Cardiovascular risk and therapeutic benefit of coronary interventions for patients with unstable angina according to the troponin T status.

AIMS: Elevation of troponin T in patients with unstable angina is predictive of adverse outcomes. Since no advanced therapeutic concept for such high-risk patients has been established, we investigated cardiac risk prior to, during, and after coronary revascularization in patients with unstable angina stratified according to the troponin T status. METHODS AND RESULTS: Out of 351 patients with unstable angina, troponin was elevated for 36% of the patients as determined by qualitative bedside tests. The patients were followed during hospitalization and 30 days after discharge for incidence of death and myocardial infarction. In troponin-positive patients, clinical symptoms were more refractory to medical treatment than in troponin-negative patients (78% vs 44%;P=0.002). Although these patients were catheterized earlier (1.6 vs 3.4 days;P=0.005) and more frequently (95% vs 69%;P<0.001), troponin-positive patients suffered a higher incidence of cardiac events prior to scheduled revascularization (death, myocardial infarction; 6.4% vs 0.4%;P<0.001). The angiogram for troponin-positive patients confirmed a more severe coronary artery disease requiring revascularization (69% vs 50%;P=0.001). Also the following coronary intervention was more complicated (death, myocardial infarction; 15.3% vs 4.8%;P=0.02). During the 30-day follow-up period, cardiac risk remained elevated for troponin-positive patients. CONCLUSIONS: Troponin T rapid testing reliably identified high-risk patients with unstable angina. A higher event rate was observed prior to and particularly in association with the coronary intervention. Coronary revascularization did not abrogate the increased risk of troponin-positive patients during the 30-day follow-up.     

Prognostic Role of Troponin T Versus Troponin I in Unstable Angina Pectoris for Cardiac Events With Meta-Analysis Comparing Published Studies

Controversy exists as to the clinical roles and relative specificities of cardiac troponin T or I in patients with unstable angina pectoris (UAP). We measured troponin T and I levels on admission in 123 patients with UAP. Of the 107 patients with normal creatine kinase during the first 24 hours, troponin T and I were elevated in 14 and 13 patients, respectively. At 30 days, 5 of 14 patients (36%) with elevated troponin T and 3 of 93 patients (3.2%) with normal troponin T had acute myocardial infarction (odds ratio [OR], 16.7; 95% confidence interval [CI] 3.4 to 81.5; p <0.001). Of 13 patients with elevated troponin I, 5 patients (39%) and 3 of 94 patients (3.2%) with normal troponin I had acute myocardial infarction (odds ratio, 21.7; 95% CI 4.3 to 110; p <0.001). No deaths occurred within 30 days. Both markers demonstrated equivalent sensitivity (63%) and specificities (troponin T: 91%; troponin I: 92%) for myocardial infarction. Meta-analysis of 12 published troponin T and 9 troponin I studies in patients with UAP produced risk ratios of 4.2 (95% CI 2.7 to 6.4, p <0.001) for troponin I compared with 2.7 (95% CI 2.1 to 3.4, p <0.001) for troponin T. Comparison of the sensitivities and specificities of both markers using summary receiver operating characteristic curves showed no significant difference in their abilities to predict acute myocardial infarction and cardiac death. Troponin T and I show similar prognostic significance for acute myocardial infarction or death in the same patients with UAP. The 2 markers are equally sensitive and specific, as confirmed by meta-analysis, and this supports a role in risk stratification.     

Elevated troponin T and C-reactive protein predict impaired outcome for 4 years in patients with refractory unstable angina, and troponin T predicts benefit of treatment with abciximab in combination with PTCA.

AIMS: Treatment with the glycoprotein IIb/IIIa receptor antagonist abciximab before and during coronary intervention in refractory unstable angina improves early outcome. We collected 4-year follow-up data to assess whether this benefit is sustained. Additionally, we investigated the predictive value of baseline troponin T and CRP for long-term cardiovascular events. METHODS AND RESULTS: Of 1265 patients enrolled in the CAPTURE trial follow-up was available in 94% of the patients alive after 6 months (median 48 months). Survival was similar in both groups. Both elevated troponin T and CRP were associated with impaired outcome, independently of other established risk factors, but with a different time course. Elevated troponin was associated with increased procedure related risk, and elevated CRP with increased risk for subsequent events. Lower rates of the composite end-point of death or myocardial infarction with abciximab vs. placebo were sustained during long-term follow up: 15.7% vs 17.2% at 4 years (P=ns), particularly in patients with elevated troponin T: 16.9% with abciximab vs 28.4% with placebo: P=0.015. Elevated CRP was not associated with specific benefit of abciximab. CONCLUSION: Troponin T as a marker of thrombosis and CRP as a marker of inflammation are independent predictors of impaired outcome at 4 years follow-up. The initial benefit from abciximab with regard to death and myocardial infarction was preserved at 4 years. No specific benefit with abciximab was observed for patients with elevated CRP, suggesting that a chronic inflammatory process is not affected by abciximab. In contrast the benefit of treatment in patients with elevated troponin T implies that the acute thrombotic process in refractory unstable angina is treated effectively.     

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.     

Prognostic value of cardiac troponin I re-elevation following percutaneous coronary intervention in high-risk patients with acute coronary syndromes.

Troponin I is a predictive marker of short- and intermediate-term adverse cardiac events in patients with acute coronary syndromes (ACS). These high-risk patients may benefit from early percutaneous coronary intervention. However, whether additional myocardial injury, defined as postprocedural troponin I elevation, may be associated with adverse short- and intermediate-term outcomes has not been fully explored. Accordingly, we studied 132 consecutive patients with non-ST-elevation ACS (62% with non-Q-wave myocardial infarction) and elevated troponin I levels at admission (>0.15 ng/ml) who underwent percutaneous coronary intervention > or =48 hours after admission. Troponin I levels were routinely measured at 6 and 18 to 24 hours after intervention and patients were stratified according to the presence or absence of troponin I re-elevation, defined as postprocedural troponin I levels >1 times the admission levels. In-hospital and cumulative 6-month clinical outcomes were compared between groups. Patients with troponin I re-elevation (n = 51) were older (68 +/- 13 vs 64 +/- 12 years, p = 0.05) and had experienced prior myocardial infarction more frequently (92.5 vs 82.1, p = 0.09), but otherwise had similar baseline clinical characteristics. Patients with troponin I re-elevation had significantly higher in-hospital mortality (9.8% vs 0%, p = 0.016) and a higher 6-month cumulative death rate (24% vs 3.7%, p = 0.001). There was a trend for an increased 6-month myocardial infarction rate in patients with troponin I re-elevation (13.7% vs 3.7%, p = 0.11) and target vessel revascularization was similar between groups (16.7% vs 17.4%, p = 0.92). By multivariate analysis, troponin I re-elevation (odds ratio [OR] 6.2, p = 0.011) and diabetes mellitus (OR 5.7, p = 0.014) were the strongest independent predictors for increased 6-month cumulative mortality, whereas creatine kinase MB-fraction re-elevation had no prognostic value. We conclude that troponin I re-elevation after percutaneous coronary intervention in high-risk patients with ACS is associated with a substantial increase in mortality and reduced event-free survival at 6-month follow-up.     

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.     

A rapid troponin I assay is not optimal for determination of troponin status and prediction of subsequent cardiac events at suspicion of unstable coronary syndromes

BACKGROUND: Troponin is a specific marker of myocardial damage. For early prediction of coronary events in patients with suspicion of acute coronary syndromes the assay also needs to be highly sensitive. METHODS AND RESULTS: A rapid troponin I assay was performed prior to inclusion in 4447 acute coronary syndrome patients in the GUSTO-IV trial. A quantitative troponin T analysis was later performed on blood samples obtained at randomization by a central laboratory. There was an agreement between the rapid troponin I assay and troponin T (< or =/>0.1 microg/l) in 3596 (80.9%) patients. A positive rapid troponin I was identifying any elevation of troponin T (>0.01 microg/l) in 1990 patients (90.4%) whereas a negative rapid troponin I was corresponding to negative troponin T (< or =0.01 microg/l) in only 1217 patients (54.2%). Patients with a positive versus negative rapid troponin I had an increased risk of death or myocardial infarction at 30 days (9.3 vs. 5.9%; odds ratio, O.R. 1.64; 95% confidence interval, 1.31-2.06). Troponin T elevation (>0.1 microg/l) provided a better (10.5 v. 4.9%, O.R. 2.26; C.I. 1.79-2.85) risk stratification. Regardless of a positive or a negative rapid troponin I, the troponin T result (>0.1 vs. < or =0.1 microg/l) stratified the patients into high and low risk of events at 30 days, (10.3 vs. 5.7%, P=0.002) and (11.5 vs. 4.8%, P<0.001), respectively. CONCLUSION: In a population with non-ST elevation acute coronary syndrome a positive rapid troponin I assay is a specific indicator of troponin elevation and a predictor of early outcome. However, a negative rapid troponin I is not a reliable indicator of the absence of myocardial damage and does not indicate a low risk of subsequent cardiac events. A rapid troponin I assay was performed prior to inclusion in 4447 acute coronary syndrome patients in the GUSTO-IV trial and related to a centrally analyzed quantitative troponin T test. A positive rapid troponin I was well corresponding to any elevation of troponin T (>0.01 microg/l) and predicted an unfavorable outcome at 30 days. However, a negative rapid troponin I was corresponding to troponin T < or =0.01 microg/l in only half of the patients. Troponin T >0.1 microg/l vs. < or =0.1 microg/l provided a better risk stratification than the rapid troponin I result. For patients with troponin T elevation (>0.1 microg/l) the 30 day event rate was high regardless of the rapid troponin I result.     

Comparison of the incidences of cardiac arrhythmias, myocardial ischemia, and cardiac events in patients treated with endovascular versus open surgical repair of abdominal aortic aneurysms

This study examines differences in cardiac arrhythmias, perioperative myocardial ischemia, troponin T release, and cardiovascular events between endovascular and open repair of abdominal aortic aneurysms (AAAs). Of 175 patients, 126 underwent open AAA repair and 49 underwent endovascular AAA repair. Continuous 12-lead electrocardiographic monitoring, starting 1 day before surgery and continuing through 2 days after surgery, was used for cardiac arrhythmia and myocardial ischemia detection. Troponin T was measured on postoperative days 1, 3, and 7 and before discharge. Cardiac events (cardiac death or Q-wave myocardial infarction) were noted at 30 days and at follow-up (mean 2.3 years). New-onset atrial fibrillation, nonsustained ventricular tachycardia, sustained ventricular tachycardia, and ventricular fibrillation occurred in 5%, 17%, 2%, and 1% of patients, respectively. Myocardial ischemia, troponin T release, and 30-day and long-term cardiac events occurred in 34%, 29%, 6%, and 10% of patients, respectively. Significantly higher heart rates and less heart rate variability were observed in the open AAA repair group. Cardiac arrhythmias were less prevalent in the endovascular AAA repair group (14% vs 29%, p = 0.04). Endovascular repair was also significantly associated with less myocardial ischemia (odds ratio 0.14, 95% confidence interval 0.05 to 0.40, p <0.001) and troponin T release (odds ratio 0.10, 95% confidence interval 0.02 to 0.32, p <0.001) and lower 30-day mortality (zero vs 8.7%, p = 0.03) and 30-day cardiac event rates (zero vs 7.9%, p = 0.04). Long-term mortality and cardiac event rates were not significantly lower in the endovascular AAA repair group. In conclusion, endovascular AAA repair is associated with a lower incidence of perioperative cardiac arrhythmias, myocardial ischemia, troponin T release, cardiac events, and all-cause mortality compared with open AAA repair.     

Superiority of combined CK-MB and troponin I measurements for the early risk stratification of unselected patients presenting with acute chest pain

BACKGROUND: Recent studies have suggested that positive troponin I tests are associated with an increased risk of cardiac death during short-term follow-up. However, it is unknown if troponin I tests alone or in addition to CK-MB measurements are superior to predict unfavorable outcome during long-term follow-up. PATIENTS AND METHODS: In a prospective, double-blind study we assessed the prevalence and prognostic value of combined troponin I and CK-MB tests in an unselected cohort of patients (n = 292) admitted to the emergency department for acute chest discomfort. Patients were grouped according to the diagnosis on discharge in those with acute myocardial infarction (1), unstable angina (2), and noncardiac chest pain (3). Six months after enrollment, death rates were obtained and follow-up interviews were performed with respect to survival, recurrence of chest pain, and myocardial infarction. RESULTS: In patients with evidence of coronary heart disease, the mortality rate for abnormal troponin I and normal CK-MB levels was 5.0%. Baseline troponin I and elevated CK-MB levels were associated with a mortality rate of 4.0%. However, the mortality rate was significantly higher (11.1%) in patients presenting with elevated troponin I and CK-MB values. In patients without myocardial infarction on admission, 10.5% with positive troponin I tests died compared to 1.6% with negative tests. The mortality rate in patients without myocardial infarction was 2.7% for patients with elevated CK-MB but normal troponin I values. In patients with both markers elevated a significantly higher mortality rate (16.7%) was found, representing a 6-fold increase in the death event rate. With the additional knowledge of troponin I values, it could be demonstrated that certain cases were misclassified as having noncardiac chest pain. At least some of the latter patients with above-normal values of troponin I were retrospectively to be reclassified as unstable angina. Acute non-Q-wave myocardial infarctions were occasionally misdiagnosed as either angina pectoris or nonischemic chest pain. CONCLUSIONS: Our data suggest the superiority of combined CK-MB and troponin I measurements in clinical practice for the early risk stratification of patients presenting with acute chest pain. In nonmyocardial infarctions, both CK-MB and troponin I convey independent prognostic information with regard to fatal outcome. Troponin I tests in addition to CK-MB measurements contribute to a lower rate of misdiagnoses.     

Cardiac troponin T in acute coronary syndrome with renal insufficiency

Cardiac troponin levels are frequently elevated in patients with chronic renal failure, hence diagnosis of myocardial necrosis is difficult. The prevalence of elevated serum troponin T was determined and its diagnostic value in acute coronary syndrome was assessed in patients with chronic renal insufficiency. A retrospective cross-sectional analysis was performed in 227 patients with chronic renal insufficiency and a diagnosis of unstable angina, non-ST or ST-segment elevation myocardial infarction. All patients had baseline serum troponin T levels measured at previous visits; the baseline troponin T level was raised in 53.3%. Cardiac troponin T levels did not correlate with creatinine levels, and were not affected by dialysis. Mortality after an acute coronary event was high (46.3%). Because of the elevated baseline cardiac troponin T levels, detection of acute coronary syndrome in patients with chronic renal failure requires evaluation of serial cardiac enzyme measurements and serial 12-lead electrocardiograms. Early and definitive cardiac interventions may contribute towards decreasing the mortality rate in this group of patients.     

Cardiac injury after percutaneous catheter ablation for atrial fibrillation

Aims: Small elevations in troponin T levels have been shown with limitedradiofrequency (RF) ablation procedures for supraventriculartachycardia, usually to levels below the threshold for ischaemiaor infarction. Left atrial catheter ablation for atrial fibrillation(AF) requires far more RF energy, therefore could be expectedto have greater elevation in troponin T. We determined troponinT levels before and after ablation in these patients to evaluatethe amount of rise with this ablation. Methods: All patients undergoing pulmonary vein isolation (PVI) fromMay 2004 to October 2004 had troponin T levels measured 4 hfollowing completion of the procedure. The first 30 patientsalso had a troponin T level measured 1 h prior to PVI to establisha baseline reference. Results: Sixty patients were studied, with 81.7% males and a mean ageof 54.6 ± 9.9 years. No patient had underlying structuralheart disease. The baseline troponin T level was normal (<0.01µg/L) in all 30 patients. Post-procedure troponin T levelswere elevated in all 60 patients compared with baseline (P <0.05), with a mean level of 0.85 µg/L and a range of 0.26–1.57µg/L after an average RF ablation time of 56 ±15 min. All levels were above the reference range for diagnosisof acute myocardial infarction (>0.15 µg/L). TroponinT level was not related to the number of RF lesions, RF time,procedure time, or associated external cardioversion. Conclusions: Troponin T elevations occurred in all patients undergoing PVI,to levels at least 20 times the normal concentration, into therange for diagnosis of acute myocardial infarction. Therefore,troponin T would not be specific for ischaemia in the settingof chest pain post-catheter ablation for AF.     

Troponin and C-reactive protein have different relations to subsequent mortality and myocardial infarction after acute coronary syndrome: a GUSTO-IV substudy

OBJECTIVES: We sought to evaluate C-reactive protein (CRP) and troponin T (TnT) as predictors of risk of the individual end points of mortality and myocardial infarction (MI) in a large cohort of patients with acute coronary syndrome (ACS). BACKGROUND: Both CRP and TnT predict risk of future coronary events in patients with ACS. However, the relationships between the levels of the markers and the individual end points are still unclear. METHODS: Baseline levels of CRP and TnT were determined in 7,108 patients with ACS not undergoing early revascularization in the Global Use of Strategies To Open occluded arteries trial IV (GUSTO-IV) trial and related to outcome at 30 days. RESULTS: Quartiles of TnT related to 30-day mortality, which was 1.1%, 3.7%, 3.7%, and 7.4% (p < 0.001) and to the rate of MI: 2.5%, 6.7%, 7.2%, and 5.6% (p < 0.001). Quartiles of CRP also related to 30-day mortality, which was 2.0%, 3.3%, 3.9%, and 6.3% (p < 0.001), whereas there was no relationship to the 30-day rate of MI: 5.6%, 4.7%, 5.2%, and 5.9% (p = 0.48). On multivariable analysis, both TnT and CRP were independent predictors of mortality, but only TnT was a predictor of MI. The combination of CRP and TnT provides an even better risk stratification of mortality, with 0.3% and 9.1% death rates, respectively, when both markers are in the bottom versus top quartiles. CONCLUSIONS: In ACS, baseline levels of TnT and CRP are independently related to 30-day mortality. Any detectable elevation of TnT, but not of CRP, is also associated with an increased risk of subsequent MI. Regarding mortality, the combination of both markers provides a better risk stratification than either one alone.     

Diagnostic efficiency of troponin T measurements in acute myocardial infarction

BACKGROUND. The present study was designed to evaluate the efficiency of a newly developed troponin T enzyme immunoassay for the detection of acute myocardial infarction. METHODS AND RESULTS. The study comprised 388 patients admitted with chest pain and suspected myocardial infarction and 101 patients with skeletal muscle damage and additional suspected myocardial cell damage. Troponin T was elevated to more than twice the analytical sensitivity of the assay (0.5 microgram/l) in all patients with non-Q wave (range, 1.2-5 micrograms/l) and Q wave infarction (range, 3-220 micrograms/l). Troponin T appeared in serum as early as 3 hours after onset of pain in 50% of the patients and remained elevated in all patients for more than 130 hours, revealing release kinetics of both free cytosolic and structurally bound molecules. The diagnostic efficiency of troponin T was superior to that of creatine kinase-MB (98% versus 97%) and remained at 98% until 5.5 days after admission, if patients with unstable angina were excluded from analysis. In the 79 patients with unstable angina, troponin T was elevated (range, 0.55-3.1 micrograms/l) in at least one blood sample from each of 37 patients (56%). Circulating troponin T was correlated to the presence of reversible ST segment or T wave changes on the electrocardiogram (p less than 0.005) and to the frequency of in-hospital complications. In the 101 patients with skeletal muscle damage and suspected additional cardiac muscle damage, troponin T was the most useful test; its efficiency was 89% or 94% (depending on the discriminator value used) as compared with 63% for creatine kinase-MB. CONCLUSIONS. Thus, the data of the study indicate that the newly developed troponin T test improves the efficiency of serodiagnostic tools for the detection of myocardial cell necrosis as compared with conventionally used cardiac enzymes.     

Early mortality of acute myocardial infarction in patients with and without prior coronary revascularization surgery. A Coronary Artery Surgery Study Registry Study.

BACKGROUND. The Coronary Artery Surgery Study (CASS) Registry is used to evaluate the effect of various baseline clinical and angiographic factors on mortality after acute out-of-hospital myocardial infarction (MI) in patients with and without prior coronary bypass surgery. METHODS AND RESULTS. Among the CASS Registry patients, there were 985 medical and 369 surgical patients who had an MI out of the hospital within 3 years after enrollment. In the medical group, 20% died before hospitalization. Medical patients with baseline three-vessel disease or left ventricular (LV) dysfunction were at high risk of immediate death. For medical patients who were hospitalized with MI, mortality was higher for older patients and those with severe angina as well as for those with extensive disease and LV dysfunction. The total 30-day mortality for medical patients was 36%. In the surgical group, 12% died before hospitalization. Surgical patients with LV dysfunction or prior MI were at highest risk of immediate death. For surgical patients hospitalized with MI, mortality was significantly increased only for patients with baseline LV dysfunction. Mortality was not significantly higher for surgical patients with multivessel disease. The total 30-day mortality for surgical patients was 21%. The prior use of aspirin or beta-blockers was not associated with reduced mortality from subsequent MI for either medical or surgical patients. Although the prevalence of cigarette smoking was high among patients who had an MI, cigarette smoking did not alter the infarct-related mortality rate. CONCLUSIONS. The surgical group had lower mortality rates than the medical group both immediately (p = 0.001), after hospitalization (p less than 0.0001), and at 30 days (p less than 0.0001).     

Prognostic value of cardiac troponin I in patients with non-ST elevation acute coronary syndrome

AIM: To elucidate relationship between initial blood levels of troponin I and occurrence of such events as death, myocardial infarction, coronary artery bypass surgery, and angioplasty in patients with non-ST elevation acute coronary syndrome. MATERIAL: One hundred one patients aged 32-78 years admitted to coronary care unit within 24 hours after onset of pain including 69 (68.3%) with unstable angina and 32 (31.7%) with non-ST elevation myocardial infarction. METHOD: Troponin I was determined by immunoassay, values below 0.4 ng/ml were considered normal. RESULTS. During 30 days of hospitalization there were 16 (35.5%) and 5 events (8.9%) events (p=0.001) among 45 patients who had elevated level of troponin I (group 1) and 56 patients with normal troponin I (group 2), respectively. By 6 months events occurred in 19 (42.2%) and 6 (10.7%) patients in groups 1 and 2, respectively (p=0.0004). CONCLUSION: Thus elevated blood level of troponin I in patients with non-ST elevation acute coronary syndrome has important value for prognosis.     

Prophylactic lidocaine use in acute myocardial infarction: incidence and outcomes from two international trials. The GUSTO-I and GUSTO-IIb Investigators

BACKGROUND: Early meta-analyses suggested that prophylactic lidocaine use reduces ventricular fibrillation but increases mortality rates after acute myocardial infarction. We determined the frequency and effect on clinical outcomes with its use in the thrombolytic era. METHODS AND RESULTS: We studied 43,704 patients enrolled in GUSTO-I or GUSTO-IIb who had ST-segment elevation, underwent thrombolysis, and survived at least 1 hour after enrollment. Odds ratios (OR) and confidence intervals (CI) were calculated for the risk of asystole, atrioventricular block, ventricular fibrillation, and ventricular tachycardia during hospitalization; for 24-hour, in-hospital, and 30-day mortality rates; and for 24-hour and 30-day mortality rates after adjustment for baseline predictors of death. In GUSTO-I and GUSTO-IIb, 16% and 3.5% of patients, respectively, received prophylactic lidocaine. They had a lower risk of death at 24 hours (OR 0.81, 95% CI 0.67 to 0.97) and trends toward lower odds of in-hospital death (OR 0.90, 95% CI 0.81 to 1.01) and death at 30 days (OR 0.92, 95% CI 0.82 to 1. 02). After adjustment for baseline characteristics, however, the odds of death were similar with or without lidocaine (OR 0.90 and 0. 97, respectively). Outside the United States, lidocaine was associated with higher incidences of all serious arrhythmias, but in US patients it conferred a lower likelihood of ventricular fibrillation and no increase in asystole, atrioventricular block, or mortality rates. CONCLUSIONS: Prophylactic lidocaine use has decreased with the advent of thrombolysis, although its use may not be associated with increased mortality rates.     

Differential impact of admission C-reactive protein levels on 28-day mortality risk in patients with ST-elevation versus non-ST-elevation myocardial infarction (from the Monitoring Trends and Determinants on Cardiovascular Diseases [MONICA]/Cooperative Health Research in the Region of Augsburg [KORA] Augsburg Myocardial Infarction Registry)

The present study investigated the association between C-reactive protein (CRP) on admission independently and in combination with troponin and short-term prognosis in an unselected sample of patients with acute myocardial infarction (AMI) from the community. The study population consisted of 1,646 patients aged 25 to 74 years who were consecutively hospitalized with AMI within 12 hours after symptom onset. They were divided into the 2 groups of CRP positive (n = 919) or CRP negative (n = 727) with respect to admission CRP (cutoff < or =0.3 mg/dl). CRP-positive patients had significantly more in-hospital complications and a higher 28-day case-fatality rate (9.6% vs 3.4%; p <0.0001). Troponin at admission (n = 1,419) also correlated with 28-day case-fatality rate (troponin-negative 3.4% vs troponin-positive patients 8.0%; p <0.002). Multivariable analysis showed that both troponin positivity and CRP positivity were associated with a 2-fold (adjusted odds ratio 1.99, 95% confidence interval 1.15 to 3.44; adjusted odds ratio 2.05, 95% confidence interval 1.09 to 3.84, respectively) increased risk of dying within 28 days after the acute event for all patients with AMI. Stratifying by AMI type showed that in patients with ST-elevation myocardial infarction (STEMI), troponin positivity, but not CRP positivity, independently predicted 28-day case fatality. In patients with non-STEMI, CRP positivity, but not troponin positivity, predicted outcome. In conclusion, admission CRP was a powerful parameter for risk stratification of patients with AMI. Stratification by AMI type and troponin showed that CRP was a better short-term risk predictor for patients with non-STEMI, and troponin was, for patients with STEMI.     

Prognostic significance of troponin T elevation in patients without chest pain

Increased cardiac troponin with chest pain is important for the diagnosis, triage, and treatment of patients in the emergency department. However, the use of troponin for the diagnosis and triage of patients without chest pain is poorly established. The aim of this study was to determine 30-day and 1-year mortality and morbidity of troponin T increases in patients without chest pain. This retrospective study compared 92 hospitalized patients without (study group) and 91 patients with chest pain (control group), followed up for 1 year. Study group patients had troponin T >0.04 mug/L, normal creatine kinase or creatine kinase-MB fraction <5%, and no electrocardiographic ischemia. Excluded were high-risk patients with end-stage kidney disease, those with left ventricular ejection fraction <40%, and the critically ill. Outcome variables included 30-day and 1-year death, myocardial infarction, unstable angina, and coronary revascularization rates. Thirty-day (13.0% vs 4.4%; p = 0.032) and 1-year (33% vs 4.6%; p <0.001) mortality rates were significantly higher in the study group, whereas myocardial infarction, unstable angina, and revascularization were infrequent. In conclusion, patients with increased troponin T and no chest pain had a high mortality rate and required careful follow-up.     

Association of culprit lesion calcium with angiographic and clinical outcomes in patients with ST-elevation myocardial infarction treated with fibrinolytic therapy

Coronary artery calcium has been associated with a greater extent of angiographically significant coronary artery stenoses, but the angiographic and clinical outcomes associated with culprit lesion calcium (CLC) have not been fully evaluated, particularly in the stetting of ST-elevation myocardial infarction. We hypothesized that CLC would be associated with adverse angiographic and clinical outcomes in patients who had ST-elevation myocardial infarction. Data were evaluated in 3,292 patients from 6 trials of fibrinolytic therapy for ST-elevation myocardial infarction; 243 culprit lesions (7.4%) were calcified. CLC was associated with advanced age, history of hypertension, previous coronary artery disease, greater extent of disease, angiographically evident residual thrombus, smaller minimum luminal diameter, and larger percent residual stenosis after fibrinolytic therapy. CLC was associated with lower rates of arterial patency after fibrinolytic therapy (63.3% vs 81.3% p <0.001), lower rates of Thrombolysis In Myocardial Infarction grade 3 flow (41.5% vs 57.2%, p <0.001), and higher (slower) Thrombolysis In Myocardial Infarction frame counts (52 vs 36 frames, p <0.0001, multivariate p = 0.02). CLC was also associated with increased 30-day mortality rates (6.2% vs 3.4%, p = 0.028) and 30-day rates of death, myocardial infarction, or congestive heart failure (16.5% vs 8.9%, p <0.001) and independently associated with 30-day rates of death, myocardial infarction, or congestive heart failure (odds ratio 1.6, p = 0.016) after multivariate adjustment for baseline clinical and lesion characteristics, epicardial flow, and performance of rescue/adjunctive percutaneous coronary intervention. In a model restricted to patients who had successful restoration of epicardial patency after fibrinolytic therapy, CLC was independently associated with 30-day mortality (odds ratio 2.2, p = 0.045). CLC is independently associated with indexes of poorer epicardial flow and a higher incidence of adverse clinical outcomes after fibrinolytic administration in patients who have ST-elevation myocardial infarction.     

Time to Positivity of a Rapid Bedside Assay for Cardiac-Specific Troponin T Predicts Prognosis in Acute Coronary Syndromes: A Thrombolysis in Myocardial Infarction (TIMI) 11A Substudy

Objectives. We sought to determine whether the rapid bedside assay for troponin T identified patients at risk for a more complicated hospital stay and a higher rate of adverse clinical events.Background. In patients with an acute coronary syndrome, the amount of cardiac-specific troponin T released bears a stoichiometric relation to the extent of myocardial damage.Methods. In 597 patients with unstable angina or non–Q wave myocardial infarction participating in the Thrombolysis in Myocardial Infarction (TIMI) 11A substudy, a rapid bedside assay and simultaneous quantitative serum measurement for troponin T were obtained at enrollment.Results. The composite end point of the sum of death, nonfatal myocardial infarction or recurrent ischemia through day 14 occurred in 33.6% of patients with a positive assay compared with only 22.5% of patients with a negative assay (p = 0.01). Those patients in whom the rapid assay became positive in ≤10 min had the highest mortality rate of 4.2% through day 14 compared with 1.1% in those patients who had either a late-appearing positive assay (>10 min) or a negative assay. The duration of hospital stay in the 116 patients (19%) with a positive rapid assay at enrollment was a median of 5 days compared with only 3 days in the 481 patients (81%) with a negative rapid assay at enrollment (p = 0.002).Conclusions. A positive rapid assay for troponin T at presentation identifies those patients at risk for higher rates of adverse clinical events and longer, more complicated hospital stays. Stratification of patients by time to development of a positive rapid assay identifies those patients at highest mortality risk.