2008 Vol. 5, No. 4
Background and Objective Overt gastrointestinal bleeding (GIB) is one of the noncardiac complications in patients with acute myocardial infarction (AMI). Identification of patients at increased risk of overt GIB could aid in targeting more aggressive treatment, and lead to improved outcomes. The aim of this study is to determine the frequency, risk factors, and prognostic significance of overt GIB in patients with AMI. Methods A retrospective review of the medical records of 1443 patients admitted to the Chinese PLA General Hospital with AMI was conducted. Charts were reviewed for clinical characteristics, possible precipitating factors and complications. Patients were categorized as having or not having overt GIB(GIB associated with hemodynamic changes or the need for transfusions). Results Twenty nine (2.0%) patients developed overt GIB within 30 days after AMI. Patients with overt GIB had higher 30-day mortality rate than those without (44.8% vs. 9.9%, P < 0.001). Multivariate logistic regression analysis showed major determinants of in-hospital overt GIB secondary to AMI were gender of female (odds ratio 2.41, 95% confidence interval [CI] 1.08 to 5.37), age=75 years (odds ratio 1.58, 95% CI 1.13 to 2.20), prior history of AMI (odds ratio 2.28, 95% CI 1.17 to 4.88), pneumonia (odds ratio 3.47, 95% CI 1.50 to 8.03) and anemia at admission (odds ratio 2.37, 95% CI 1.04 to 5.37). Conclusions In patients with AMI, overt GIB is associated with higher in-hospital mortality, and female sex, older age, prior AMI, pneumonia and anemia at admission are predictors of overt GIB during hospitalization.
Objective Multiple organ dysfunction syndrome (MODS) is one of the leading causes of death in ICU patients. However, there have been few studies on the role of MODS as a cause of death in patients with acute myocardial infarction (AMI), particularly in those at advanced age. Our study aimed to investigate the incidence and to identify the predicting factors of MODS in elderly patients with AMI. Methods We identified consecutive patients with AMI who were discharged from the Chinese PLAGeneral Hospital between January 1993 to June 2006. Medical records of 800 consecutive patients aged 60 years or over were analyzed retrospectively. Multivariate logistic regression was used to determine factors predicting in-hospital development of MODS. Results Twenty-seven (3.4%) patients developed MODS within 30 days after AMI. Compared with patients without MODS, patients with MODS had higher in-hospital mortality rates (55.6% vs 11.6%, P<0.001) and more frequent complications of cardiogenic shock (25.9% vs 6.2%, P<0.001), heart failure (HF) (59.3% vs 18.2%, P<0.001), cardiac arrhythmia (44.4% vs 26.4%, P<0.05) and pneumonia (55.6% vs 16.3%, P<0.001). Multivariate logistic regression analysis showed the major predictors for the occurrence of MODS secondary to AMI were advanced age (≥75 years, odds ratio 2.64, 95% confidence interval [CI] 1.13 to 6.61), heart rate≥100 bpm on admission (odds ratio 1.74, [CI] 1.14 to 2.64), in-hospital complication of HF (odds ratio 3.03, [CI] 1.26 to 7.26) and pneumonia (odds ratio 2.82, [CI] 1.18 to 6.77). Conclusions MODS is not the uncommon complication in elderly patients with AMI and is associated with poor prognosis. Advanced age, heart failure and pneumonia are predictors of the development of MODS in patients with AMI.
Background and Objective Percutaneous coronary intervention (PCI) is becoming a common practice in the treatment of patients with coronary heart disease (CHD) of all age. Depression is considered to be a risk factor for the development of CHD and deteriorates the outcome after cardiac rehabilitation efforts. The aim of our study was to evaluate the presence of clinically relevant anxiety and depression in patients before and after PCI. Additionally we evaluated their relationship to age because of the increasing number of elderly patients undergoing PCI. Methods One hundred and twelve consecutive patients in three Sanatoria for Retired Cadres in Beijing who underwent PCI were asked to fill in the Hospital Anxiety and Depression Scale (HADS) to measure depression and anxiety scores two days before and ten days after PCI. Differences between these pre- and post-surgical scores were then calculated as means for changes, and the amount of elevated scores was appraised. In order to investigate the relationship between age and anxiety and depression, respectively, Spearman correlations between age and the difference scores were calculated. In addition, ANOVA procedures with the factor “age group” and McNemar tests were calculated. Results 25.8% of the patients were clinically depressed before and 17.5% after PCI; 34.0% of the patients were clinically anxious before and 24.7% after PCI. This overall change is not significant. We found a significant negative correlation between age and the difference between the two time points for anxiety (Spearman rho = -.218, P = 0.03), but not for depression (Spearman rho = -.128, P = 0.21). ANOVA and McNemar tests revealed that anxiety scores and the number of patients high in anxiety declined statistically meaningful only in the youngest patient group. Such a relationship could not be found for depression. Conclusions Our data show a relationship between age and anxiety. Younger patients are more anxious before PCI than older ones and show a decline in symptoms while elderly patients show hardly any change.
Background and Objective The atherosclerotic plaque vulnerability may be related to inflammation, immunity, metabolism and blood clotting. One of the key factors affecting plaque stability is inflammatory reaction. This study was to investigate the relationship between vulnerability of coronary artery plaque evaluated with coronary angiography (CAG), intravascular ultrasound (IVUS) and the levels of plasma inflammatory markers. Methods Fifty-eight consecutive patients with acute coronary syndrome who had coronary lesion of a single vessel were divided into 3 groups based on angiographic morphology of the lesions: type I lesion group (n =16), type II lesion group (n =25) and type III lesion group (n =17). The control group consisted of 17 patients with stable angina. Plasma levels of high sensitivity C reaction protein (hs-CRP), matrix metalloproteinase (MMP, including MMP-2 and MMP-9), CD40 ligand (CD40L) and pregnancy associated plasma protein-A (PAPP-A) were measured by ELISA. Asubgroup of 28 patients (including 18 ACS patients and 10 stable angina control patients) who underwent IVUS study, were analyzed. Results The plasma levels of MMP-2, MMP-9 and PAPP-A in type II lesion group were significantly higher than those in other groups (all P<0.05). In type II lesion group, linear correlation analyses showed significant positive correlation between levels of hs-CRP andMMP-2 (r=0.508); MMP-2 and MMP-9, CD40L, PAPP-A (r=0.647, 0.704 and 0.751, respectively); MMP-9 and CD40L, PAPP-A (r=0.491 and 0.639, respectively); CD40L and PAPP-A (r=0.896). IVUS subgroup analysis showed that the area of plaques and plaque burden in culprit lesion, the incidence of high-risk plaques, remodeling index (RI) and positive remodeling percentage in ACS patients were significantly greater than those in control subgroup (P=0.000, 0.037, 0.028, 0.015 and 0.040, respectively). Compared with control subgroup, the plasma levels of hs-CRP, MMP-2, MMP-9 and PAPP-A were markedly elevated (P=0.033, 0.000, 0.000 and 0.027, respectively). Conclusions CAG and IVUS combined with study on plasma levels of inflammation mediators are helpful in judging the vulnerability of coronary artery plaques.
Objectives To compare the clinical effects of intravenously and orally administered aspirin in the treatment for acute coronary syndrome (ACS), and to evaluate the adverse effects of intravenous administration of aspirin. Methods One hundred and twentyfive patients with unstable angina pectoris or acute myocardial infarction were randomized into three groups: group 1 received intravenous aspirin (300mg/d, n =40), while groups 2 (n =42) and 3 (n =43) received orally administered aspirin (100mg/d and 300mg/d, respectively). The control group included 30 patients with no heart disease or blood disease, and they had never taken aspirin and clopidogrel. Blood samples were taken at 2nd and 7th day of hospitalization. Platelet aggregation and the level of platelet activation marker CD62p were measured and compared among the groups. Patients were followed up for 6 months for the occurrence of major adverse cardiovascular events. Results There were no statistically significant differences in the decrease in adenosine diphosphate (ADP)-induced platelet aggregation rate (12.01± 10.45%, 6.76± 14.62% and 9.73± 16.72%for group 1, group2 and group 3, respectively), the decrease in arachidonic acid (AA)-induced platelet aggregation rate (6.73± 11.34%, 6.95± 12.45% and 7.57 ± 13.11%, respectively), and the decrease in CD62p level (10.89± 18.62%, 8.92± 11.57% and 7.05± 15.67% , respectively). At six months, there were 4 deaths (10%) in group 1, 4 deaths (9.5%) in group 2 and 5 deaths (11.6%) in group 3 (P>0.05). Conclusions Intravenous administration of aspirin provides a new approach as an anti-platelet treatment for ACS patients, especially those who can not tolerate oral administration of aspirin.
Objective The paper aims to determine whether the inflammation, a powerful risk factor that has been demonstrated for the development of coronary artery disease, plays a role in no-reflow phenomenon in patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI). Methods We prospectively analyzed 656 patients with AMI after primary PCI. Based on post-PCI angiography data, patients were divided into two groups: the no-reflow group (TIMI=2, n =60) and the reflow group (TIMI=3, n =596). Results Our results showed that the inflammatory factors including leukocyte count (×109/L) (10.90±4.04 vs. 9.12±2.98 P =0.002), hs-CRP (5.04±0.71 vs. 4.70±0.75 P =0.001) and other factor platelet count (×109/L) (210.96±33.42 vs. 196.41±46.06 P =0.033) in no-reflow group are significantly higher than those in reflow group, major adverse cardiac events happened in the patients with no-reflow are higher than in reflow patients no matter in hospital or at the end of follow-up.We also found the left ventricular ejection fraction (LVEF) dramatically decreased (58.65±9.34 vs. 51.29±11.38, P<0.001) and left ventricular end-diastolic dimension (LVEDD) significantly increased (49.94±6.75 mm vs. 54.66±6.68mm, P<0.001) in no-reflow patients at the end of followup. Conclusions Our results suggest that inflammation factors function in no-reflow phenomenon, and no-reflow is a serious complication after primary PCI which predicts poor left ventricular systolic functional recovery and mortality in patients with AMI.
Background and Objective Although coronary heart disease (CHD) and stroke share important risk factors, some associations differ between these two components of cardiovascular diseases. The objective of this study was to compare vascular risk factor profiles and in-hospital outcomes in acute stroke (AS) and acute myocardial infarction (AMI) patients. Methods We evaluated 383 consecutive patients who were admitted to the 94th Hospital of Chinese PLA and the Third Hospital of Nanchang with diagnoses of AS (ischemic stroke or intracerebral hemorrhage; n = 310) or AMI (n = 73) during a 2-year period. The frequency of risk factors and inhospitalmortality rates were assessed in both groups. Results AS patients were significantly older than AMI patients ( 68.9 ± 9.1 years vs. 62.8 ± 11.7 years; P < 0.01). AMI was significantly more common than AS in patients younger than 65 years; 51% of this group had AMI and 26% had AS (P < 0.001). Hypertension was more common in AS patients than in AMI patients (69% vs. 58%; P = 0.042). Patients who died did not differ significantly in age between the groups. In-hospital mortality rates were significantly higher in AS than AMI cases (31% vs. 12%, P < 0.001 for all patients; 37% vs.5%, P < 0.001 for men). Women hospitalized for AMI were more likely to die in hospital than men (28% vs. 5%; P = 0.002). Conclusions Patients with stroke and with AMI differ in their risk factor profile. Age at the time of presentation was a significant differentiating factor between patients with AS and AMI. We observed significantly higher in-hospital mortality for patients with AS (when adjusted for age) than for patients with AMI.
Objective To investigate the relationship between severity of cerebrovascular atherosclerosis stenosis and that of coronary atherosclerosis stenosis. Methods Cerebral angiography and coronary angiography were performed in 34 patients who had coronary disease with cerebral ischemia. Patients were divided into 3 subgroups according to the degree of stenosis on angiography, concomitant diseases, risk factors and biochemical data. Results The follow-up study showed that the incidence of cardiac and cerebrovascular death increased significantly in patients with moderate to severe stenosis of coronary and cerebral arteries; the severity of stenosis in the coronary artery parallels that in the solitary carotid artery, or dual carotid and vertebral arteries. Conclusions Patients with coronary and cerebral artery stenosis, especially those with multi-risk factors, such as hypertension, diabetes and cigarette smoking, should receive intensive treatment to reduce cardiac and cerebrovascular events.
Background Our previous studies have suggested that angiopoietin-related protein 2 (Arp2) may improve rat cardiac function after acute myocardial infarction (AMI) by accelerating angiogenesis. We want to study the efficacy of the adenoviral vector-mediated gene transfer of Arp2 (Ad.Arp2) in inducing angiogenesis and in improving the myocardial perfusion and function in a porcine acute myocardial ischemic model. Methods The minipigs underwent ligation of the proximal circumflex coronary artery (LCx) and were randomly assigned to treatment with Ad.Arp2, adenoviral vectors with no transgene (Ad.Null) or PBS. Four weeks later, the animals were evaluated using echocardiography, cardiac perfusion imaging and pathologic observation. Results Four weeks after treatment, the Arp2 protein was revealed in the myocardium of Ad.Arp2 animals, but was not found in the Ad.Null or PBS animals. Also, a significant revival of myocardial perfusion was found in the ischemic area in Ad.Arp2-treated animals, whose global and regional myocardial function was greatly improved. The quantitation of new capillaries was much greater in the Ad.Arp2 group than in the Ad. Null or PBS groups. Conclusion Treatment with Ad.ARP2 offers the obvious advantage of greatly improving the blood supply and the heart function.
Backgroud and objective Plaque rupture, platelet aggregation, and thrombogenesis are the main mechanisms of acute coronary syndrome (ACS), and inflammation factors play key roles in plaque unstability. Psychological stress promotes acute inflammatory response, leading to increased circulating levels of C-reactive protein (CRP), IL-6, and serum intercellular adhesion molecule (sICAM)-1. But it is not clear that whether psychological stress has a direct effect on atherosclerotic plaque stability. The purpose of this study was to investigate effects of chronic psychological stress on inflammatory marker (ICAM-1) in atherosclerotic plaque, and inflammatory markers in peripheral blood. Materials and methods Sixty male rabbits were randomized into 2 groups: the control group (n =10) and the atherosclerotic group (n =50). The latter were fed on high fatty diet and were given a large dose of vitamin D3 (3 600 000IU/kg) via intraperitoneal injection. After 8 weeks, the atherosclerotic model was estaslished. Then the 50 atherosclerotic model rabbits were divided into 3 subgroups: no-stress subgroup (n =16), physiological stress subgroup (n =16) and psychological stress subgroup (n =18). In physiological stress subgroup and psychological stress subgroup, drinking was cut from twice a day to once a day. At the same time, psychological stress subgroup was given empty bottle stress, and this process lasted for 2 weeks. One hour after the last stress, the blood samples were collected and the serum levels of CRP, IL-6 amd ICAM-1 were tested by radioimmunoassay or enzyme linked immunosorbent assay. The aorta and heart were extracted for pathology examination, and the express of ICAM-1 was tested by immunohistochemical examination. Results (1) After effective atherosclerotic animal model construction, the expression of ICAM-1 in aorta was higher in atherosclerotic group than that in control group (P<0.01), and was notably higher in psychological stress subgroup than that in no-stress subgroup or in physiological stress subgroup (2.18±0.17 vs 1.58±0.22, 1.22±0.15, P<0.001, respectively). The expression in physiological stress subgroup was higher than that in no-stress subgroup (58±0.22 vs 1.22±0.15, P=0.001). (2) The serum level of IL-6 (51.80±4.60 pg/ml vs 27.60±4.19 pg/ml,8.01±1.39 pg/ml,7.83±1.37 pg/ml), sICAM-1(1.24±0.25 vs 0.85±0.09, 0.62±0.17, 0.57±0.11), CRP (1.00±0.37 vs 0.90±0.29,1.01±0.22, 0.71±0.13) in psychological stress group were significantly higher than that in other groups (All P<0.05). There was a positive relationship between the serum level of CRP, IL-6 and ICAM-1 and the expression of ICAM-1 in aorta wall ( r =0.59, r =0.75, r =0.87, P<0.01, respectively). Conclusions Psychological stress induces an increased expression of ICAM-1 in aortic atherosclerotic plaque, a higher serum level of CRP, IL-6, and sICAM-1 expression. Psychologial stress has a direct effect on the transition from stability to unstability through in-plaque and outplaque inflammation. The serum level of CRP, IL-6 and ICAM-1 can reflex the inflammatory degree in atherosclerotic plaque.
Objective To investigate the effect of sea anemone toxin anthopleurin-Q (AP-Q) on potassium currents in isolated rats and guinea pig ventricular myocytes. Methods The ventricular cells of guinea pigs and SD rats were obtained by enzymatic dissociation method. Whole cell patch clamp technique was used to record potassium currents (Ito, IK, and IK1). Results AP-Q 3-100 nmol/L increased Ito in a concentration-dependent manner, with an EC50 value of 12.7 nmol/L. At a potential of +50mV, AP-Q 10nmol/L increased Ito from (13.3±3.4) pA pF-1 to (19.46±4.3) pA pF-1. AP-Q 0.1-100 nmol/L increased IK and IK tail in a concentrationdependent manner with EC50 values of 4.7 nmol/L and 5.0 nmol/L, respectively. AP-Q 1 pmol/L-100 nmol/L increased IK1 in dosedependent manner, with an EC50 of 0.2 nmol/L. Conclusions The effect of AP-Q on Ito, IK and IK1 may partly explain its mechanism in shortening APD and increasing RP.
Objective To explore the protective effects of trimetazidine on vascular endothelial cells injury induced by hydrogen peroxide (H2O2) and its pharmacological mechanisms of anti-oxidation. Methods Human umbilical vein endothelial cells (HUVECs) were injured by H2O2. Next, the cells were treated with three different concentrations of trimetazidine (1μmol/L,10μmol/L,100μmol/L, respectively). The viability of cells was detected by methyl thiazoeyl tetrazolium (MTT) assay. In addition, malondialdehyde (MDA) contents, superoxide dismutase (SOD) and secretion of NO were measured. Results Trimetazidine could enhance the viability of the injured HUVECs induced by oxidation, decrease the level of MDA, enhance the SOD activity, and increase the secretion of nitrogen monoxide. These effects were in a certain dose-dependent manner and the difference was significant among the three concentrations (P<0.05). Conclusions Our results suggest that trimetazidine may protect lipid peroxidation and prevent oxidation-induced cellular dysfunction of HUVECs.
Both acute myocardial infarction (MI) and acute ischemic stroke are leading causes of death and disability in our world—the former in mostAmerican and European countries and the latter in many of Asian countries.1 Although these common acute vascular disorders share some similarities, there are important differences regarding pathophysiology, diagnostic evaluation, and management. The differences between acuteMI and acute ischemic stroke are manifold, and imply different prevention and treatment strategies. Given that the paradoxical differences in incidence density of coronary heart disease (CHD) and stroke between different populations has long been known, and the great burden placed by these disorders on human being, one may wonder at the paucity of literature to compare them. In this issue of the Journal of Geriatric Cardiology, we publish two articles2,3 addressing the similarity and differences of CHD and stroke to highlight this important question in medicine. Wei et al.3 performed cerebral angiography and coronary angiography in 34 patients who had both coronary and cerebral ischemia related symptoms and found significant correlation between the severity of these two vascular beds; Yu and Wu2 analyzed data of patients admitted to their hospitals because of either acute stroke or acute MI, and they found that acute stroke patients were significantly older than acute MI patients while hypertension was more common in acute stroke patients than in acuteMI patients.