C-reactive protein as a marker for acute coronary syndromes

BACKGROUND: For several years, acute coronary syndromes have been perceivedas causing the most hospital admissions, and even hospital mortality.The syndrome of unstable angina frequently progresses to acutemyocardial infarction but its pathogenesis is poorly understood,and prognosis determination is still problematic. We testedthe hypothesis that measurement of the C-reactive protein inpatients admitted for chest pain could be a marker for acutecoronary syndromes. METHODS AND RESULTS: We studied 110 patients admitted with suspected ischaemic heartdisease, but without elevated serum creatine-kinase levels atthe time of hospital admission. Patients were subsequently dividedinto two groups based on their final diagnosis: group 1 comprisedpatients with unstable angina; group 2 patients with acute myocardialinfarction. We measured the C-reactive protein at the time ofhospital admission. The concentration of C-reactive proteinwas elevated in 59% of the patients with a final diagnosis ofacute myocardial infarction, and in 5% of the patients witha final diagnosis of unstable angina, (P<0·001). CONCLUSION: This study indicates that C-reactive protein levels measuredat the time of admission in patients with suspected ischaemicheart disease could be a marker for acute coronary syndromes,and helpful in identifying patients at high risk for acute myocardialinfarction. Measurement of C-reactive protein may have practicalclinical significance in the management of patients hospitalizedfor suspected acute coronary syndromes.     

Improved long-term prognosis for patients with unstable coronary syndromes 1988-1995.

AIMS: A more aggressive approach to unstable coronary syndromes has developed over the last decade. We set out to examine the long-term outcome among patients with acute coronary syndromes with respect to period of admission since 1988. METHODS: 3918 patients with unstable angina or a non-Q wave myocardial infarction who were admitted to the coronary care unit at Ostra Hospital in the period 1988-1997 were included. Standardized criteria were used to define a non-Q wave myocardial infarction and included fulfilment of the following: (1) typical enzyme changes (serial serum aspartate aminotransferase above 0.7 microkat x l(-1), serial creatine kinase above 3.3 microkat x l(-1) or serial creatine kinaseMB subunit mass concentration above 15 microg x l(-1)), and at least one of the following: (2) chest pain, shock, syncope or pulmonary oedema suggestive of a myocardial infarction, (3) development of electrocardiographic changes with serial ST-T changes without Q waves. The standardized criteria for unstable angina pectoris were fulfilment of at least one of the following: (1) a clear worsening of a previous stable pattern of angina pectoris, (2) chest pain at rest or minimal effort with transient ST-segment elevation or depression on electrocardiogram or elevation of cardiac enzymes not reaching the criteria for myocardial infarction. Information on vital status and cause of death after discharge was collected from the national cause-specific mortality register. RESULTS: Two-year mortality decreased from 30% in 1988 to 19% in 1995 (relative risk per year 0.94 (0.90-0.97), 95% confidence interval). The improvement was consistent regardless of differences in age, prior myocardial infarction, diabetes mellitus, hypertension, development of non-Q wave myocardial infarction, treatment with heparin or thrombolytics or performance of acute coronary angiograms. The cumulative survival at 10 years was 53% in the unstable angina group and 36% in the non-Q wave myocardial infarction group (P<0.0001). CONCLUSION: Against a background of a more aggressive approach to acute coronary syndromes a decrease in long-term mortality is seen between 1988 and 1995.     

Homocysteine predicts adverse clinical outcomes in unstable angina and non-ST elevation myocardial infarction: implications from the folate intervention in non-ST elevation myocardial infarction and unstable angina study

BACKGROUND: Unstable angina and non-ST elevation myocardial infarction (NSTEMI) are common acute coronary events. Homocysteine is a novel risk factor for coronary heart diseases. Together with the conventional risk factors, they may affect the outcome of non-ST coronary events. OBJECTIVE: This study aims to determine the effect of clinical risk factors that are responsible for the occurrence of mortality, and the composite outcome of mortality, nonfatal myocardial infarction and serious rehospitalization within 6 months after the onset of non-ST acute coronary syndromes. METHODS: A total of 124 Filipino patients were interviewed and tested for blood homocysteine levels and lipid profiles. Outcomes were assessed after 6 months. RESULTS: Homocysteinemia (>16 micromol/l) is associated with increased mortality and composite outcomes (mortality, nonfatal reinfarction, and serious rehospitalization), even if adjusted for conventional risk factors. No association was detected for the conventional risk factors. Earlier acute coronary syndrome was found to be positively associated with mortality and the composite outcomes. Early stroke is associated with increased composite outcomes, whereas greater mortality and adverse outcomes were observed in NSTEMI compared with intermediate-risk unstable angina. CONCLUSION: Increased homocysteine level is associated with mortality and serious nonfatal outcomes in patients with unstable angina and NSTEMI.     

Clinical characteristics determining the mode of presentation in patients with acute coronary syndromes

Objectives. The purpose of this study was to examine clinical characteristics of patients with acute coronary syndromes to identify factors that influence the mode of presentation.

Background. In acute coronary syndromes, presentation with myocardial infarction or unstable angina has major prognostic implications, yet clinical factors affecting the mode of presentation are not well defined.

Methods. A prospective cohort study was made of 1,111 patients with acute coronary syndromes. Baseline demographic, clinical and biochemical data were compared in groups with myocardial infarction (n = 633) and unstable angina (n = 478).

Results. The risk of myocardial infarction relative to unstable angina was increased by age >70 years (odds ratio [OR] 2.21; 95% confidence interval [CI] 1.33 to 3.66), male gender (OR 1.56; CI 1.13 to 2.16) and cigarette smoking (OR 1.49; CI 1.09 to 2.03). A rise in admission creatinine from the 10th to the 90th centile of the distribution also increased the odds of myocardial infarction (OR 1.30; CI 1.05 to 1.94). Conversely, the risk of myocardial infarction relative to unstable angina was reduced by previous treatment with aspirin (OR 0.37; CI 0.27 to 0.52), hypertension (OR 0.64; CI 0.47 to 0.86) and previous acute coronary syndromes (OR 0.36; CI 0.26 to 0.51) and revascularization procedures (OR 0.36; CI 0.21 to 0.62).

Conclusions. The clinical presentation of acute coronary syndromes may be influenced by various factors that have the potential to influence the coagulability of the blood, the collateralization of the coronary circulation and myocardial mass. Myocardial infarction is favored by cigarette smoking, advanced age and renal impairment, while unstable angina is favored by treatment with aspirin, hypertension, previous revascularization and previous coronary syndromes.     

Excess triiodothyronine as a risk factor of coronary events

BACKGROUND: Abnormalities in cardiac function, eg, arrhythmias and congestive heart failure, often accompany thyrotoxicosis. A relationship between thyroid hormone excess and the cardiac complications of angina pectoris and myocardial infarction (MI) remains largely speculative. METHODS: The results of thyroid function studies on blood samples drawn from a total of 1049 patients (aged 40 years or older) immediately on emergency medical admission were related to frequencies of angina pectoris and myocardial infarction as determined according to current diagnostic algorithms. After 3 years, those patients who had initially presented with angina pectoris or acute MI were observed for subsequent coronary events; of these (n=185), 98% of the subjects (n=181) could be reevaluated. RESULTS: On hospital admission, the relative rate of angina pectoris and MI was markedly high (odds ratio, 2.6; 95% confidence interval, 1.3-5.2; P=.007) in patients with elevated serum free and total triiodothyronine (T(3)) levels. An initially elevated free T(3) level was a risk factor for subsequent coronary events during the 3-year follow-up (adjusted odds ratio, 4.8; 95% confidence interval, 1.3-17.4; P=.02). CONCLUSIONS: An elevation of serum free T(3) levels at hospital admission is associated with a 2.6-fold greater likelihood of the presence of a coronary event. Moreover, an initially elevated T(3) level is associated with a 3-fold higher risk of developing a subsequent coronary event during the next 3 years. Excess T(3) seemed to be a factor associated with the development and progression of acute myocardial ischemia.     

Acute Coronary Syndromes

Acute coronary syndromes represent a broad spectrum of ischemic myocardial events including unstable angina, non-ST elevation myocardial infarction and acute ST elevation myocardial infarction, which are associated with high morbidity and mortality. They constitute the most frequent cause of hospital admission related to cardiac disease. Early diagnosis and risk stratification are essential for initiation of optimal medical and invasive management. Therapeutic measures comprise aggressive antiplatelet, antithrombotic, and anti-ischemic agents. In addition, patients with high-risk features, notably positive troponin, ST segment changes and diabetes, benefit from an early invasive as compared to a conservative strategy. Importantly, lifestyle interventions, modification of the risk factor profile, and long-term medical treatment are of pivotal importance in reducing the long-term risk of recurrence.     

No long-lasting or intermittent mast cell activation in acute coronary syndromes

BACKGROUND: Unstable coronary syndromes, such as acute myocardial infarction and unstable angina pectoris are mostly due to rupture of an atherosclerotic plaque. Recently mast cells were found to participate actively in the inflammatory process of atherosclerosis by excreting proteolytic and pro-inflammatory substances with the ability to cause plaque instability and rupture. Mast cell activity can be determined by measuring serum levels of tryptase, as has been demonstrated in patients with anaphylaxis and mastcytosis. HYPOTHESIS: Acute coronary events (acute myocardial infarction and unstable angina pectoris) are associated with increased mast cell activity, reflected by elevated serum tryptase levels. METHODS: Serum levels of tryptase were determined in the following three groups of patients: 13 patients with acute myocardial infarction, 10 patients with unstable angina pectoris, and 14 patients without ischaemic cardiovascular disease who were used as controls. Patients with known IgE mediated allergic diseases and/or anti-histaminical drugs were excluded. RESULTS: The groups were comparable for sex, blood pressure, smoking and cholesterol levels. The controls tended to be younger (P=0.05). Levels of tryptase did not differ between patients with acute myocardial infarction (7.9+/-4.6 microg/l), unstable angina pectoris (6.0+/-2.1 microg/l) or controls (6.9+/-4.1 microg/l), nor could a relation with levels of C-reactive protein be demonstrated. CONCLUSION: Serum levels of tryptase are not elevated in patients with acute coronary syndromes. This implies that increased mast cell activity, if any, in unstable coronary syndromes is not reflected systemically. Other, more specific methods will be needed to determine the activity of the mast cell in vivo.     

Prognostic value of fibrinogen in patients admitted with suspected unstable angina and non-q-wave myocardial infarction

INTRODUCTION AND OBJECTIVE: In recent years, the relation between biological markers of inflammation and prognosis in patients suffering from acute coronary syndromes has been investigated. The aim of this study was to evaluate the association between baseline fibrinogen concentrations and the development of clinical events in patients admitted with suspicion of unstable angina and non-Q-wave myocardial infarction. MATERIAL AND METHOD: Levels of fibrinogen at enrollment were analyzed in 325 consecutive patients with acute coronary syndromes. Fibrinogen values were divided into tertiles and the incidence of clinical events was evaluated at each level. The combination of death and/or myocardial infarction was the main endpoint. RESULTS: Fibrinogen levels were significantly higher in patients who subsequently had myocardial infarction, cardiac death, or both during follow up. The probabilities of death and/or myocardial infarction were 6%, 13%, and 29% (p < 0.0001), respectively, in patients grouped by fibrinogen tertiles (304, 305-374 and 375 mg/dl). Multivariate predictors of combined events were age, previous angina, ST-segment depression in the admission ECG, and fibrinogen into tertiles. The adjusted hazard ratio (95% CI) for patients in the upper tertile was 4.8 (1.6-14; p = 0.004). CONCLUSIONS: High fibrinogen levels were related to a less favorable long-term or short-term outcome in patients admitted for suspicion of unstable angina and non-Q-wave myocardial infarction. This association persists after adjustment for other classical risk factors such as age, prior angina, and ST-segment depression in the ECG.     

Acute and convalescent changes in plasma homocysteine concentrations in acute coronary syndromes

BACKGROUND—Raised plasma homocysteine is a risk factor for coronary artery disease. Patients with myocardial infarction or unstable angina show greater activation of coagulation, greater troponin release, and a worse outcome.OBJECTIVE—To examine variations in plasma homocysteine concentration in relation to C reactive protein (CRP) in patients presenting with acute coronary syndromes.METHODS—Consecutive patients presenting with acute myocardial infarction (22) and unstable angina pectoris (12) were studied. Plasma samples were obtained on admission (before clinical intervention), on days 2, 7, and 28, and again six months after admission. Plasma homocysteine, assayed by high performance liquid chromatography, and CRP were both determined at the same time points. Changes were assessed by analysis of variance.RESULTS—CRP concentrations showed a classical rise on day 2, followed by a gradual decline to normal values taken at six months from admission in both myocardial infarction (p < 0.0001) and unstable angina (p = 0.02). Homocysteine concentrations in myocardial infarction (median, 25th to 75th interquartile range) were: 11.9 (10.7 to 12.6), 11.5 (9.1 to 13.4), 12.1 (11.4 to 14.1), 12.4 (11.1 to 14.4), and 12.1 (11.2 to 14.0) µmol/l, for days 1, 2, 7, 28, and 180, respectively (p = 0.02). Significant differences were observed only between day 2 and day 7 (p < 0.05). The final homocysteine measurement was not different from the admission level. Homocysteine concentrations in unstable angina did not differ between admission and convalescence (12.5 (9.1 to 14.5) µmol/l and 12.3 (7.7 to 14.9) µmol/l, respectively).CONCLUSIONS—Plasma homocysteine concentrations are minimally influenced by acute phase variations with reliable measurements obtained on admission in patients with myocardial infarction and unstable angina.     

Clinical outcomes, risk stratification and practice patterns of unstable angina and myocardial infarction without ST elevation: Prospective Registry of Acute Ischaemic Syndromes in the UK (PRAIS-UK)

AIMS: To determine characteristics, outcomes, prognostic indicators and management of patients with acute coronary syndromes without ST elevation. METHODS AND RESULTS: A prospective registry was carried out with follow-up for 6 months after index hospital admission. A history of acute cardiac chest pain was required plus ECG changes consistent with myocardial ischaemia and/or prior evidence of coronary heart disease. Patients with ST elevation or those receiving thrombolytic therapy were excluded. A total of 1046 patients were enrolled from 56 U.K. hospitals. The mean age was 66+/-12 years and 39% were female. The rate of death or non-fatal myocardial infarction at 6 months was 12.2% and of death, new myocardial infarction, refractory angina or re-admission for unstable angina at 6 months was 30%. In a multivariate analysis, patients >70 years had a threefold risk of death or new myocardial infarction compared with those <60 years (P<0.01) and those with ST depression or bundle branch block on the ECG had a five-fold greater risk than those with normal ECG (P<0.001). Aspirin was given to 87% and heparin to 72% of patients in hospital. At 6 months 56% received no lipid-lowering therapy at all. The 6-month rate of coronary angiography was 27% and any revascularization 15%. CONCLUSIONS: In this cohort there was a one in eight chance of death or myocardial infarction, and a one in three chance of death, new myocardial infarction, refractory angina or re-admission for unstable angina, over 6 months. Age and baseline ECG were useful markers of risk. Aspirin, heparin and statins were not given to about one-sixth, one-third and one-half respectively. Rates of angiography and revascularization appear low. A review of treatment strategies of unstable angina and myocardial infarction without ST elevation is warranted in the U.K. to ensure that patients are receiving optimum treatments to reduce mortality and morbidity.     

Prognostic value of quantitative troponin T measurements in unstable angina/non-ST-segment elevation acute myocardial infarction treated early and predominantly with percutaneous coronary intervention

PURPOSE: To evaluate the effect of baseline cardiac troponin T measurements on in-hospital and long-term outcomes in patients with unstable angina/non-ST-segment elevation myocardial infarction who are treated with an early invasive strategy. METHODS: We conducted a prospective cohort study involving 1024 consecutive patients with unstable angina/non-ST-segment elevation myocardial infarction. Patients were stratified according to quantitative troponin T measurements on admission, and underwent coronary angiography and subsequent coronary stenting of the culprit lesion as the primary revascularization strategy within 24 hours. The primary endpoint was all-cause mortality. RESULTS: The risk of in-hospital and long-term mortality increased with absolute levels of troponin T. In-hospital mortality was 0.7% (3/449) in patients with levels <0.010 microg/L, 2.0% (4/197) in those with levels from 0.010 to 0.035 microg/L, 3.2% (6/186) in those with levels from 0.035 to 0.229 microg/L, and 4.7% (9/192) in patients with levels >0.229 microg/L. Cumulative 2-year mortality rates were 2.8%, 8.0%, 10.5%, and 14.8% from the lowest to highest troponin T groups (P <0.001). In contrast, the risk of nonfatal myocardial infarction assumed an inverted U-shaped curve and was lower in the lowest and highest troponin T groups. CONCLUSION: Troponin T remains a strong predictor of mortality, even at low levels, in patients with unstable angina/non-ST-segment elevation myocardial infarction who are treated with early revascularization. The risk associated with elevated levels is linear for death but not for myocardial infarction.     

Serum profiles of matrix metalloproteinases and their tissue inhibitor in patients with acute coronary syndromes. The effects of short-term atorvastatin administration

There is increasing evidence that abnormal cytokine expression and increased metalloproteinase activity are implicated in the pathophysiology of acute coronary syndromes. This study investigates the serum profiles of representative metalloproteinases (MMP-1, -2, -9) and their tissue inhibitor (TIMP-1) in patients with myocardial infarction (MI) and unstable angina (UA) in relation to circulating proinflammatory cytokine (TNF-alpha and IL-6) activity. Furthermore, we examined the effects of a 30-day treatment with atorvastatin on serum levels of these inflammatory factors. Serum concentrations of MMP-1, -2, -9, TIMP-1, IL-6 and TNF-alpha were measured (enzyme-linked immunosorbent assay (ELISA) method) in 23 acute myocardial infarction patients and 20 unstable angina patients on 0 day, 1st, 3rd, 7th and 30th day after admission. Sixteen normal volunteers were used as healthy controls. Additionally, 12 patients of myocardial infarction group and 11 patients of unstable angina group were treated with atorvastatin (20 mg/day) for 30 days in a randomized design. In patients with myocardial infarction and unstable angina, serum levels of MMP-2, -9, TIMP-1, TNF-alpha and IL-6 were significantly higher than those of healthy controls in all time frames (p<0.05). In the group of unstable angina patients, we observed a statistically significant reduction in the levels of MMP-9, TIMP-1 and IL-6 after the 30-day atorvastatin administration. Our results suggest that serum MMPs, TIMP-1 and proinflammatory cytokines play an important role in the pathophysiology of the acute coronary syndromes. The reduction of these factors by short-term atorvastatin administration may provide a new insight into the pleiotropic effects of statins on unstable coronary artery disease.     

Relative contributions of a single-admission 12-lead electrocardiogram and early 24-hour continuous electrocardiographic monitoring for early risk stratification in patients with unstable coronary artery disease

Patients with unstable coronary syndromes are a heterogeneous group with varying degrees of ischemia and prognosis. The present study compares the prognostic value of a standard electrocardiogram (ECG) obtained at admission to the hospital with the information from 24-hour continuous electrocardiographic monitoring obtained immediately after admission. The admission ECGs and 24 hours of vectorcardiographic (VCG) monitoring from 308 patients admitted with unstable coronary artery disease were analyzed centrally regarding standard electrocardiographic ST-T changes, ST-vector magnitude (ST-VM), and ST change vector magnitude episodes. End points were death, acute myocardial infarction, and refractory angina pectoris within a 30-day follow-up period. ST-VM episodes (> or = 50 microV for > or = 1 minute) during VCG monitoring was the only independent predictor of death or acute myocardial infarction by multivariate analysis. ST-VM episodes during vectorcardiography was associated with a relative risk of 12.7 for having a cardiac event, hypertension was associated with a relative risk of 1.7, and ST depression on the admission ECG was associated with a relative risk of 5.7. Patients with ST depression at admission had an event rate (death or acute myocardial infarction) of 17% at 30-day follow-up. Patients without ST depression could further be risk stratified by 24 hours of VCG monitoring into a subgroup with ST-VM episodes at similar (8%) risk and a subgroup without ST-VM episodes at low (1%) risk (p = 0.00005). Continuous VCG monitoring provides important information for evaluating patients with unstable coronary artery disease. It is recommended that patients not initially estimated at high risk based on the admission ECG are referred for 24 hours of VCG monitoring for further risk stratification.     

Anti-human skeletal muscle glycolipid antibodies in unstable angina

BACKGROUND: We studied whether the level of anti-skeletal muscle glycolipid antibodies (AGA), a marker of acute rejection in heart transplantation, may be associated with an adverse prognosis in unstable angina. METHODS AND RESULTS: The in-hospital evolution of 50 patients with unstable angina (Braunwald class III B) was assessed. We determined the incidence of death, myocardial infarction, and refractory angina. Blood was collected at admission and 24 hours later for determination of AGA levels by enzyme-linked immunosorbent assay. Twenty-three patients showed a decrease in the AGA level at 24 hours after admission. Ten in-hospital cardiac events occurred in these patients (43.4%) as compared with 4 (14.8%) in the 27 patients who did not show a decrease (P =.025). In patients with previous myocardial infarction (n = 26), the AGA assay was a powerful predictor of outcome. In this subgroup, 66.6% of patients who had decreased AGA levels (8 of 12) had cardiac events as compared with 14.2% (2 of 14) of those who did not have that decrease (P =.001). CONCLUSIONS: We conclude that a decrease of AGA levels 24 hours after admission is associated with a complicated in-hospital course. This finding may provide new insights in the phenomenon of plaque instability involved in the development of acute coronary syndromes.     

Akute Koronarsyndrome – ein Update Teil I: Pathogenese und medikamentöse Therapie

BACKGROUND: Unstable angina accounts for more than one million hospital admissions annually. 6-8% of patients with this condition have non-fatal myocardial infarction or die within the first year after diagnosis. Recently, the term "acute coronary syndromes" has been used to describe the spectrum of conditions that includes unstable angina, non-Q-wave myocardial infarction (which generally presents without ST-segment elevation), and Q-wave myocardial infarction (which generally presents with ST-segment elevation). PATHOGENESIS: Disruption of a formed plaque is a complex pathologic process that is central to the initiation of the acute coronary syndromes. Local thrombosis occurring after plaque disruption results from complex interactions among the lipid core, smooth-muscle cells, macrophages, and collagen. TREATMENT: Multiple huge clinical trials confirmed that aspirin reduces the risk of death from cardiac causes and fatal and non-fatal myocardial infarction by about 50-70% in patients presenting with unstable angina. Ticlopidine may be substituted for aspirin in patients with hypersensitivity to aspirin or gastrointestinal intolerance. Clopidogrel acts similarly to ticlopidin but has fewer side effects than ticlopidine and has not been reported to cause neutropenia. High-risk patients with refractory unstable angina and elevated troponin levels may have substantial benefit of glycoptotein (GP) IIb/IIIa inhibition. Current practice guidelines support the use of the combination of unfractionated heparin and aspirin for the treatment of unstable angina. Clinical studies have demonstrated that the incidence of the composite end point of death, myocardial infarction, or recurrent angina was lower with enoxaparin than with unfractionated heparin. Beta-blockers, nitrates, and calcium-channel blockers are useful for antiischemic therapy in patients with acute coronary syndromes.     

Early statin therapy in acute coronary syndromes

Patients who survive an acute coronary syndrome of unstable angina or myocardial infarction are at much higher risk of a recurrent event within the following year than patients with stable coronary syndromes. Statin therapy is justified for many of these patients, not only for long-term benefit but also to reduce the risk of recurrent events within weeks of the primary event. The mechanisms that underlie this benefit are probably related to improvements in endothelial function, a decrease in vascular inflammation, and reduced prothrombotic factors. The effects of statins may be mediated by cholesterol reduction, cholesterol-independent effects (particularly decreasing isoprenoids), and mechanisms that are independent of inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase. Observational studies consistently show an early reduction in mortality with statin therapy started before discharge from hospital after an acute coronary syndrome. Several randomized controlled trials also support an early benefit of risk reduction from statins started during the hospital admission for an acute coronary syndrome. Early statin therapy is also related to improved compliance and use of statins several years after a coronary event. Thus, early statin therapy may improve both early and long-term secondary prevention efforts.     

Long-term prognostic value of serial troponin T bedside tests in patients with acute coronary syndromes

The early presence of troponin T in serum strongly predicts short-term mortality and myocardial infarction in patients with acute coronary syndromes. We investigated the long-term outcome of the prognostic significance of the troponin T rapid bedside assay (TROPT) and compared this with the quantitative troponin T assay (cTnT enzyme-linked immunosorbent assay), myoglobin and creatine kinase-MB (CK-MB) mass. One hundred sixty-three patients with chest pain and suspected acute coronary syndromes were studied and followed prospectively for 3 years. Serial blood specimens were obtained at admission and at 3, 6, 12, 24, 48, 72, and 96 hours after admission. Patients were classified as having acute myocardial infarction in 99 patients (61%), unstable angina in 34 patients (21%), and no evidence for acute cardiac ischemia in 30 patients (18%). At 3 years, 28 patients (17%) had died of which 25 deaths (15%) were for cardiac reasons. Twenty-one patients (13%) had a nonfatal (recurrent) myocardial infarction. At admission 29% of the patients were TROPT positive (> or = 0.2 microg/L), another 31% became positive within 12 hours, and 39% remained negative. When adjusted for baseline variables, a positive TROPT (any sample 0 to 12 hours) was independently associated with a higher risk of cardiac mortality (RR 4.3, 95% confidence interval [CI] 1.3 to 14.0). Because troponin T stays elevated up to 2 weeks, later TROPT results between 24 and 96 hours remained significantly predictive for mortality. The cTnT enzyme-linked immunosorbent assay (any sample 0 to 12 hours; cutoff > or = 0.2 microg/L) was similarly predictive (RR 2.9, 95% CI 1.0 to 8.6). Early myoglobin results were significantly prognostic for cardiac mortality up to 12 hours after admission (RR 3.7; 95% CI 1.0 to 12.0). In contrast, serial CK-MB mass measurements were not predictive of mortality. Thus, a combination of a baseline TROPT and an additional TROPT 12 hours or later identifies a subgroup of patients at high risk for subsequent mortality and reinfarction, both at short-term but also at long-term.     

Angiotensin receptor blockers vs. angiotensin converting enzyme inhibitors and acute coronary syndrome outcomes in elderly patients: a population-based cohort study (UMPIRE study results)

Inhibitors of the renin-angiotensin system remain a cornerstone of cardiovascular pharmacotherapy. Although angiotensin converting enzyme inhibitors (ACEIs) have been demonstrated to afford cardiovascular risk reduction in patients with atherosclerosis and preserved left ventricular function, at the present time it is unclear if angiotensin receptor blockers (ARBs) exert similar benefits. We performed a population-based comparative study to compare the rates of hospital admission for acute coronary syndromes between users of ARBs relative to the use of ACEIs. A retrospective cohort study using population-based administrative databases in Ontario, Canada covering over 1.4 million residents age 65 years and older with access to universal healthcare coverage was conducted. We compared the hospital admission for acute coronary syndromes (ACS) among patients initiated on ARBs as compared to propensity-score matched patients started on ACEIs from 1999 through 2002, using a 3:1 (ACEI:ARB) matching strategy. Each individual was observed for up to 2 years. The primary outcome of interest was an ACS event, defined as the composite of hospital admission for myocardial infarction and/or unstable angina. During over 71,000 person-years of follow-up, we observed 1,295 hospitalizations for ACS. Relative to ACEI users (n = 49,037), rate of hospitalizations for ACS was similar in patients initiated on ARBs (n = 16,456) (adjusted relative risk [aRR] 0.89, 95% confidence interval [CI] 0.76-1.04. Pre-specified secondary analysis, performed in patients with atherosclerosis, diabetes, and heart failure, also revealed no difference in rates of myocardial infarction and acute coronary syndromes in users of ARBs compared to ACEIs (adjusted relative risk, diabetes: 0.79, 95% CI 0.58-1.07; heart failure: 0.84, 95% CI 0.59-1.20; atherosclerosis: 0.85, 95% CI 0.70-1.04). These data represent the first and largest population based comparative evaluation of ACEI and ARBs on hospitalizations for ACS among new users of each therapy. Our findings suggest that ARBs offer similar reduction in acute coronary syndrome outcomes in elderly patients with atherosclerosis, diabetes or heart failure. These data have important clinical implications, especially since patients over the age of 65 represent the largest users of risk reduction therapy.     

血清同型半胱氨酸与冠心病的相关性研究

目的探讨冠心病患者血清同型半胱氨酸(homocysteine,Hcy)水平变化的临床意义。方法检测106例冠心病患者和50例健康对照组的血清Hcy的水平。结果冠心病患者血清Hcy水平较健康对照组明显升高(P0.01);稳定型心绞痛、不稳定型心绞痛及急性心肌梗死三组Hcy比较水平依次升高,差异有统计学意义(P0.05)。Hcy水平随着冠状动脉病变支数的增加依次升高,有显著性差异(P0.05)。结论血清Hcy水平变化与冠状动脉病变的严重程度相关,是冠状动脉病变程度的重要危险因素之一。     

Endothelial adhesion molecules ICAM-1, VCAM-1 and E-selectin in patients with acute coronary syndrome

INTRODUCTION AND OBJECTIVES: The acute inflammatory response is an important phenomenon in the pathogenesis of myocardial damage during acute coronary syndrome. Endothelial dysfunction has been found in unstable angina and acute myocardial infarction, although the results are controversial. The purpose of this study was to determine the levels of the soluble endothelial adhesion molecules ICAM-1, VCAM-1 and E-selectin, in patients with unstable angina and acute myocardial infarction, compare the results in both groups, and analyze their relation with the degree of myocardial injury. METHODS: Serum concentrations of ICAM-1, VCAM-1, and E-selectin were measured in 37 control subjects and 43 patients (32 with acute myocardial infarction and 11 with unstable angina). Measurements were made at the time of admission and ten days later using commercial enzyme-linked immunoabsorbent assay (ELISA) kits (R&D Systems, UK). RESULTS: There was a significant increase in E-selectin (p < 0.05) in patients with unstable angina at admission and ten days later. In contrast, patients with acute myocardial infarction showed no significant differences in E-selectin compared with the control group at admission or ten days later. A significant increase in VCAM-1 levels was demonstrated in both groups of patients and ICAM-1 levels in acute myocardial infarction, but the concentrations of VCAM-1 and ICAM-1 in both groups of patients at admission and ten days later did not differ significantly. There was no relation between soluble endothelial adhesion molecule levels and the severity of myocardial damage estimated by cardiac enzymes or electrocardiographic changes. CONCLUSION: This study indicates that serum levels of E-selectin, measured at time of admission and ten days later, could be a marker for unstable angina and might be useful in the differential diagnosis with myocardial infarction.