First precision mass measurements of refractory fission fragments.

Atomic masses of 95-100Sr, 98-105Zr, and [corrected] 102-110Mo and have been measured with a precision of 10 keV employing a Penning trap setup at the IGISOL facility. Masses of 104,105Zr and 109,110Mo are measured for the first time. Our improved results indicate significant deviations from the previously published values deduced from beta end point measurements. The most neutron-rich studied isotopes are found to be significantly less bound (1 MeV) compared to the 2003 atomic mass evaluation. A strong correlation between nuclear deformation and the binding energy is observed in the two-neutron separation energy in all studied isotope chains.

Exclusive measurement of quasifree proton-neutron bremsstrahlung.

Data on proton-neutron bremsstrahlung have been obtained from a measurement of the quasifree breakup channel in proton-deuteron bremsstrahlung. This high-precision measurement, with an incident proton energy of 190 MeV, is fully exclusive; i.e., the protons, the neutron, and the photon have been detected. The quasifree differential cross sections obtained are compared with microscopic calculations and calculations based on soft-photon models. There are sizable differences between the models and also between the models and the data obtained for this simple process.

Chronology of particle emission from the E/A=61 MeV 36Ar+27Al reaction.

The emission time chronology of neutrons, protons, and deuterons from the E/A=61 MeV 36Ar+27Al reaction is deduced from two-particle correlation functions.

Strong predictive value of TIMI risk score analysis for in-hospital and long-term survival of patients with right ventricular infarction.

BACKGROUND: While right ventricular myocardial infarction is associated with increased in-hospital morbidity and mortality, prognostic risk factors for in-hospital and long-term mortality are poorly defined. OBJECTIVES: To evaluate the prognostic value of TIMI (Thrombolysis in Myocardial Infarction) risk score analysis in patients with right ventricular myocardial infarction (RVI). DESIGN: Retrospective analysis of a community population. SETTING: Mayo Clinic Coronary Care Unit. PATIENTS: One hundred and two patients with RVI from 580 consecutive patients from Rochester, Minnesota admitted to the Coronary Care Unit with acute inferior or lateral wall myocardial infarction from January 1988 through March 1998. MEASUREMENT: Combined TIMI risk score analysis with in-hospital and long-term mortality. RESULTS: In-hospital morbidity (RVI: 54.9% vs non-RVI: 22.2%; P<0.001) and mortality (RVI: 21.6% vs non-RVI: 6.9%;P <0.001) were increased in patients with RVI. The TIMI risk score predicted risk (per one point increase in TIMI score) for in-hospital mortality (OR 1.23, 95% CI 1.02-1.51, P=0.037) and long-term mortality (OR 1.57, 95% CI 1.25-1.96, P<0.001). Patients with RVI whose TIMI risk score was >or=4 had significantly worse long-term survival compared to those patients with RVI and TIMI score <4 (P=0.006). CONCLUSIONS: In-hospital morbidity and mortality, and long-term mortality are increased by right ventricular infarction and can be accurately predicted by the initial TIMI risk score.

Matrix protein and another viral component contribute to induction of apoptosis in cells infected with vesicular stomatitis virus.

The induction of apoptosis in host cells is a prominent cytopathic effect of vesicular stomatitis virus (VSV) infection. The viral matrix (M) protein is responsible for several important cytopathic effects, including the inhibition of host gene expression and the induction of cell rounding in VSV-infected cells. This raises the question of whether M protein is also involved in the induction of apoptosis. HeLa or BHK cells were transfected with M mRNA to determine whether M protein induces apoptosis when expressed in the absence of other viral components. Expression of M protein induced apoptotic morphological changes and activated caspase-3 in both cell types, indicating that M protein induces apoptosis in the absence of other viral components. An M protein containing a point mutation that renders it defective in the inhibition of host gene expression (M51R mutation) activated little, if any, caspase-3, while a deletion mutant lacking amino acids 4 to 21 that is defective in the virus assembly function but fully functional in the inhibition of host gene expression was as effective as wild-type (wt) M protein in activating caspase-3. To determine whether M protein influences the induction of apoptosis in the context of a virus infection, the M51R M protein mutation was incorporated onto a wt background by using a recombinant infectious cDNA clone (rM51R-M virus). The timing of the induction of apoptosis by rM51R-M virus was compared to that by the corresponding recombinant wt (rwt) virus and to that by tsO82 virus, the mutant virus in which the M51R mutation was originally identified. In HeLa cells, rwt virus induced apoptosis faster than did rM51R-M virus, demonstrating a role for M protein in the induction of apoptosis. In contrast to the results obtained with HeLa cells, rwt virus induced apoptosis more slowly than did rM51R-M virus in BHK cells. This indicates that a viral component other than M protein contributes to induction of apoptosis in BHK cells and that wt M protein acts to delay induction of apoptosis by the other viral component. tsO82 virus induced apoptosis more rapidly than did rM51R-M virus in both HeLa and BHK cells. These two viruses contain the same point mutation in their M proteins, suggesting that sequence differences in genes other than that for M protein affect their rates of induction of apoptosis.

Impact of community-based education on health care evaluation in patients with acute chest pain syndromes: the Wabasha Heart Attack Team (WHAT) project.

BACKGROUND: Community education programmes focused on raising public awareness of the symptomatology of acute coronary syndromes have had mixed results. OBJECTIVES: The Wabasha Heart Attack Team project, a unique multidisciplinary public education effort in Minnesota, sought to educate area citizens about signs and symptoms of acute myocardial infarction (MI). METHODS: After an intensive 1-month education period, we compared presentations for emergency evaluation of chest pain during the study period with baseline data from the same seasonal period of the preceding year. RESULTS: Visits to the Emergency Room for symptomatic heart disease increased significantly during the study period (56 patients versus 46 patients during the baseline period), as did the percentage of patients presenting with acute MI (18% versus 12%, P < 0.05). Use of emergency medical services for pre-hospital evaluation was significantly increased (41% versus 27%, P < 0.05). CONCLUSION: A community education campaign can significantly increase use of pre-hospital emergency medical service resources and may increase the number of patients presenting with acute chest pain symptoms, including MI.

T-cell immunity in acute coronary syndromes.

Acute coronary syndromes (ACS) are complications of atherosclerotic vascular disease that are triggered by the sudden rupture of an atheroma. Atherosclerotic plaque stability is determined by multiple factors, of which immune and inflammatory pathways are critical. Unstable plaque is characterized by an infiltrate of T cells and macrophages, thereby resembling a delayed hypersensitivity reaction. On activation, T cells secrete cytokines that regulate the activity of macrophages, or the T cells may differentiate into effector cells with tissue-damaging potential. Constitutive stimulation of T cells and macrophages in ACS is not limited to the vascular lesion but also involves peripheral immune cells, suggesting fundamental abnormalities in homeostatic mechanisms that control the assembly, turnover, and diversity of the immune system as a whole. This review gives particular attention to the emergence of a specialized T-cell subset, natural killer T cells, in patients with ACS. Natural killer T cells have proinflammatory properties and the capability of directly contributing to vascular injury.

Early coronary angiography improves long-term survival in unstable angina.

BACKGROUND: The role of early coronary angiography in the evaluation of patients with unstable angina has been controversial. This study was designed to determine the effect of early coronary angiography on long-term survival in patients with unstable angina. METHODS: We reviewed the Olmsted County Acute Chest Pain Database, a population-based epidemiologic registry that includes all patients residing within Olmsted County who were seen for emergency department evaluation of acute chest pain from 1985 to 1992. Patients with symptoms consistent with myocardial ischemia qualifying as unstable angina were classified as undergoing early (

Obesity is associated with premature occurrence of acute myocardial infarction.

BACKGROUND: The American Heart Association has classified obesity as a major modifiable risk factor for coronary artery disease, but its relationship with age at presentation with acute myocardial infarction (AMI) is poorly documented. HYPOTHESIS: The study was undertaken to evaluate the impact of obesity on age at presentation, and on in-hospital morbidity and mortality in patients with AMI. METHODS: Our analysis includes a consecutive series of 906 Olmsted County patients (mean age 67.7 years, 51% male) admitted with AMI to the Mayo Clinic Coronary Care Unit (CCU). The patients were entered into the Mayo CCU Database, a prospective registry of data pertaining to patients admitted to the Mayo Clinic CCU with AMI. Age at AMI occurrence and in-hospital morbidity and mortality were noted. RESULTS: Obese patients (body mass index [BMI] >30) with AMI were significantly younger than patients with AMI in the overweight (BMI 25-30) and normal-weight (BMI < 30) groups (62.3+/-13.1 vs. 66.9+/-13.2 and 72.9+/-13.4, respectively. p < 0.001). Obesity and overweight status were associated with male gender, diabetes mellitus, hypercholesterolemia, and smoking history; however, after multivariate adjustment for these risk factors, excess weight and premature AMI remained significantly associated. Compared with normal-weight patients, overweight patients presenting with AMI were 3.6 years younger (p < 0.001, confidence interval [CI] 1.9-5.4) and obese patients 8.2 years younger (p < 0.001, Cl 6.2-10.1). No significant increase in in-hospital morbidity and mortality was seen. CONCLUSION: In this population-based study, overweight and obese status are independently associated with the premature occurrence of AMI, but not with an increased incidence of in-hospital complications.

An anti-CD11/CD18 monoclonal antibody in patients with acute myocardial infarction having percutaneous transluminal coronary angioplasty (the FESTIVAL study).

Maximal benefits of coronary reperfusion after acute myocardial infarction (AMI) with ST-segment elevation may be attenuated by neutrophil-mediated reperfusion injury. Inflammatory mediators released from potentially viable myocytes cause activation of neutrophils, which traverse the endothelium and enter the myocardium. This process involves interaction between the neutrophil-expressed CD11/CD18 and endothelial-expressed intercellular adhesion molecule-1 (ICAM-1). Preclinical studies have shown that monoclonal antibodies (MAb) to CD18 can limit infarct size and preserve left ventricular function. We sought to determine the initial clinical safety and tolerability of Hu23F2G (LeukArrest), a humanized MAb to CD11/CD18, in patients with AMI who underwent percutaneous transluminal coronary angioplasty (PTCA). Sixty patients with AMI were randomized to low- (0.3 mg/kg) or high-dose (1.0 mg/kg) Hu23F2G or to placebo immediately before PTCA. We found no clinically significant differences in vital signs, physical examination, laboratory evaluation, or need for subsequent cardiac interventions. In Hu23F2G treatment groups, serum concentration of Hu23F2G increased rapidly to 3,234 +/- 1,298 microg/L (low-dose group) and 15,558 +/- 4409 microg/L (high-dose group) between 5 and 60 minutes, then declined over 72 hours to near-baseline values. Myocardial single-photon emission computed tomographic imaging 120 to 260 hours after PTCA showed no statistically significant differences in final left ventricular defect size. Hu23F2G was well tolerated, with no increase in adverse events, including infections. Thus, Hu23F2G appears safe and well tolerated in patients undergoing PTCA for AMI.

Comparison of two aspirin doses on ischemic stroke in post-myocardial infarction patients in the warfarin (Coumadin) Aspirin Reinfarction Study (CARS).

The Coumadin Aspirin Reinfarction Study demonstrated that combination treatment with fixed dose warfarin (1 or 3 mg) + aspirin 80 mg was not superior to aspirin 160 mg alone after myocardial infarction for reducing nonfatal reinfarction, nonfatal stroke, and cardiovascular death. In this analysis, we examined the importance of aspirin dose in the protection against the secondary end point of ischemic stroke. The comparison arms for this analysis were warfarin 1 mg + aspirin 80 mg versus aspirin 160 mg. In the Coumadin Aspirin Reinfarction Study, 2,028 patients were randomized to aspirin 80 mg plus warfarin 1 mg, and 3,393 were randomized to aspirin 160 mg alone. A predictive model for ischemic stroke was developed using the Cox proportional-hazards model. A reduced Cox proportional-hazards model was developed to test for the effect of aspirin dose on ischemic stroke in predefined subgroups. The incidence of ischemic stroke was lower in patients treated with aspirin 160 mg than in patients treated with aspirin 80 mg + warfarin 1 mg (0.6% vs 1.1%; p = 0.0534). Age, previous stroke or transient ischemic attack, and aspirin dose were independent predictors of ischemic stroke. In addition, the highest risk patients, those with Q-wave myocardial infarction and male patients, appeared to receive greater benefit from aspirin 160 mg than from aspirin 80 mg + warfarin 1 mg. The results of this secondary analysis suggest that aspirin 160 mg is more effective than aspirin 80 mg + warfarin 1 mg in preventing ischemic stroke in post-myocardial infarction patients.

Length of stay in myocardial infarction.

OBJECTIVE: We evaluated the association between length of hospital stay (LOS) and clinical factors, treatment intensity, and use of percutaneous coronary revascularization from 1988 to 1997. BACKGROUND: Multiple factors contribute to the observed reduction in LOS for patients with myocardial infarction. METHODS: We studied a series of 849 consecutive patients admitted with acute myocardial infarction to the Mayo Clinic Coronary Care Unit within three time periods: period I (1988-1990), period II (1991-1993), and period III (1994-1997). RESULTS: Median LOS decreased significantly between 1988 and 1997 (9 days to 5 days, 36% reduction, p < 0.0001), with significant reductions (p < 0.001) associated with certain therapies: primary reperfusion (6 days vs 7 days), b-blockers (6 days vs 8 days), and aspirin (6 days vs 8 days). Hospitalizations were lengthened by coronary artery bypass grafting (12 vs 6 days) and by serious complications (10 vs 6 days). The era of the admission (period I vs II vs III) is a significant, powerful predictor of LOS, even after adjustment for other key variables. CONCLUSION: The 36% reduction in LOS for acute myocardial infarction between 1988 and 1997 is related both to therapeutic modalities and temporal trends. Further study is needed to clarify whether the trend for decreasing LOS persists and influences outcome and health care quality variables.

Initiation of hormone replacement therapy after acute myocardial infarction is associated with more cardiac events during follow-up.

OBJECTIVES: This study explored the association between the initiation of hormone replacement therapy (HRT) and early cardiac events (<1 year) in women with a recent myocardial infarction (MI). BACKGROUND: Observational studies have linked postmenopausal hormone use with a reduced risk of death from heart disease. However, a recent randomized trial of HRT found no long-term benefit, primarily due to an increase in cardiac events in the first year. METHODS: The Coumadin Aspirin Reinfarction Study (CARS) database contains information on HRT use and menopausal status for women with a recent MI. We classified the 1,857 postmenopausal women in CARS as prior/current HRT users if they took HRT before enrollment, new users if they began HRT during the study period or never users. We assessed the incidence of cardiac events (death, MI, unstable angina [UA]) during follow-up. RESULTS: In our cohort, 28% (n = 524) used HRT at some point. Of these, 21% (n = 111) began HRT after their MI. New users had a higher incidence of death/MI/UA (41% vs. 28%, p = 0.001) during follow-up than never users, largely due to a higher incidence of UA (39% vs. 20%, p = 0.001). After adjustment, new users still had a significantly higher risk of death/MI/UA than never users during follow-up (relative risk [RR] = 1.44 [1.05-1.99]). Prior/current users had no excess risk of the composite end point after adjustment. Users of estrogen/progestin had a lower incidence of death/MI/UA during follow-up than users of estrogen only (RR = 0.56 [0.37-0.85]). CONCLUSIONS: Postmenopausal women who initiated HRT after a recent MI had an increased risk of cardiac events largely due to excess UA during follow-up.

Bundle branch block as a predictor of long-term survival after acute myocardial infarction.

Using a community-based population of patients with acute myocardial infarction (AMI), we sought to: (1) determine the prevalence of bundle branch block (BBB) on the presenting electrocardiogram (ECG), (2) compare the clinical characteristics and the treatment administered to patients with and without BBB, and (3) determine the association of BBB with mortality. We analyzed the admission ECGs of 894 consecutive patients with AMI from Olmsted County, Minnesota, seen at our institution from January 1988 to March 1998. Of these, 53 had left BBB (LBBB) (5.9%) and 60 had right BBB (RBBB) (6.7%). Patients with BBB were more likely to be older, have a history of AMI or hypertension, and to be in Killip class >I at presentation. They were less likely to receive primary reperfusion therapy, beta blockers, or heparin, but more likely to receive angiotensin-converting enzyme inhibitors. They had lower mean predischarge ejection fractions (38 +/- 16% vs 50 +/- 15%, p <0.0001). In-hospital mortality was 13.3%, 17.0%, and 9.1% for patients with RBBB, LBBB, and no BBB, respectively (p = 0.11). Respective postdischarge survival at 1, 3, and 5 years was 80%, 60%, and 50% in the RBBB group, 78%, 56%, and 51% in the LBBB group, and 92%, 85%, and 76% in the group without BBB (p <0.0001). Although BBB was not an independent predictor of mortality on multivariate analysis, the presence of transient or persistent BBB with AMI is an easily recognized clinical marker of increased mortality. Our conclusion from this study is that in a community-based population, patients who had LBBB or RBBB at the time of AMI had lower predischarge ejection fractions and higher in-hospital and long-term unadjusted mortality.

Characteristics of presenting electrocardiograms of acute myocardial infarction from a community-based population predict short- and long-term mortality.

To investigate the relevance of presenting electrocardiographic (ECG) patterns to short- and long-term mortality in nonreferral patients with acute myocardial infarction (AMI), 6 ECG patterns were analyzed. A consecutive series of 907 patients from Olmsted County, Minnesota, admitted to the Mayo Clinic Cardiac Care Unit from January 1, 1988 to March 31, 1998 for acute myocardial infarction comprised the study population. ECG patterns and distribution in the population were: (1) ST elevation alone (20.8%), (2) ST elevation with ST depression (35.2%), (3) normal or nondiagnostic electrocardiograms (18.5%), (4) ST depression alone (11.8%), (5) T-wave inversion only (10.7%), and (6) new left bundle branch block (LBBB) (3.0%). Seven- and 28-day mortalities varied significantly (p <0.01) among the 6 ECG groups. Respective mortalities were 3.0% and 6.0% for patients with normal or nondiagnostic electrocardiograms, 3.1% and 5.2% for T-wave inversion only, 7.4% and 10.6% for ST elevation alone, 9.4% and 13.1% for ST depression alone, 10.3% and 13.8% for ST elevation with ST depression, and 18.5% and 22.2% for new LBBB. Length of hospital stay (LOS) also varied among the ECG pattern groups (p <0.001) with the longest average LOS being in the new LBBB group (12.5 days). Long-term survival was similar among 5 ECG pattern groups (45% to 55% at 8 years from discharge) with the exception of LBBB (20% at 8 years). Among non-LBBB groups, ST-segment depression with or without ST elevation was associated with increased short-term mortality. Also, in this community-based population, 18.5% of patients had normal or nondiagnostic electrocardiograms.

Effect of concomitant or very early statin administration on in-hospital mortality and reinfarction in patients with acute myocardial infarction.

In a retrospective analysis, 66 patients identified as having received a statin drug within 24 hours of admission for acute myocardial infarction were matched 3:1 with a control group of 198 patients not treated with a statin agent. End points of in-hospital mortality and in-hospital reinfarction were significantly lower in the statin-treated group, pointing to a benefit from very early statin treatment in acute myocardial infarction.

Molecular fingerprint of interferon-gamma signaling in unstable angina.

BACKGROUND: Activation of circulating monocytes in patients with acute coronary syndromes may reflect exposure to bacterial products or stimulation by cytokines such as IFN-gamma. IFN-gamma induces phosphorylation and nuclear translocation of transcription factor STAT-1, which initiates a specific program of gene induction. To explore whether monocyte activation is IFN-gamma driven, patients with unstable (UA) or stable angina (SA) were compared for nuclear translocation of STAT-1 complexes and upregulation of IFN-gamma-inducible genes CD64 and IP-10. METHODS AND RESULTS: Peripheral blood mononuclear cells were stained for expression of CD64 on CD14(+) monocytes and analyzed by PCR for transcription of IP-10. Expression of CD64 was significantly increased in patients with UA. Monocytes from UA patients remained responsive to IFN-gamma in vitro, with accelerated transcriptional competency of CD64. IP-10-specific sequences were spontaneously detectable in 82% of the UA patients and 15% of SA patients (P<0.001). Most importantly, STAT-1 complexes were found in nuclear extracts prepared from freshly isolated monocytes of patients with UA, which provides compelling evidence for IFN-gamma signaling in vivo. CONCLUSIONS: Monocytes from UA patients exhibit a molecular fingerprint of recent IFN-gamma triggering, such as nuclear translocation of STAT-1 complexes and upregulation of IFN-gamma-inducible genes CD64 and IP-10, which suggests that monocytes are activated, at least in part, by IFN-gamma. IFN-gamma may derive from stimulated T lymphocytes, which implicates specific immune responses in the pathogenesis of acute coronary syndromes.

Nonsteroidal antiinflammatory drug-induced mucosal lesions of the upper gastrointestinal tract and their relationship to Helicobacter pylori.

The aim of the present study was to determine the prevalence of Helicobacter pylori infection in a group of patients hospitalized at the clinic of rheumatology who presented peptic ulcers and erosions associated with nonsteroidal antiinflammatory drugs (NSAIDs). Of a group of 4,256 hospitalized patients receiving therapy with NSAIDs, 221 patients with persistent dyspepsia underwent endoscopic examination of the upper segment of the gastrointestinal tract. Among them, mucosal abnormalities in the stomach and duodenum were confirmed in 69 patients. H. pylori was found in 42% (29/69) of the examined patients. Peptic ulcers were confirmed in 19 patients. Localization was gastric in 12 patients and duodenal in seven. H. pylori was found in only 17% of the patients (2/12) with gastric ulcers, but in as many as 86% (6/7) of those with duodenal ulcers. Patients with H. pylori taking NSAIDs were at higher risk of developing duodenal mucosal abnormalities, both ulcers (OR: 10.17; 95% CI: 1.08-23.88, p = 0.013) and erosions (OR: 2.67; 95 CI: 1.94-3.66, p = 0.001). Concomitant administration of corticoids and NSAIDs did not increase the risk of gastrotoxicity in patients with positive finding of H. pylori (OR: 0.32; 95% CI: 0.1-0.96). In conclusion, a close association was found between H. pylori infection and duodenal ulcers and erosions, but not between gastric ulcers and gastric erosions in a group of patients hospitalized for rheumatic diseases and undergoing NSAID therapy.

Intercessory prayer and cardiovascular disease progression in a coronary care unit population: a randomized controlled trial.

OBJECTIVE: To determine the effect of intercessory prayer, a widely practiced complementary therapy, on cardiovascular disease progression after hospital discharge. PATIENTS AND METHODS: In this randomized controlled trial conducted between 1997 and 1999, a total of 799 coronary care unit patients were randomized at hospital discharge to the intercessory prayer group or to the control group. Intercessory prayer, ie, prayer by 1 or more persons on behalf of another, was administered at least once a week for 26 weeks by 5 intercessors per patient. The primary end point after 26 weeks was any of the following: death, cardiac arrest, rehospitalization for cardiovascular disease, coronary revascularization, or an emergency department visit for cardiovascular disease. Patients were divided into a high-risk group based on the presence of any of 5 risk factors (age = or >70 years, diabetes mellitus, prior myocardial infarction, cerebrovascular disease, or peripheral vascular disease) or a low-risk group (absence of risk factors) for subsequent primary events. RESULTS: At 26 weeks, a primary end point had occurred in 25.6% of the intercessory prayer group and 29.3% of the control group (odds ratio [OR], 0.83 [95% confidence interval (CI), 0.60-1.14]; P=.25). Among high-risk patients, 31.0% in the prayer group vs 33.3% in the control group (OR, 0.90 [95% CI, 0.60-1.34]; P=.60) experienced a primary end point. Among low-risk patients, a primary end point occurred in 17.0% in the prayer group vs 24.1% in the control group (OR, 0.65 [95% CI, 0.20-1.36]; P=.12). CONCLUSIONS: As delivered in this study, intercessory prayer had no significant effect on medical outcomes after hospitalization in a coronary care unit.