number of AVs were found in the region bordering the infarction. Compared with the infarction region and the normal region, the formation of AV was significantly increased in the region bordering the infarction (P < 0.05). The expression of autophagy- and anti-apoptotic-related proteins was significantly increased in the region bordering the infarction. Meanwhile, the expression of apoptotic-related proteins was significantly increased in the infarction region. In the chloroquine intervention group, a large number of initiated AVs (AVis) were found in the necrotic myocardial region. At 2 weeks after AMI, AVs were frequently observed in myocardial cells in the AMI group, the carvedilol group and the sham group, and the number of AVs was significantly increased in the carvedilol group compared with both the AMI group and the sham group (P < 0.05). The expression of autophagy- and anti-apoptotic-related proteins was significantly increased in the carvedilol group compared with that in the AMI group, and the positive expression located in the infarction region and the region bordering the infarction.</p><p><b>CONCLUSIONS</b>AMI induces the formation of AV in the myocardium. The expression of anti-apoptosis-related proteins increases in response to upregulation of autophagy. Carvedilol increases the formation of AVs and upregulates autophagy and anti-apoptosis of the cardiac myocytes after AMI.</p>

Serum troponin I level in patients with hypertrophic cardiomyopathy / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe serum troponin I (TNI) level in patients with hypertrophic cardiomyopathy (HCM).</p><p><b>METHOD</b>Six hundreds and twelve HCM patients were analyzed prospectively from January 1990 to November 2007.Ultracardiography were detected for all the patients. The diagnostic criteria of HCM is ventricular wall thickness more than 15 mm. Serum TNI level was measured in 116 patients with HCM. Clinical data including age, gender, history, main symptoms, NYHA grade, coronary angiograph, electrocardiogram and echocardiography were compared between patients with normal and increased TNI levels.</p><p><b>RESULTS</b>In 116 patients who detected TNI, 62 of them (53.4%) had a degree higher than normal. The median TNI value of all these patients is 0.07 ng/ml (0 - 4.38 ng/ml). Sixty-nine patients (59.5%) had undergone coronary angiography. Only 9 of them (13.0%) could be diagnosised as coronary heart disease. The TNI values of HCM patients with or without coronary heart disease were similar. The factors related to a higher TNI value included maximal depth of ventricule (P < 0.05), significant T inversion (P < 0.01) and chest pain (P < 0.05). Compared to all the 612 patients, the ones who detected serum TNI were likely to have chest pain (45.7% vs. 34.5%, P < 0.01) and significant T inversion (75.9% vs. 30.1%, P < 0.01).</p><p><b>CONCLUSION</b>Increased serum TNI could be seen in half of HCM patients, especially in those patients with chest pain or significant T inversion. It is therefore important to different these patients from patients with acute coronary syndrome.</p>

Impact of admission heart rate on in-hospital mortality in patients with acute myocardial infarction / 中华心血管病杂志

<p><b>OBJECTIVE</b>To evaluate the impact of admission heart rate (HR) on in-hospital mortality in patients with acute myocardial infarction.</p><p><b>METHOD</b>The data of 904 in-hospital patients with ST-elevation myocardial infarction were collected from database of Beijing Anzhen Hospital during 2003--2004. The patients were divided into three groups according to the admission HR: < 80 beats/min, 80 - 90 beats/min and > 90 beats/min. Left ventricular ejection fraction (LVEF), left ventricular end diastolic dimension (LVEDD), left ventricular end systolic dimension (LVESD) and the cases of in-hospital death were analyzed.</p><p><b>RESULT</b>(1) Age, gender, smoking, hypertension, diabetes, the number of diseased vessel detected by coronary angiography were similar among three groups. LVEDD in group > 90 beats/min [(51.9 +/- 7.5) mm] and group 80 - 90 beats/min [(51.6 +/- 5.8) mm] were significantly larger compared with group < 80 beats/min [(50.3 +/- 5.3) mm, all P < 0.05]; LVESD in group > 90 beats/min [(39.5 +/- 8.7) mm] were also significantly increased compared with group 80 - 90 beats/min [(37.1 +/- 7.1) mm] and group < 80 beats/min [(34.8 +/- 6.2) mm, all P < 0.05]; LVEF was significantly lower in group > 90 beats/min (46.0% +/- 10.6%) compared with group 80 - 90 beats/min (49.5% +/- 11.3%) and group < 80 beats/min (54.6% +/- 10.8%, all P < 0.05). In-hospital mortality was significantly higher in group > 90 beats/min (18.2%) than those in group 80 - 90 beats/min and in group < 80 beats/min (8.5%, 3.9%, all P < 0.05). (2) Multivariate analysis showed that admission HR was an independent risk factor for in-hospital mortality (OR = 1.025, 95% CI 1.008 - 1.043, P = 0.005).</p><p><b>CONCLUSION</b>The high level of admission HR was a powerful predictor of in-hospital mortality and ventricular remodeling in patients with acute myocardial infarction.</p>

Safety and efficacy comparison of myocardial contrast enhancement-guided and angio-pressure-guided transcoronary ablation of septal hypertrophy for patients with hypertrophic obstructive cardiomyopathy / 中华心血管病杂志

<p><b>OBJECTIVE</b>To compare the safety and efficacy of myocardial contrast enhancement (MCE)-guided and angio-pressure (AP)-guided transcoronary ablation of septal hypertrophy (TASH) for patients with hypertrophic obstructive cardiomyopathy (HOCM).</p><p><b>METHODS</b>TASH was performed under MCE-guide (n = 47, group I) or AP-guide (n = 25, group II) for drug-refractory patients with HOCM. Myocardial perfusion imaging (MPI) data as well as other clinical data were compared.</p><p><b>RESULTS</b>TASH both under MCE-guide or AP-guide resulted in similar and significant reduction of left ventricular outflow tract gradient (PG) and associated with significant symptom improvement (all P < 0.001). Dosage of ethanol use, peak-level of CK-MB and ablated myocardial area and incidence of arrhythmia were also similar between the two groups.Similar left ventricular/atrial dimension changes post TASH were observed in the 2 groups during follow-up. However, the first selected septal vessels were changed under MCE in 6 patients.</p><p><b>CONCLUSIONS</b>Our data demonstrated that the MCE-guided TASH was not superior to AP-guided TASH in safety and efficacy. However, MCE-guided TASH can avoid the misplace of ethanol to avoid innocent myocardial ablation.</p>

The primary observation on the effect of pravastatin to non-ischemic heart failure / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the efficacy and safety of adding pravastatin (Pra) on top of standard therapy in non-ischemic heart failure patients.</p><p><b>METHODS</b>A total of 61 patients hospitalized in our hospital from Jan 2005 to Jul 2006 were randomly divided into pravastatin group (Pra 20 mg/d on top of standard therapy, n = 30) and control group (standard therapy, n = 31) and followed 6 months. The changes on cardiac function, flow-mediated vasodilatation (FMD) of brachial artery, plasma TNF-alpha level, liver and kidney function were observed.</p><p><b>RESULTS</b>In Pra treated patients, FMD of brachial artery significantly increased after 3 months treatments and NYHA stage significantly improved, plasma BNP, TNF-alpha levels and left ventricular end-diastolic dimension significantly decreased, LVEF significantly increased significantly 6 months post therapy compared to baseline (all P < 0.01). In control group, the patients' NYHA stage also significantly improved (P < 0.05) and LVEF tended to be higher (P = 0.052) while FMD, plasma BNP and TNF-alpha levels remained unchanged at 6 months post therapy compared to baseline. In Pra group, the level of TC (P < 0.05) and LDL-C (P = 0.051) also significantly decreased while HDL-C remained unchanged 6 months post therapy. One patient in Pra group discontinued the study drug because of anaphylaxis. No event on liver and kidney dysfunction was noticed.</p><p><b>CONCLUSION</b>Pravastatin was effective and safe in treating non-ischemic heart failure patients and can significantly improve left ventricular remodeling, endothelial and cardiac functions as well as reduce the levels of inflammatory factors.</p>

Simvastatin inhibits hypertension-induced cardiac hypertrophy in rats through activation of heme oxygenase-1/carbon monoxide pathway / 生理学报

To investigate the anti-cardiac hypertrophic mechanism of statins, thirty-eight male Wistar rats were randomly allocated to four groups. Rats in model group received nitric oxide synthase inhibitor, N-nitro-L-arginine (L-NNA) 15 mg/(kg.d) by peritoneal injection. Rats in simvastatin treatment groups were given simultaneously L-NNA as those in model group and simvastatin 5 or 30 mg/(kg.d) intragastrically respectively. Rats in control group received the same volume of normal sodium. Left ventricular function, left ventricular mass index (LVMI), the content of brain natriuretic peptide (BNP) in plasma and myocardium, myocardial hydroxyproline and heme oxygenase activity were determined after 6 weeks. The results showed that rats in model group developed significant cardiac hypertrophy associated with reduced left ventricular function compared with the control group. However, compared with the model group, L-NNA-induced cardiac hypertrophy of rats was significantly relieved in simvastatin treatment groups, associated with improved left ventricular function, decreased LVMI, lower BNP levels in plasma and myocardium, lower content of myocardial hydroxyproline, and increased myocardial heme oxygenase (HO) activity. In cultured rat neonatal cardiomyocytes, simvastatin (30 or 100 mumol/L) significantly increased heme oxygenase-1 (HO-1) mRNA expression, HO activity as well as the production of CO in cardiomyocytes. Cultured with zinc protoporphyrin, a HO inhibitor, or simvastatin alone did not change [(3)H]leucine uptake of cardiomyocytes. However, cocultured with simvastatin significantly inhibited the cardiomyocyte [(3)H]leucine uptake induced by angiotensin II in a concentration-dependent manner. Cotreatment with zinc protoporphyrin significantly abolished the suppressive effect of simvastatin on cardiomyocyte [(3)H]leucine uptake. These data suggest that the activation of HO-1/CO pathway may be one of the important mechanisms by which statins inhibit cardiac hypertrophy caused by hypertension.

Effect of metabolic syndrome on prognosis and clinical characteristics of revascularization in patients with coronary artery disease / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>People with metabolic syndrome are at higher risk for developing coronary artery disease (CAD). The effect of the metabolic syndrome on outcomes in patients with preexisting CAD has not been well studied. This study was conducted to assess the prevalence, characteristics, in hospital and long term prognosis of CAD with metabolic syndrome and to determine the factors influencing the prognosis of the disease.</p><p><b>METHODS</b>The DESIRE registry contains data of 3696 patients with CAD between 2001 and 2004. Mean long term followup was (829 +/- 373) days. Diagnosis of metabolic syndrome was based on modified International Diabetes Federation (IDF) Worldwide Definition of the Metabolic Syndrome, using body mass index (BMI) instead of waist circumference.</p><p><b>RESULTS</b>Of 2596 patients with complete records of height, weight, and so on, 1280 (49.3%) were identified with metabolic syndrome. The patients with metabolic syndrome had higher level of body mass index, systolic blood pressure, diastolic blood pressure, fasting glucose and disordered blood lipid (all P < 0.0001), with higher creatinine [(10.5 +/- 4.3) mg/L vs (9.9 +/- 2.9) mg/L, P < 0.0001] and the number of white blood cells [(7.49 +/- 2.86) x 10(9)/L vs (7.19 +/- 2.62) x 10(9)/L, P = 0.008) compared with those without metabolic syndrome. The patients with metabolic syndrome showed severer coronary angiographic alterations (left main artery and/or > or = 2-vessel) (73.6% vs 69.6%, P = 0.031). There were no significant differences of major adverse cardiac and cerebral events (MACCE) or mortality in hospital between the two groups. During followup, the ratio of MACCE in CAD with metabolic syndrome patients increased significantly (11.8% vs 10.0%, P = 0.044). Fasting blood glucose (> or = 1000 mg/L) and triglyceride (TG, > or = 1500 mg/L) were responsible for most of the increased risk associated with the metabolic syndrome (adjusted OR 1.465, 95% CI 1.037 - 1.874, P = 0.032; OR 1.378, 95% CI 1.014 - 1.768, P = 0.044).</p><p><b>CONCLUSIONS</b>The prevalence of metabolic syndrome was very high in CAD patients. The metabolic syndrome confers a higher risk of long term MACCE in patients with CAD, and dysglycaemia and hypertriglycaemia appear to be responsible for most of the associated risk.</p>

Clinical study of pravastatin with different dosage in early admission period in patients with unstable angina / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effect of early intervention by pravastatin with two different dosage on inflammatory factors and endothelial vasodilator function in patients with unstable angina (UA).</p><p><b>METHODS</b>108 patients with UA were investigated consecutively and divided randomly into three groups (group 20 mg, n = 37; group 10 mg, n = 37; group control, n = 34). Blood samples were examined at admission and 4, 8 weeks after the therapy of pravastatin. Fourty patients of UA were chosen from those three groups (15, 15 and 10 cases respectively). The endothelium-dependent vasodilation and the function of vascular endothelium of them were measured. In the dosage of 20 mg pravastatin group non-endothelium-dependent vasodilation in brachial artery was also tested by ultrasound before and 8 weeks after the therapy. Cardiac events were followed up for 2 months.</p><p><b>RESULTS</b>(1) The use of pravastatin in early admission period of UA could significantly reduce inflammatory factors and improve vascular endothelium function, which was more obviously in the group of 20 mg/d than in group of 10 mg/d. These benefits occurred in 4th week and more obviously in 8th week after the therapy. (2) The lipid lowering therapy in the early stage of admission (24 - 48 h) resulted in the reduction of cardiac events in the hospital.</p><p><b>CONCLUSION</b>The use of pravastatin 20 mg/d seems better than that of 10 mg/d in all the fields as above in early admission period of UA patients.</p>

Evaluation of early invasive or initially conservative strategies in patients with non-ST-segment elevation acute coronary syndrome at intermediate or high risk / 中华心血管病杂志

<p><b>OBJECTIVE</b>To demonstrate the effect of early strategies and revascularization patterns on in-hospital major adverse cardiac events (MACE) in patients with non-ST-segment elevation acute coronary syndrome (ACS) at intermediate or high risk.</p><p><b>METHODS</b>910 Patients with non-ST-segment elevation ACS at intermediate or high risk were divided into either early invasive (n = 237) or initially conservative (n = 673) group according to whether or when coronary angiography (CAG) was performed after admission (<or= 48 h or > 48 h) in order to demonstrate the impact of early strategies and revascularization patterns on in-hospital MACE events (death, new-onset myocardial infarction or repeat revascularization).</p><p><b>RESULTS</b>Compared with those of the initially conservative group, patients in the early invasive group had a shorter hospital stay and increased rate of MACE (6.3% vs 2.5%, OR 0.384, 95% CI 0.188 - 0.781, P = 0.006) or new-onset myocardial infarction (4.6% vs 0.9%, OR 0.185, 95% CI 0.068 - 0.505, P = 0.001), which was partly due to increased procedures of revascularization (86.9% vs 67.5%, P < 0.001). No differences were found among in-hospital mortality or rate of repeat revascularization between the two groups. During subgroup analysis, patients receiving PCI in the early invasive or initially conservative group had comparable rates of new-onset myocardial infarction, repeat revascularization or MACE events, whereas patients receiving CABG in the early invasive group had a higher rate of new-onset myocardial infarctions than those in the initially conservative group (7.5% vs 1.8%, P = 0.027).</p><p><b>CONCLUSIONS</b>An early invasive strategy in patients with non-ST-segment elevation ACS had comparable in-hospital mortality and higher rate of in-hospital myocardial infarction compared with an initially conservative strategy, an early invasive strategy with PCI seems safe and feasible without increased risk of adverse clinical events. The impact of early CABG on in-hospital adverse events warrants further investigation.</p>