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At least 343 records · Page 19Linked to original sources
PubMed2003

Serum myoglobin/carbonic anhydrase III ratio as a marker of reperfusion after myocardial infarction.

BACKGROUND: Coronary patency is important for short- and long-term outcome after myocardial infarction. Serum myoglobin concentration is a sensitive marker of myocardial damage and its specificity can be improved by simultaneous measurement of carbonic anhydrase III, a skeletal muscle marker. In the present study we evaluated the role of myoglobin/carbonic anhydrase III ratio as a non-invasive marker of reperfusion. METHODS: We measured myoglobin, carbonic anhydrase III and creatine kinase MB-fraction release serially in 29 patients with acute myocardial infarction treated with thrombolysis and in 28 patients treated with primary coronary angioplasty. RESULTS: Thrombolytic therapy was followed by a 9.1+/-2.2-fold increase in myoglobin and 10.8+/-3.3-fold increase in creatine kinase MB-fraction during the first hour of treatment, while carbonic anhydrase III remained unchanged. The peak value of myoglobin/carbonic anhydrase III ratio was found at 2 h and that of creatine kinase MB-fraction at 8 h after thrombolysis. Knowledge of the reperfusion time point during primary angioplasty and follow-up of cardiac markers revealed that cut-off points of 3 and 10 h for the peak values of myoglobin/carbonic anhydrase III ratio and creatine kinase MB-fraction can be used as indicators for reperfusion, respectively. Myoglobin/carbonic anhydrase III ratio measured before treatment and at 2 and 4 h after the onset of treatment screened 23 of those 25 patients with probable reperfusion after thrombolysis. CONCLUSIONS: We conclude that measuring myoglobin/carbonic anhydrase III ratio during the first hours after initiation of thrombolysis may be useful in evaluating the success of reperfusion after acute myocardial infarction.

Angioplasty, Balloon, Coronary↗
PubMed2003

Cardiac troponin T and I and creatine kinase-MB as markers of myocardial injury and predictors of outcome following percutaneous coronary intervention.

AIMS: This study was performed to determine the most sensitive biochemical marker for the detection of cardiac myocyte damage potentially sustained during percutaneous coronary intervention (PCI) and to assess whether such a marker can be used to identify patients at increased risk of poor subsequent clinical outcome. METHODS AND RESULTS: We studied 109 consecutive patients presenting with clinical stable and unstable angina and undergoing PCI at our institution. Blood was sampled for creatine kinase-MB (CK-MB), cardiac Troponin T (cTnT) and I (cTnI) immediately before and at 6, 14 and 24 h post-PCI. Five patients with raised cardiac markers pre-PCI were excluded from further analysis. The occurrence of major adverse cardiac events (MACE) was documented in-hospital, at 30 days and at long-term clinical follow up of up to 20 months. MACE occurred in 26/109 (24%) patients: death=1, QWMI=4, NQWMI=5, repeat PCI=16 (nine target vessel revascularisations and seven de-novo lesions), CABG=5. cTnI had the highest detection rate for myocardial damage, with 58 cTnI-positive patients, 38 cTnT-positive patients and 28 CK-MB-positive patients in the 24 h following PCI (Pearson's Chi square test, P<0.01). The type of interventional strategy per se was not significantly associated with post-procedural cardiac marker concentrations (Kruskal-Wallis ANOVA, P>0.05). There was a significant association between post-procedural cardiac marker concentrations of CK-MB, cTnT and cTnI and the occurrence of procedural angiographic complications (P=0.0003, 0.0002, 0.001, respectively). All three markers, at each sampling time point between 6 and 24 h post-PCI, showed a significant predictive relationship with MACE in-hospital and at long-term follow up (ROC curve AUC analysis, P<0.05). All three markers provided equally predictive information at each of the three post-procedural sampling time points between 6 and 24 h following PCI. All levels of cardiac marker elevation above the clinically discriminant cut-off values were significantly predictive of outcome at long-term follow up. CONCLUSIONS: cTnI proved to be the most sensitive marker in detecting myocardial necrosis following PCI. CK-MB, cTnT and cTnI all provided similarly reliable prognostic information, with cTnT and cTnI being marginally superior in predicting MACE at follow up.

Angina Pectoris↗
PubMed2004

Pericardial fluid level of heart-type cytoplasmic fatty acid-binding protein (H-FABP) is an indicator of severe myocardial ischemia.

BACKGROUND: Heart-type cytoplasmic fatty acid-binding protein (H-FABP) has been reported as a sensitive and specific marker for the early diagnosis of acute myocardial infarction. Our hypothesis was that serum or pericardial fluid levels of H-FABP can reflect not only myocardial infarction but also myocardial ischemia. METHODS: A total of 34 patients with unstable angina, who had anginal symptoms and/or ST-changes in ECG monitoring within 24 h before operation, were classified into group A (n=17), and those without these symptoms and changes into group B (n=17). Blood and pericardial fluid samples were obtained immediately after median sternotomy, and serum and pericardial fluid levels of creatine kinase-MB, cardiac troponin-T, and H-FABP were measured. RESULTS: Serum H-FABP levels were slightly elevated compared with their normal values in both groups. While they showed no difference between groups A and B (group A vs. B: 8.5+/-1.0 vs. 7.1+/-0.7 ng/ml, P=0.25), pericardial fluid levels of H-FABP were significantly higher in group A than in group B (16.3+/-2.0 vs. 9.6+/-1.0 ng/ml, P=0.0046). H-FABP showed a weak correlation between its serum levels and pericardial fluid levels (r=0.40). CONCLUSIONS: Pericardial fluid levels of H-FABP reflect myocardial ischemia occurring within 24 h of their measurements. H-FABP may be secreted into the interstitial space by increased permeability of the myocardial cell membrane associated with severe myocardial ischemia. Thus, pericardial fluid reflects pathophysiological conditions of cardiomyocytes more sensitively than circulating blood.

Aged↗
PubMed2003

Myonecrosis following isolated coronary artery bypass grafting is common and associated with an increased risk of long-term mortality.

AIMS: We sought to evaluate the risk of long-term mortality with respect to post-operative elevation of the isoenzyme CK-MB following first-time isolated coronary artery bypass grafting (CABG) surgery. METHODS: Patients undergoing first-time isolated CABG between September 1992 and December 2001, at the Mid America Heart Institute, were included in this registry analysis. A sole CK-MB measurement was obtained at an average of 15.2h following CABG. The main endpoint was long-term mortality. RESULTS: There were 3667 patients included in this registry. The mean follow up was 5.1 years. The event-free survival rate was 80%, 78% and 73%, for the normal, 1-3 and >3 times by ULN groups respectively; log-rank p=0.0058. The event-free survival for the four CK-MB groups was 80%, 78%, 75% and 72% for the normal, 1-3 times, >3-5, and >5 times ULN groups respectively, log-rank p=0.0078. The CK-MB elevation following CABG remained a significant predictor following multivariate adjustment. With a point estimate of 1.04, 95% confidence limits 1.009-1.062, p=0.007. CONCLUSION: Elevation of the isoenzyme CK-MB is an important predictor of longterm mortality following coronary bypass grafting. These data support routine use of creatinine kinase measurement following bypass surgery to further delineate long-term risk.

Biomarkers↗
PubMed2003

Role of cardiac troponin T in the long-term risk stratification of patients undergoing percutaneous coronary intervention.

AIMS: To investigate the long-term prognostic significance of pre- and post-procedure troponin T (TnT) elevations in patients undergoing percutaneous coronary intervention (PCI). METHODS AND RESULTS: TnT and CK-MB were measured pre- and post-procedure in 212 patients undergoing PCI. Major adverse events (composite of death, myocardial infarction and revascularization) were ascertained 6 years later. Pre-procedural TnT was a significant independent predictor of time to major events (hazard ratio [HR] 1.75, 95% confidence interval [CI] 1.16-2.64) and death or myocardial infarction. Post-procedural TnT elevation above normal was the only independent predictor of the primary end-point at 1 year (HR 2.39, 95% CI 1.09-5.26) but was not significantly related to event-free survival throughout follow-up. Post-PCI elevation of TnT 5x above normal, however, did significantly predict time to events during the entirety of follow-up. By contrast, CK-MB was not an independent predictor in any of the analyses. CONCLUSIONS: Our study confirms the long-term prognostic value of pre-procedural TnT elevation in patients undergoing PCI, and demonstrates the superior predictive ability of a post-procedural increase in TnT 5x normal for long-term adverse events. Whether the prognostic significance of smaller post-procedural TnT elevations extends beyond the intermediate-term awaits further investigation.

Adult↗
PubMed2004

Lack of utility of telemetry monitoring for identification of cardiac death and life-threatening ventricular dysrhythmias in low-risk patients with chest pain.

STUDY OBJECTIVE: Low-risk patients with chest pain are often admitted to monitored beds; however, the use of telemetry beds in this cohort is not evidence based. We tested the hypothesis that monitoring admitted low-risk patients with chest pain for dysrhythmia is low yield (<1% detection of life-threatening dysrhythmias requiring treatment). METHODS: We conducted a prospective cohort study of emergency department (ED) patients with chest pain with a Goldman risk score of less than 8%, a normal initial creatine kinase-MB level, and a negative initial troponin I level admitted to non-ICU monitored beds. Investigators followed the hospital course daily. The main outcome was cardiovascular death and life-threatening ventricular dysrhythmia during telemetry. RESULTS: Of 3,681 patients with chest pain who presented to the ED, 1,750 patients were admitted to non-ICU monitored beds. Of these, 1,029 patients had a Goldman risk score of less than 8%, a troponin I level of less than 0.3 ng/mL, and a creatine kinase-MB level of less than 5 ng/mL (accounting for 59% of all chest pain telemetry admissions). During hospitalization, there were no patients with sustained ventricular tachycardia/ventricular fibrillation requiring treatment on the telemetry service (0%; 95% confidence interval [CI] 0% to 0.3%). There were 2 deaths: neither was cardiovascular in nature or preventable by monitoring (cardiovascular preventable death rate=0%; 95% CI 0.0% to 0.3%). CONCLUSION: The routine use of telemetry monitoring for low-risk patients with chest pain is of limited utility. Admission to nonmonitored beds might help alleviate ED crowding without increasing risk of adverse events caused by dysrhythmia in patients with a Goldman risk of less than 8%, an initial troponin I level of less than 0.3 ng/mL, and a creatine kinase-MB level of less than 5 ng/mL.

Arrhythmias, Cardiac↗
PubMed2003

Prognostic value of cardiac markers in ESRD: Chronic Hemodialysis and New Cardiac Markers Evaluation (CHANCE) study.

BACKGROUND: Cardiac disease is the main cause of mortality in long-term hemodialysis patients. Cardiac troponins (cTn) have been proposed to be markers of cardiac damage, but their value is still debated in hemodialysis patients. The aim of this prospective study is to assess the prognostic value of biochemical cardiac markers in long-term hemodialysis patients. METHODS: We measured serum levels of cTn I (cTnI), cTn T (cTnT), and creatine kinase-MB (CK-MB) in 258 asymptomatic patients (mean age, 60 +/- 15 years; 150 men) before the dialysis treatment. All causes of death and major adverse cardiac events (MACEs: cardiac death, myocardial infarction, or unstable angina) were recorded at 1 and 2 years of follow-up. A Cox proportional hazard regression model was used to identify factors predictive of mortality. RESULTS: On inclusion, 48 patients (18.6%) had cTnT levels greater than 0.1 ng/mL, 46 patients (17.8%) had cTnI levels greater than 0.15 ng/mL, and 18 patients (7.0%) had CK-MB levels greater than 3 ng/mL. Of 246 patients followed up at 2 years, 64 patients (26%) had died, including 29 patients (11.8%) of cardiac disease, and 49 patients (19.9%) experienced at least 1 MACE. MACEs were significantly greater for patients with elevated predialysis serum cTnT and CK-MB levels (>0.1 ng/mL and 3 ng/mL, respectively) than for patients with normal levels of these cardiac markers (31.9% versus 17.1%; P = 0.01; 38.9% versus 18.4%; P = 0.02, respectively). No differences were found for cTnI levels. In multivariate analysis, age (relative risk [RR], 1.04; P = 0.002), previous ischemic heart disease (RR, 2.5; P = 0.0001), and serum cTnT levels greater than 0.1 ng/mL (RR, 1.9; P = 0.04) were independent significant factors for MACEs. CONCLUSION: Increased predialysis serum levels of cTnT and CK-MB, but not cTnI, were predictive of a high risk for overall mortality and MACEs at 2 years in asymptomatic hemodialysis patients.

Aged↗
PubMed2003

[Applicability of a new definition of myocardial infarction and the opinion of Spanish cardiologists].

INTRODUCTION AND OBJECTIVES: The Working Group on Ischemic Heart Disease and Coronary Care Units of the Spanish Society of Cardiology evaluated the applicability of a new definition of infarction in Spanish hospitals, its current use, and the opinion of Spanish cardiologists. METHODS: A telephone survey was made (from late 2001 to early 2002) in Spanish hospitals to evaluate the availability of troponin or creatine kinase MB mass determinations. A questionnaire was sent to all members of the Spanish Society of Cardiology to query about the availability of determinations of cardiac necrosis markers at their respective hospitals, use of the new definition, and whether they agreed with the new definition. RESULTS: An important proportion of Spanish hospitals cannot determine myocardial necrosis markers (troponin or creatine kinase MB mass), mainly due to low-volume activity (fewer than 200 beds). The new definition of myocardial infarction was used by Spanish cardiologists always (24%), frequently (31%), sometimes (17%), seldom (14%), and never (11%). Agreement with the definition was complete in 21%, almost complete in 33%, half and half in 26%, rare in 10%, and absent in 7% of Spanish cardiologists. CONCLUSIONS: A large percentage of Spanish hospitals cannot use the new definition of myocardial infarction because they cannot determine specific cardiac necrosis markers. Spanish cardiologists are not generally using the new definition and many do not agree with it.

Biomarkers↗
PubMed2003

[Long-term prognostic value of troponin I in patients admitted to a coronary unit for unstable angina].

INTRODUCTION AND OBJECTIVES: Troponin I (TnI) is a useful marker of myocardial damage for the diagnosis and prognosis of acute coronary syndrome. The purpose of this study was to analyze the long-term prognostic value of the peak TnI concentration obtained within 48 h of admission to the coronary unit for unstable angina. METHODS: The study included 149 consecutive patients. Serial determinations were made of the MB fraction of creatine kinase (CK-MB) and TnI. Patients without CK-MB elevation were classified into two groups depending on the presence of high (n = 58) or normal (n = 91) troponin I values. We prospectively analyzed the clinical and evolutive factors related to the probability of death, new acute coronary event, or coronary revascularization at one-year of follow-up. RESULTS: There were no differences in the clinical characteristics between groups, except that patients in the group with high TnI values were older (69 vs. 64 years, p = 0.01). At one year of follow-up there were no differences in the incidence of new acute coronary events or coronary revascularization procedures; however there was a higher mortality in the group with high TnI (13 vs. 4%; p = 0.01). The independent predictors of mortality were prior myocardial infarction (RR = 3), elevated troponin I (RR = 3.2), left ventricular ejection fraction < 35% (RR = 10), and age > 70 years (RR = 15). CONCLUSIONS: In patients with unstable angina a high troponin I value in the first 48 h of admission was associated with a higher mortality rate at one-year of follow-up.

Adult↗
PubMed2003

[Chest pain in clinical practice: impact of routine troponin determination on clinical manifestations and care].

UNLABELLED: INTRODUCTION AND OBJECTIVES. To study the significance of chest pain in the clinical practice of a Spanish hospital and to evaluate the impact of routine troponin determination. METHODS: In our institution, routine serial measurements of troponins I and T were made in the evaluation of chest pain in 2000. We compared the results obtained in 1999 for all patients who visited the emergency room for chest pain and the patients who were hospitalized. We recorded the diagnosis at discharge, duration of the hospital stay, and associated costs. RESULTS: In 2000, 1,820 patients with chest pain visited the emergency department, which was equivalent to 1.9% of visits and 7.5 cases per 1,000 people and year: 43% of these patients were hospitalized for suspected acute coronary syndrome as compared to 49% in 1999 (-12%; p > 0.001). Among the patients admitted, 28% were discharged with a diagnosis of non-ischemic chest pain. Troponin determinations were associated with a lower probability of admission due to unstable angina (11.5 vs 16.0%; -28%; p < 0.001) and non-ischemic chest pain (12.1 vs 14.5%; -16%; p < 0.05), and an increase in diagnoses of non-Q wave acute myocardial infarction (3.4% vs 1.8%; +89%; p < 0.01). Non-ST elevation acute coronary syndrome ACS required 3,751 days of hospitalization and 1,003,420 euros of cost, and troponin determinations were associated with a reduction in hospital stays of 832 days (-18.2%) and 185,100 euros (-15.6%). CONCLUSION: Chest pain had a high incidence, 7.5, and generates high costs in hospital admissions. The routine use of serial troponin determinations was associated with a reduction in hospital admissions due to unstable angina and non-ischemic chest pain, and costs.

Angina, Unstable↗
PubMed2001

Clinical application of rapid quantitative determination of cardiac troponin-T in an emergency department setting.

OBJECTIVES: We analysed the clinical use of Troponin-T compared to creatine kinase MB in a non-trauma emergency department setting. BACKGROUND: A newly established single specimen quantitative Troponin T assay allows the clinical application of this parameter. METHODS. Five-hundred Troponin T tests were provided for use by emergency physicians who could combine them with the routine laboratory tests without restriction as to the indication or number of tests per patient. The number of tests per patient, time frame, final diagnosis and additional clinical information gained were recorded. All patients were followed for at least 6 months to verify the diagnosis and to assess the occurrence of cardiac events (nonfatal AMI or cardiac death). The ability of Troponin T and creatine kinase MB tests to predict cardiac events within 6 months were compared. RESULTS: The 500 Troponin T tests were used in 249 patients (median two tests per patient (range 1-5)) within 41 days. The final diagnosis revealed coronary heart disease in 85, non-coronary heart disease in 39, non-cardiac chest pain in 86 and other diagnoses in 39 of the patients. In 14 patients with an elevated creatine kinase MB, myocardial damage could safely be ruled out by a negative Troponin T, in six patients with a normal creatine kinase MB minor myocardial damage could be detected by a positive Troponin T. During follow up 28 cardiac events were recorded. Troponin T had a significantly higher specificity, positive predictive value and proportion of correct prediction for cardiac events within 6 months compared to creatine kinase MB. CONCLUSIONS: Troponin T has proved to be an useful method for diagnosing myocardial damage in routine clinical use in the non-trauma emergency department.

Austria↗
PubMedDate not supplied

Serum potassium levels, CPK-MB and ECG in children suffering asthma treated with beclomethasone or beclomethasone-salmeterol.

Asthma morbidity and mortality has increased. One of the possible causes is the excessive use of beta agonists. The aim of this study is to compare the effects of six week treatment with beclomethasone alone (Ibec) or the combination of beclomethasone-salmeterol (Ibe + Isal) on serum potassium (K), CPK-MB and ECG in children suffering asthma. It was a prospective, randomised, open cross-over trial. Patients received either Ib2 (2 puff/12 hr, 100 micrograms per puff) or Ibe + Isal (B 2 puff/12 hr, 100 micrograms per puff and S 2 puff/12 hr, 25 micrograms per puff) with dose meter inhaler by 6 weeks, with a four-week wash-out period between the treatments. K, CPK-MB and ECG were assessed at baseline, and after each treatment period. There were 9 girls and 20 boys, aged 11 +/- 2.18 (mean +/- SD) years, baseline K was 4.57 +/- 0.43 mEq/l, after B K 4.38 +/- 0.39 IU and after BS K 4.38 +/- 0.40. The CPK-MB level were baseline 14.75 +/- 4.5, after B 20.10 +/- 6.9 and after BS 21 +/- 8.05 (p < 0.05). Baseline QTc was 0.416 +/- 0.02 msec, after B 0.425 +/- 0.027, and after BS 0.415 +/- 0.029. We conclude that the treatment of children with asthma with 400 micrograms per day of Ibec or concomitantly with 100 micrograms of Isal for 6 weeks does not alter the serum K+ or the QTc. However, the CPK-MB has a significant increment with both treatments but without clinical and/or ECG changes. We can't affirm that Ibec or Ibec plus Isal have a cardiotoxic side-effect by the only presence of high levels of CPK-MB. We agree that it is necessary a close follow up of these apparently asymptomatic patients not induce important cardiovascular changes although CPK-MB was increased.

Adolescent↗
PubMed2003

Can CK-MB and cTn-I be detected in the peripheral circulation within the first 10 min of acute coronary ischemia?

There are approximately 4 million patients hospitalized with suspected acute coronary syndromes (ACS) annually. However, the current standard tools for assessing ACS in the Emergency Department are felt to have insufficient sensitivity and specificity. Animal studies have demonstrated that CK-MB and troponin-I are released in a biphasic pattern with an initial transient release which peaks and falls within the first 10 min of ischemia. We hypothesize that transient elevations of CK-MB and troponin-I can be detected in the peripheral circulation within the first 10 min of ischemia in a human model of brief coronary ischemia. We also present results from our pilot study that failed to confirm this hypothesis; however, this pilot studied was insufficiently powered to detect potentially clinically important results.

Creatine Kinase↗
PubMed2001

Serum markers in the emergency department diagnosis of acute myocardial infarction.

No currently used cardiac-specific serum marker meets all the criteria for an "ideal" marker of AMI. No test is both highly sensitive and highly specific for acute infarction within 6 hours following the onset of chest pain, the timeframe of interest to most emergency physicians in making diagnostic and therapeutic decisions. Patients presenting to the ED with chest pain or other symptoms suggestive of acute cardiac ischemia therefore cannot make a diagnosis of AMI excluded on the basis of a single cardiac marker value obtained within a few hours after symptom onset. The total CK level is far too insensitive and nonspecific a test to be used to diagnose AMI. It retains its value, however, as a screening test, and serum of patients with abnormal total CK values should undergo a CK-MBmass assay. Elevation in CK-MB is a vital component of ultimate diagnosis of AMI, but levels of this marker are normal in one fourth to one half of patients with AMI at the time of ED presentation. The test is highly specific, however, and an abnormal value (particularly when it exceeds 5% of the total CK value) at any time in a patient with chest pain is highly suggestive of an AMI. There have been several improvements of CK-MB assay timing and subform quantification that appear highly useful for emergency physicians. Rapid serial CK-MB assessment greatly increases the diagnostic value of the assay in a timeframe suitable for ED purposes but unfortunately still misses about 10% of patients ultimately diagnosed with acute MI. Assays of CK-MB subforms have very high sensitivity, and, although unreliable within 4 hours of symptom onset, have excellent diagnostic value at 6 or more hours after chest pain begins. Automated test assays recently have become available and could prove applicable to ED settings. The cardiac troponins are highly useful as markers of acute coronary syndromes, rather than specifically of AMI, and abnormal values at any time following chest pain onset are highly predictive of an adverse cardiac event. The ED applicability of the troponins is severely limited, however, because values remain normal in most patients with acute cardiac events as long as 6 hours following symptom onset. Myoglobin appeared promising as a marker of early cardiac ischemia but appears to be only marginally more sensitive than CK-MB assays early after symptom onset and less sensitive than CK-MB at 8 hours or more after chest pain starts. Rapid serial myoglobin assessment, however, appears highly useful as an early marker of AMI. The marker has a very narrow diagnostic window. The clinician is left with several tests that are highly effective in correctly identifying patients with AMI (or at high risk for AMI), but none that can dependably exclude patients with acute coronary syndromes soon after chest pain onset. A prudent strategy when assessing ED patients with chest pain and nondiagnostic ECGs is to order CK-MB and troponin values on presentation in the hope of making an early diagnosis of AMI or unstable coronary syndrome. Although it is recognized that normal values obtained within 6 hours of symptom onset do not exclude an acute coronary syndrome, patients at low clinical risk and having normal cardiac marker tests could be provisionally admitted to low-acuity hospital settings or ED observation. After 6 to 8 hours of symptom duration has elapsed, the cardiac-specific markers are highly effective in diagnosing AMI, and such values obtained can be used more appropriately to make final disposition decisions. At no time should results of serum marker tests outweigh ECG findings or clinical assessment of the patient's risk and stability.

Biomarkers↗
PubMed2001

Reactivation of ischemic events in acute coronary syndromes: results from GUSTO-IIb. Gobal Use of Strategies To Open occluded arteries in acute coronary syndromes.

OBJECTIVES: We sought to determine the incidence of and risk factors for thrombotic events early after discontinuing antithrombin therapy in patients with acute coronary syndromes. BACKGROUND: Discontinuation of treatment with heparin and other thrombin inhibitors in patients with unstable coronary syndromes has related to clinical and biochemical evidence of early reactivation of thrombosis. METHODS: We studied 8,943 of the 12,142 patients with acute coronary syndromes enrolled in the Global Use of Strategies To Open occluded arteries in acute coronary syndromes trial of hirudin versus heparin. We excluded patients who received no study drug, lacked timing data, died or had myocardial (re)infarction [(re)MI] during study-drug infusion, or began heparin treatment within 2 h after treatment with the study drug was stopped. We assessed the incidence and timing of (re)MI by type and timing of antithrombin treatment. RESULTS: In all, 215 patients (2.4%) suffered (re)MI, 49 within 12 h of antithrombin therapy discontinuation and 166 between hour 12 and hospital discharge. The duration of infusion did not differ between the hirudin and heparin groups. The rate of early re(MI) after drug therapy discontinuation was significantly higher in patients given heparin versus hirudin (0.8% vs. 0.3%, p = 0.002). Patients with (re)MI had higher mortality at 30 days (23.6% vs. 2.4%, p = 0.001) and 1 year (35.2% vs. 6.7%, p = 0.001) compared with patients without (re)MI. CONCLUSIONS: The incidence of (re)MI was clustered within 12 h of heparin therapy discontinuation, with the greatest risk within 4 h. There was no evidence of early reactivation of thrombotic events after hirudin. Patients who had (re)infarction had worse outcomes. Better understanding of the mechanism and possible prevention of recurrent thrombosis is needed.

Aged↗