Home  About us  Contact
 

Infarction Patients (infarction + patient)

Distribution by Scientific Domains
Medical Sciences84%
Life Sciences15%
Distribution within Medical Sciences
General & Internal Medicine27%
Cardiovascular Disease17%

Kinds of Infarction Patients

  • acute myocardial infarction patient
    		•
  • myocardial infarction patient
    		•

    Selected Abstracts

    Percutaneous Coronary Intervention, Comorbidities, and Mortality among Emergency Department,Admitted ST-Elevation Myocardial Infarction Patients in Florida

    JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 3 2010
    ELIZABETH BARNETT PATHAK Ph.D., F.A.H.A., M.S.P.H.
    Background: Risk of mortality following an ST-elevation myocardial infarction (STEMI) can be significantly reduced by prompt percutaneous coronary intervention (PCI). National guidelines specify primary PCI as the preferred recommended treatment for STEMI. In this study, we examined same-day PCI as an independent predictor of in-hospital mortality, after adjustment for comorbidities, other patient factors, and hospital PCI-volume using unselected surveillance data from Florida. Methods: We analyzed hospital discharge data for adults, 18+ years old, with a primary diagnosis of STEMI who were admitted to PCI-capable hospitals through the emergency department during 2001,2005 (n = 43,849). Hierarchical (multilevel) logistic regression models were used for analysis. Results: Overall, 4,143 STEMI patients (9.4%) did not survive to hospital discharge. In late 2005, the in-hospital mortality rates were 1.9% for those who received same-day PCI versus 13.0% for those who did not. After adjustment for multiple patient factors, same-day PCI was a significant predictor of in-hospital survival with a strong protective effect (adjusted OR = 0.35, 95% CI 0.31,0.38 P < 0.0001). Restriction of the analysis to those patients who survived the first day of admission did not appreciably change this result (adjust OR = 0.37, 95% CI 0.33,0.42, P < 0.0001). Hospital PCI-volume did not significantly impact mortality risk. Conclusions: Same-day PCI markedly reduced the risk of in-hospital mortality among STEMI patients after multivariate adjustment. Serious comorbidities and complications, older age, and female gender continued to predict elevated risk of mortality after control for treatment status. Our results provide additional evidence in support of national clinical recommendations and aggressive treatment of STEMI. (J Interven Cardiol 2010;23:205,215) [source]

    Impact of an Audit Program and Other Factors on Door-to-balloon Times in Acute ST-elevation Myocardial Infarction Patients Destined for Primary Coronary Intervention

    ACADEMIC EMERGENCY MEDICINE, Issue 4 2009
    Chao-Lun Lai MD
    Abstract Objectives:, This before,after study investigated the association between an audit program and door-to-balloon times in patients with acute ST-elevation myocardial infarction (STEMI) and explored other factors associated with the door-to-balloon time. Methods:, An audit program that collected time data for essential time intervals in acute STEMI was developed with data feedback to both the Department of Emergency Medicine and the Department of Cardiology. The door-to-balloon times for 76 consecutive acute STEMI patients were collected from February 16, 2007, through October 31, 2007, after the implementation of the audit program, as the intervention group. The control group was defined by 104 consecutive acute STEMI patients presenting from April 1, 2006, through February 15, 2007, before the audit was applied. A multivariate linear regression model was used for analysis of factors associated with the door-to-balloon time. Results:, The geometric mean 95% CI of the door-to-balloon time decreased from 164.9 (150.3, 180.9) minutes to 141.9 (127.4, 158.2) minutes (p = 0.039) in the intervention phase. The median door-to-balloon time was 147.5 minutes in the control group and 136.0 minutes in the intervention group (p = 0.09). In the multivariate regression model, the audit program was associated with a shortening of the door-to-balloon time by 35.5 minutes (160.4 minutes vs. 195.9 minutes, p = 0.004); female gender was associated with a mean delay of 58.4 minutes (208.9 minutes vs. 150.5 minutes; p = 0.001); posterolateral wall infarction was associated with a mean delay of 70.5 minutes compared to anterior wall infarction (215.4 minutes vs. 144.9 minutes; p = 0.037) and a mean delay of 69.5 minutes compared to inferior wall infarction (215.4 minutes vs. 145.9 minutes; p = 0.044). The use of a glycoprotein IIb/IIIa inhibitor was associated with a 46.1 minutes mean shortening of door-to-balloon time (155.7 minutes vs. 201.8 minutes; p < 0.001). Conclusions:, The implementation of an audit program was associated with a significant reduction in door-to-balloon times among patients with acute STEMI. In addition, female patients, posterolateral wall infarction territory, and nonuse of glycoprotein IIb/IIIa inhibitor were associated with longer door-to-balloon times. [source]

    Hospital Costs and Revenue Are Similar for Resuscitated Out-of-hospital Cardiac Arrest and ST-segment Acute Myocardial Infarction Patients

    ACADEMIC EMERGENCY MEDICINE, Issue 6 2010
    Robert Swor DO
    Abstract Objectives:, Care provided to patients who survive to hospital admission after out-of-hospital cardiac arrest (OOHCA) is sometimes viewed as expensive and a poor use of hospital resources. The objective was to describe financial parameters of care for patients resuscitated from OOHCA. Methods:, This was a retrospective review of OOHCA patients admitted to one academic teaching hospital from January 2004 to October 2007. Demographic data, length of stay (LOS), and discharge disposition were obtained for all patients. Financial parameters of patient care including total cost, net revenue, and operating margin were calculated by hospital cost accounting and reported as median and interquartile range (IQR). Groups were dichotomized by survival to discharge for subgroup analysis. To provide a reference group for context, similar financial data were obtained for ST-segment elevation myocardial infarction (STEMI) patients admitted during the same time period, reported with medians and IQRs. Results:, During the study period, there were 72 admitted OOCHA patients and 404 STEMI patients. OOCHA and STEMI groups were similar for age, sex, and insurance type. Overall, 27 (38.6%) OOHCA patients survived to hospital discharge. Median LOS for OOHCA patients was 4 days (IQR = 1,8 days), with most of those hospitalized for ,4 days (n = 34, 81.0% dying or discharged to hospice care). Median net revenue ($17,334 [IQR $7,015,$37,516] vs. $16,466 [IQR = $14,304,$23,678], p = 0.64) and operating margin ($7,019 [IQR = $1,875,$15,997] vs. $7,098 [IQR = $3,767,$11,138], p = 0.83) for all OOHCA patients were not different from STEMI patients. Net income for OOCHA patients was not different than for STEMI patients (,$322 vs. $114, p = 0.72). Conclusions:, Financial parameters for OOHCA patients are similar to those of STEMI patients. Financial issues should not be a negative incentive to providing care for these patients. ACADEMIC EMERGENCY MEDICINE 2010; 17:612,616 © 2010 by the Society for Academic Emergency Medicine [source]

    Prehospital Electrocardiograms (ECGs) Do Not Improve the Process of Emergency Department Care in Hospitals with Higher Usage of ECGs in Non,ST-segment Elevation Myocardial Infarction Patients

    CLINICAL CARDIOLOGY, Issue 12 2009
    Michael T. Cudnik
    Background This article will describe the impact of prehospital electrocardiogram (ECG) use on emergency department (ED) processes of care for non,ST-segment elevation myocardial infarction (NSTEMI) patients and assess the characteristics associated with prehospital ECG use. Methods This is a retrospective, multicenter, observational analysis of NSTEMI patients captured by the National Cardiovascular Data Registry-Acute Coronary Treatment and Intervention Outcomes Network Registry,Get with the Guidelines (NCDR ACTION-GWTG) in 2007. Patient and hospital data were stratified by documentation of a prehospital ECG (pECG). Hospitals were stratified into tertiles of pECG use by higher pECG (>5.6%, n 91), lower pECG (, 5.6%, n = 83), or no pECG (n = 100). Statistical evaluation was done via Wilcoxon rank sum and ,2 tests. Results There were 21 251 patients eligible for analysis. A pECG was documented in 1609 (7.6%) patients. Of 274 hospitals, 100 (36.5%) had no pECGs recorded. Median ED length of stay (LOS) was shorter at no pECG hospitals vs lower pECG hospitals (3.97 h vs 4.12 h, P < 0.05), but not higher pECG hospitals vs no pECG hospitals (3.85 h vs 3.97 h, P = not significant [NS]). A pECG was not associated with an improvement in ED performance metrics (use of aspirin, ,-blocker, any heparin) in the higher pECG hospitals vs no pECG hospitals or the lower pECG hospitals vs no pECG hospitals. Conclusions Use of prehospital ECG in NSTEMI patients is uncommon. In contrast to its impact on reperfusion times in ST-segment elevation myocardial infarction (STEMI) patients, its use does not appear to be associated with an improvement in ED processes of care at the hospital level. Copyright © 2009 Wiley Periodicals, Inc. [source]

    Cardiac hypertrophy and failure: lessons learned from genetically engineered mice

    ACTA PHYSIOLOGICA, Issue 1 2001
    Y. Takeishi
    Congestive heart failure is a major and growing public health problem. Because of improved survival of myocardial infarction patients produced by thrombolytic therapy or per-cutaneous revascularization it represents the only form of cardiovascular disease with significantly increased incidence and prevalence. Clinicians view this clinical syndrome as the final common pathway of diverse pathologies such as myocardial infarction and haemodynamic overload. Insights into mechanisms for heart failure historically derived from physiological and biochemical studies which identified compensatory adaptations for the haemodynamic burden associated with the pathological condition including utilization of the Frank Starling mechanism, augmentation of muscle mass, and neurohormonal activation to increase contractility. Therapy has largely been phenomenological and designed to prevent or limit the deleterious effects of these compensatory processes. More recently insights from molecular and cell biology have contributed to a more mechanistic understanding of potential causes of cardiac hypertrophy and failure. Many different analytical approaches have been employed for this purpose. These include the use of conventional animal models which permit serial observation of the onset and progression of heart failure and a sequential analysis of underlying biochemical and molecular events. Neonatal murine cardiomyocytes have been a powerful tool to examine in vitro subcellular mechanisms devoid of the confounding functional effects of multicellular preparations and heterogeneity of cell type. Finally, significant progress has been made by utilizing tissue from human cardiomyopathic hearts explanted at the time of orthotopic transplantation. Each of these methods has significant advantages and disadvantages. Arguably the greatest advance in our understanding of cardiac hypertrophy and failure over the past decade has been the exploitation of genetically engineered mice as biological reagents to study in vivo the effects of alterations in the murine genome. The power of this approach, in principle, derives from the ability to precisely overexpress or ablate a gene of interest and examine the phenotypic consequences in a cardiac specific post-natal manner. In contrast to conventional animal models of human disease which employ some form of environmental stress, genetic engineering involves a signal known molecular perturbation which produces the phenotype. [source]

    Quantitative assessment of human serum high-abundance protein depletion

    ELECTROPHORESIS, Issue 21 2008
    Rene Stempfer
    Abstract The aim of this study is to quantify the effectivity of the depletion of human high-abundance serum and plasma proteins for improved protein identification and disease marker candidate discovery and to assess the risk of concomitant removal of relevant marker proteins. 2-DE and bottom-up shotgun MS combining 2-D capillary chromatography with MS/MS were applied in parallel for the analysis of fractions resulting from the depletion procedure. For many proteins the factors of enrichment by the depletion were obvious allowing their enhanced detection and identification upon high-abundance protein depletion. Nano-liquid chromatography linked MS allowed the efficient identification of several low-abundant proteins that were not identified on the 2-DE gels. Resolving the fractions that were eluted from the matrix upon depletion indicated unspecific binding of disease relevant proteins in plasma samples from acute myocardial infarction patients. The unspecific binding to the depletion matrix of inflammatory markers spiked into the serum was found to depend on the type of capturing agent used. Polyclonal avian antibodies (IgY) displayed the least unspecific binding due to the high immunogenicity of mammalian proteins in avian hosts. [source]

    Plasma urocortin in acute myocardial infarction patients

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2010
    Arintaya Phrommintikul
    Eur J Clin Invest 2010; 40 (10): 874,882 Abstract Background, Despite its proposed cardioprotective effect, the role of plasma urocortin in acute myocardial infarction (AMI) remains unknown. We investigated plasma profile of urocortin in AMI patients and evaluated its long-term prognostic performance. Material and methods, Sixty-six AMI patients and 21 healthy subjects were included in this study. Blood samples for urocortin were collected on days 0 (onset), 1, 3 and 5 and at 3 and 6 months. Primary endpoint was mortality within 1 year of follow-up. Secondary endpoint was combined death and nonfatal adverse cardiac events (i.e. myocardial reinfarction, urgent revascularization or hospitalization due to heart failure) within 1 year. Results, During follow-up at 1 year, 38 (57·6%) patients were alive without cardiac events, nine (13·6%) had nonfatal cardiac events and 17 (25·8%) died. Plasma urocortin in AMI patients were increased on days 0, 1, 3 and 5 (P < 0·05 vs. control). The receiver-operating characteristic curve showed an area under curve (AUC) of day 0 urocortin to be 0·750 with 95% confidence interval (CI) of 0·619,0·881 (P = 0·004), whereas AUC of NT-proBNP was 0·857 (95% CI, 0·722,0·992; P = 0·003). Sensitivity values for predicting the mortality of urocortin NT-proBNP and a combined urocortin and NT-proBNP were 0·81 (95% CI, 0·54,0·95), 0·86 (95% CI, 0·42,0·99) and 1·0 (95% CI, 0·56,1·0), respectively. Conclusions, Plasma urocortin level is elevated in AMI patients for 5 days from onset. High plasma urocortin within 24 h after the onset is associated with increased mortality. Combined urocortin and NT-proBNP enhance prognostic performance in AMI patients. [source]

    Atorvastatin therapy improves exercise oxygen uptake kinetics in post-myocardial infarction patients

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2007
    M. Guazzi
    Abstract Background Statins represent a modern mainstay of the drug treatment of coronary artery disease and acute coronary syndromes. Reduced aerobic work performance and slowed VO2 kinetics are established features of the clinical picture of post-myocardial infarction (MI) patients. We tested the hypothesis that statin therapy improves VO2 exercise performance in normocholesterolaemic post-MI patients. Materials and methods, According to a double-blinded, randomized, crossover and placebo-controlled study design, in 18 patients with uncomplicated recent (3 days) MI we investigated the effects of atorvastatin (20 mg day,1) on gas exchange kinetics by calculating VO2 effective time constant (tau) during a 50-watt constant workload exercise, brachial artery flow-mediated dilatation (FMD) as an index of endothelial function, left ventricular function (echocardiography) and C-reactive protein (CRP, as an index of inflammation). Atorvastatin or placebo was given for 3 months each. Results, Atorvastatin therapy significantly improved exercise VO2 tau and FMD, and reduced CRP levels. We did not observe changes in cardiac contractile function and relaxation properties during all study periods in either group. Conclusions, In post-MI patients exercise performance is a potential additional target of benefits related to statin therapy. Endothelial function improvement is very likely implicated in this newly described therapeutic property. [source]

    Risk adjusted resource utilization for AMI patients treated in Japanese hospitals

    HEALTH ECONOMICS, Issue 4 2007
    Edward Evans
    Abstract Though risk adjustment is necessary in order to make equitable comparisons of resource utilization in the treatment of acute myocardial infarction patients, there is little in the literature that can be practically applied without access to clinical records or specialized registries. The aim of this study is to show that effective models of resource utilization can be developed based on administrative data, and to demonstrate a practical application of the same models by comparing the risk-adjusted performance of the hospitals in our dataset. The study sample included 1748 AMI cases discharged from 10 large, private teaching hospitals in Japan, between 10 April 2001 and 30 June 2004. Explanatory variables included procedures (CABG and PCI), length of stay, outcome, patient demographics, diagnosis and comorbidity status. Multiple linear regression models constructed for the study were able to account for 66.5, 27.7, and 58.4% of observed variation in total charges, length of stay and charges per day, respectively. The performance of models constructed for this study was comparable to or better than performance reported by other studies that made use of explanatory variables extracted from clinical data. The use of administrative data in risk adjustment makes broad scale application of risk adjustment feasible. Copyright © 2006 John Wiley & Sons, Ltd. [source]

    A search for cyclophilin-A gene (PPIA) variation and its contribution to the risk of atherosclerosis and myocardial infarction

    INTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 2 2008
    M. Palacín
    Summary Cyclophilin A is secreted by vascular smooth muscle cells in response to inflammatory stimuli, and could thus contribute to atherosclerosis. We hypothesized that the genetic variation at the cyclophilin A gene (PPIA) could affect the risk for developing atherosclerosis and myocardial infarction. This study included 250 myocardial infarction patients (all male and < 60 years; 95% are smokers). All these cases had at least one atherosclerotic diseased coronary vessel. DNA was obtained from patients and from 250 healthy controls. The variation at the PPIA gene was determined in the patients through single-strand conformation analysis and direct sequencing of seven polymerase chain reaction fragments. Allele and genotype frequencies were compared between patients and controls. The effect of a promoter polymorphism (,11 G/C) on gene expression was in vitro analysed with luciferase-reporter assays. We found two common polymorphisms in the PPIA promoter (,11 G/C) and the 5, non-translated (+36 G/A) regions. Cells transfected with luciferase-plasmids containing the ,11 G had significantly higher luciferase activity. Genotype frequencies for these polymorphisms did not differ between patients and controls. In conclusion, we reported a functional variant in the PPIA promoter. However, the PPIA variation did not significantly contribute to the risk of suffering from myocardial infarction among patients with atherosclerotic diseased vessels. [source]

    Does a telephone follow-up intervention for patients discharged with acute myocardial infarction have long-term effects on health-related quality of life?

    JOURNAL OF CLINICAL NURSING, Issue 9 2009
    A randomised controlled trial
    Aims., An earlier combined proactive and reactive telephone follow-up intervention for acute myocardial infarction patients after discharge from hospital showed positive effects after six months. The aim of the present study was to assess whether the intervention has long-term effects up to 18 months after discharge. Design., A prospective randomised controlled trial with 18 months follow-up. Method., The trial was conducted with 288 patients allocated to a telephone follow-up intervention group (n = 156) or control group (n = 132). The primary endpoint was health-related quality of life using the SF-36. Secondary endpoints included smoking and exercise habits, return to work and rehospitalisation due to chest pain. Results., There were significant improvements over time on most dimensions of health-related quality of life in both the intervention and control group to US norm population levels on most SF-36 dimensions and summary scores. The intervention group showed no overall significant improvement beyond six months in the physical or mental summary scores, but there was a significant effect for those aged 70 or above. Although there was a promising effect for rehospitalisation due to chest pain, no significant differences were found between the groups on the secondary endpoints after six months. Conclusion., This study demonstrated that despite positive short-term effects at six months, the telephone follow-up intervention had no long-term effects on health-related quality of life or secondary endpoints. However, the potential for improvement beyond six months was less than anticipated reflecting a reduced morbidity among acute myocardial infarction patients. Relevance to clinical practice., Telephone follow-up after discharge from hospital is an easy implementable follow-up intervention enabling individualised provision of information and support in a time often experienced as stressful by patients. Our study indicates that six months is an adequate support period. Despite positive results six months after discharge no significant added long-term effects of telephone follow-up, compared to usual care were found in this study. [source]

    Left atrioventricular plane displacement determined by echocardiography: a clinically useful, independent predictor of mortality in patients with stable coronary artery disease

    JOURNAL OF INTERNAL MEDICINE, Issue 5 2003
    E. Rydberg
    Abstract. Rydberg E, Erhardt L, Brand B, Willenheimer R (Malmö University Hospital, University of Lund, Malmö, Sweden). Left atrioventricular plane displacement determined by echocardiography: a clinically useful, independent predictor of mortality in patients with stable coronary artery disease. J Intern Med 2003; 254: 479,485. Background. Echocardiographically determined left atrioventricular plane displacement (AVPD) is strongly related to prognosis in patients with chronic heart failure and in postmyocardial infarction patients. We aimed at exploring whether AVPD, unlike ejection fraction, is related to mortality in patients with stable coronary artery disease (CAD). Methods and results. Atrioventricular plane displacement was assessed by two dimensionally guided M-mode echocardiography in the four and two chamber views, in 333 consecutive patients with stable CAD and an abnormal coronary angiogram. Patients were followed up for an average of 41 months. AVPD was lower in patients who died (n = 30, 9.0 %) compared with survivors (9.0 ± 2.2 vs. 11.5 ± 2.1 mm, P < 0.0001). Amongst patients with prior myocardial infarction (n = 184) AVPD was 8.7 ± 2.3 mm in those who died (n = 17) and 11.2 ± 2.3 mm in the survivors (P < 0.0001). In patients without prior myocardial infarction (n = 149), AVPD was 9.4 ± 2.1 (n = 13) and 11.8 ± 1.8 mm, respectively (P < 0.0001). Age, AVPD and four other echocardiographical variables correlated significantly with prognosis in univariate logistic regression analysis. In multiple logistic regression analysis only AVPD (P < 0.0001) correlated independently with mortality. Conclusion. Echocardiographically determined AVPDis a clinically useful, independent prognostic tool in patients with stable CAD. The presence of a documented previous myocardial infarction does not influence this observation. [source]

    Co-localization of von Willebrand factor with platelet thrombi, tissue factor and platelets with fibrin, and consistent presence of inflammatory cells in coronary thrombi obtained by an aspiration device from patients with acute myocardial infarction

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 1 2006
    Y. HOSHIBA
    Summary.,Background:,Detailed histochemical analysis of coronary thrombi obtained freshly from acute phase of myocardial infarction patients may provide information necessary to understand the mechanism of coronary occlusive thrombus formation. Methods and Results:,Coronary thrombi causing myocardial infarction were obtained from 10 consecutive patients of myocardial infarction in the acute phase, using a newly developed aspiration catheter. All the fixed specimens of coronary thrombi, by hematoxylin and eosin staining, were found to contain three major constituents, namely, platelets, densely packed fibrin and inflammatory cells, including polymorphonuclear and mononuclear cells, although their distribution in each specimen is totally heterogeneous. Immunohistochemical staining revealed the prominent presence of von Willebrand factor (VWF) at the sites of platelet accumulation, presence of tissue factor and platelets at the sites of deposition of fibrin fibrils. It also revealed the presence of CD16-, CD45- and CD34-positive cells, yet the functional roles of these cells have still to be elucidated. There are weak positive correlation between the number of inflammatory cells involved in the unit area of coronary thrombi specimen and the time of collection of the specimens after the onset of chest pain. Conclusions:,In spite of various limitations, our results contain information suggesting the possible role of VWF in platelet-thrombus formation, possible important role played by tissue factor and activated platelets in the formation of fibrin fibrils, and the positive relationship between inflammatory cells migration and the formation of occlusive thrombi in human coronary arteries. [source]