Prognosis In Unstable Angina Research Articles

Unstable Angina Risk Stratification Using High-Sensitivity Cardiac Troponin and Coronary Angiography

Patients formerly diagnosed with unstable angina (UA) are being reclassified as non-ST-elevation myocardial infarction (NSTEMI) with the widespread adoption of sensitive troponin assays (hsTn), leading to significant changes in the incidence and prognosis of UA. The main purpose of this study was to evaluate the value of hsTn and the presence of significant obstructive CAD in the risk stratification of patients with unstable angina. We conducted a retrospective, single-centre study of 742 patients hospitalized for UA between 2016-2021. The primary endpoint of this study was all-cause mortality. The secondary outcome (MACE) was defined as a composite of nonfatal myocardial infarction (MI), hospitalization for heart failure (hHF), and repeated coronary angiography due to recurring UA (rUA) after the index event. Outcomes were assessed within one month, one year, and up to 5 years of follow-up. The average follow-up duration was 45±24 months, and 37.2% (N=276) of patients completed a 5-year follow-up. No in-hospital death was observed, and 6.9% of patients died during follow-up, which was more commonly a late event (>12 months). The composite secondary endpoint (MI+hHF+rUA) was observed in 16.7% of the patients. There was 3.2% nonfatal MI, 2.3% hHF, and 11.6% rUA during follow-up. We developed a risk model (UA Mortality Risk) using variables with the highest discriminatory power: age, hsTn, and ST-segment deviation. Our model performed well against the GRACE and TIMI risk scores in predicting death during follow-up. Obstructive CAD on coronary angiography was the only independent predictor of MACE during follow-up. In conclusion, a contemporary cohort of patients with UA presented with favourable prognosis, particularly within the first year after the index event. Non-significant increases in HsTn levels add to the risk stratification of UA patients, and the presence of obstructive CAD was the only independent predictor of MACE, highlighting the potential importance of assessing coronary anatomy.

Comparison of ticagrelor and clopidogrel on platelet function and prognosis in unstable angina

PurposeThis study aims to compare the effects of ticagrelor and clopidogrel on platelet function, cardiovascular prognosis, and bleeding in patients with unstable angina pectoris.MethodsPatients with unstable angina pectoris undergoing percutaneous coronary intervention (PCI) were enrolled (January 2018–December 2019). In total, 212 patients were treated with ticagrelor (90 mg twice daily) and 210 patients were treated with clopidogrel (75 mg once daily). Thromboelastography and light transmission aggregometry were used to measure the platelet aggregation rate (PAR). High-sensitivity troponin T (hs-TnT), pro-brain natriuretic peptide (NT-proBNP), high-sensitivity C-reactive protein (CRP), and heart-type fatty acid–binding protein (h-FABP) were measured to assess myocardial injury after PCI. Cardiovascular prognosis and bleeding events were evaluated in hospital and 12 months after discharge.ResultsThe PAR was significantly slower with ticagrelor (P < 0.001). hs-TnT, NT-proBNP, CRP, and h-FABP increased after compared with before PCI in both groups (P < 0.05). hs-TnT (P < 0.001) and h-FABP (P < 0.001) increased more significantly with clopidogrel. The in-hospital and 12-month major adverse cardiovascular event (MACE) rates were not significantly different between the two groups. The in-hospital total bleeding event rate was higher with ticagrelor (P < 0.05). Minor bleeding and total bleeding were more frequent at the 12-month follow-up in the ticagrelor group (P < 0.05).ConclusionTicagrelor was more effective in suppressing the PAR than clopidogrel and reduced PCI-induced myocardial injury in patients with unstable angina pectoris. However, it increased in-hospital and 12-month bleeding events and had no benefit on in-hospital and 12-month MACEs.

P5525Impact of clinical presentation at admission on long-term clinical outcomes in patients undergoing percutaneous coronary interventions - a contemporary registry data

Abstract Background Both unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI) are still classified together in non-ST-elevation acute coronary syndromes despite the fact they substantially differ in both clinical profile and prognosis. Purpose The aim of the present study was to evaluate contemporary clinical characteristics and outcomes of UA patients after percutaneous coronary intervention (PCI) in comparison with stable angina (SCAD) and myocardial infarction (NSTEMI as well as STEMI) in Swietokrzyskie District of Poland in years 2014–2017. Methods A total of 7'187 patients after PCI from ORPKI Registry (38% with diagnosis of UA) were included into the analysis. Impact of clinical presentation (UA, SCAD, NSTEMI, STEMI) on 3-year outcomes were determined. Results UA patients were older that SCAD but younger than NSTEMI individuals. Diabetes and hypertension were more often encountered into UA group than in NSTEMI but less often than in SCAD cases. In UA group the percentage of previous myocardial infarction (MI), PCI or coronary artery bypass grafting (CABG) was the highest among all analyzed groups. In 3-year observation the risk of death as well as myocardial infarction (MI) and major adverse cardiac events (MACE) in unstable angina after PCI was higher than in stable angina but considerably lower than in NSTEMI group. Multivariate analysis confirmed that prognosis in NSTEMI was substantially worse in comparison with UA (RR 1.365, 95% CI: 1.126–1.655, p=0.0015). On the contrary there were no difference in mortality risk between UA and SCAD patients (RR 1.189, 95% CI: 0.932–1.518, p=0.1620). Parallel results were observed in respect of MI and MACE. Independ predictors of death were: age, kidney disease, hypertension, diabetes, previous stroke or previous PCI. Multivariate logistic regression analyse Clinical presentation Death Myocardial infarction MACE RR 95% CI p-value RR 95% CI p-value RR 95% CI p-value NSTEMI/UA 1.365 1.126–1.655 0.0015 1.822 1.076–3.055 0.0260 1.514 1.267–1.807 &lt;0.0001 NSTEMI/SCAD 1.624 1.251–2.109 0.0003 1.882 0.982–3.789 0.0568 1.604 1.275–2.094 &lt;0.0001 UA/SCAD 1.189 0.932–1.518 0.1620 1.033 0.557–2.034 0.9219 1.060 0.855–1.323 0.6023 MACE, major adverse cardiac events; NSTEMI, non-ST-segment elevation myocardial infarction; UA, unstable angina; SCAD, stable angina. Conclusion Unstable angina accounted for 38% of all cases and was the most common diagnosis in patients that underwent PCI in that time. 3-year prognosis in UA was considerable better in comparison with NSTEMI. On contrary there was no difference in outcomes (death, MI, MACE) between UA and SCAD patients.

Level of C-Reactive Protein in Prognosis of Unstable Angina and Non St Elevation Myocardial Infarction

Level of C-Reactive Protein in Prognosis of Unstable Angina and Non St Elevation Myocardial Infarction

MiR-28-5p Involved in LXR-ABCA1 Pathway is Increased in the Plasma of Unstable Angina Patients

Previous studies confirmed that the intronic miRNAs participated in regulating host gene-primed biological processes. The coordinated roles of miR-28 with its host gene, LIM domain lipoma-preferred partner (LPP), remain unknown in atherosclerosis. In this study, we determined to assess circulating levels of miR-28-5p in unstable angina patients, compared with age- and sex- matched control subjects by quantitative PCR. Furthermore, we attempted to explore whether miR-28-5p could influence the expression of ATP-binding cassette transporter A1 (ABCA1) and liver X receptor (LXR), major mediators of high density lipoprotein (HDL) synthesis and transportation in hepatic cells and macrophages. It was found that plasma levels of miR-28-5p were significantly increased in unstable angina patients with or without type 2 diabetes mellitus. Notably, miR-28-5p upregulated ABCA1 expression at transcription and translation levels, strongly correlated with translational activation of LXRα in HepG2 and THP-1-derived macrophages. Our findings suggest that circulating miR-28-5p, involved in LXRα-ABCA1 pathway, may be a potential biomarker for diagnosis and prognosis of unstable angina.

Mean Platelet Volume and Prognosis of Unstable Angina

Objective: Clopidogrel therapy is the standard of care in patients with unstable angina. However, a percentage of subjects are nonresponders to clopidogrel and this leads to increased adverse outcome. On the other way round, some responsive patients are exposed to bleeding complications. Detection of both in daily practice is important in order to tailor the treatment protocol. In this study we aimed to estimate the cutoff value of mean platelet volume (MPV) for both platelet responsiveness and bleeding risks. Methods: The study was planned as a prospective cohort study. A total number of 230 patients admitted to our CCU with unstable angina over a period of one year (from June 2013 to May 2014) were enrolled. Exclusion criteria were: severe anemia, throm-bocytopenia, myelodysplastic syndrome, coagulopathy and recent blood transfusion. In all patients clopidogrel was initially started and maintained during the hospital stay. Blood (2 ml) was collected in dipotassium EDTA tubes from all patients on the first day of admission by a clean puncture. Samples for MPV analysis were drawn on admission, and analyzed within 1 hour of admission after sampling by Beckman Caulter LH 780 Analyzer. Grouping was then done according to MPV of the patients into group (I) who had a low MPV less than or equal to 7.00 fl, and group (II) with MPV equal to or higher than 9.00 fl. Demographical and clinical variables of the patients were recorded. Routine laboratory parameters were also recorded. Clinical manifestations during the admission period were meticulously reported. Major complications as bleeding or, urgent need for percutaneous coronary intervention (PCI) were also studied. Results: Among the 230 patients analyzed, 175 patients (76%) were found to have MPV ≤7.00 fl (group (I)) and 55 patients (24%) had MPV ≥9.00 fl (group (II)) with mean ± SD MPV (8.4 ± 1.5 fl, vs 11.7 ± 1.2 fl respectively) (p < 0.001). Observation of clinical course during admission period revealed a statistically more significant clinical deterioration in group (II) than group (I) and the presence of more frequent AMI cases in group (II) having a high MPV. A high cutoff value of 9.7 fl for MPV was detected in prediction of clopidogrel nonresponsiveness (group (II)) with a sensitivity of 78.2% and specificity of 66.8%, and a low cutoff value for bleeding tendency lower than 6.3 fl was detected in group (I) with a sensitivity of 71.4% and specificity of 62.5%. Conclusion: This study showed that MPV can be used as a simple bedside predictor for detection of clopidogrel response in patients with unstable angina. And a cutoff value for both platelet responsiveness and risk of bleeding is now reached. This may lead to enhancement in our decision for early intervention and attention for bleeding risk during clopidogrel therapy.

1059G/C polymorphism within the exon 2 of the C-reactive protein gene: relationship to C-reactive protein levels and prognosis in unstable angina

Patients with unstable angina (UA) and high C-reactive protein (CRP) have increased cardiovascular risk. Whether genetic factors such as the synonymous 1059G/C polymorphism within the exon 2 of the human CRP gene determine CRP levels and outcome is unclear. In 105 consecutive patients with UA, we assessed the CRP 1059G/C polymorphism, CRP plasma levels and interleukin-6 production after in-vitro stimulation of whole blood with lipopolysaccharide (1 ng/ml). Coronary events during a 24-month follow-up were recorded. CRP levels (median, range) were significantly lower among C-allele carriers (2.3 mg/l, 0.5-26.9) than among GG homozygotes (5.9 mg/l, 0.8-72.12, P=0.009). Interleukin-6 production was lower in C-allele carriers (1645 pg/ml, 832.0-9522) than in GG homozygotes (3929 pg/ml, 670.8-10 582), (P=0.085). At follow-up, 1059C-allele carriers experienced fewer coronary events than 1059GG homozygotes (13 vs. 47%, P=0.021). At multivariable analysis, a CRP level >3 mg/l, but not the 1059G/C polymorphism, was an independent predictor of coronary events (odds ratio 10.04, 95% confidence interval 2.84-35.44, P=0.0002). This study shows that the CRP synonymous 1059G/C polymorphism affects CRP levels. No independent association was, however, observed between this polymorphism and clinical outcome in UA.

Interleukin-6 and the Risk of Future Cardiovascular Events in Patients With Angina Pectoris and/or Healed Myocardial Infarction

The aim of this study was to evaluate the prognostic value of interleukin-6 (IL-6) for myocardial infarction (MI) and mortality in a population with stable coronary artery disease (CAD) during a mean period of 6.3 years. IL-6 is a major proinflammatory cytokine of acute phase response; elevated levels are associated with worse prognosis in unstable angina and after acute MI. However, data regarding its long-term prognostic value in stable CAD are limited and controversial. A nested case-control study design was used. Of 3,090 patients with stable CAD, 129 with an adequate blood sample for IL-6 and who reached the end points (MI or sudden death) were randomly selected. Each case was 1:1 matched with 129 controls (alive at the end of the study and free of cardiovascular events) according to age, gender, and treatment. Of the 129 cases, 113 had a MI as the initial event, and for the other 16 the initial event was sudden death. There were 8 patients who first had a MI and later died suddenly. IL-6 was significantly higher in cases (2.34 pg/ml) than in controls (1.65 pg/ml) (p = 0.0004). IL-6 was significantly correlated with C-reactive protein (r = 0.2, p = 0.002); a borderline significance was also found for fibrinogen (r = 0.11, p = 0.07). Each increase of 1 pg/ml in IL-6 was associated with a 1.70 (range 1.23 to 2.45) increased relative odds of subsequent MI or sudden death. Events rate per 1,000 patients-years for the 5 quintiles of IL-6 were 72.26, 89.61, 79.76, 142.53, and 181.08, respectively (p <0.0001). A significantly higher risk in the upper quintile was found (odds ratio, 3.44; 95% confidence interval 1.57 to 8.13). In conclusion, elevated IL-6 levels are strongly associated with future cardiac events and mortality in a population with stable CAD during a long-term follow-up.

Chlamydia pneumoniae in the atherosclerotic plaques of patients with unstable angina undergoing coronary artery bypass grafting: does it have prognostic implications?

Objective: This study sought to evaluate the prognostic significance of the presence of DNA of Chlamydia pneumoniae in the coronary atherosclerotic lesions of patients with unstable angina. Background: C. pneumoniae has been implicated in the pathogenesis of coronary artery disease by serological and pathological studies, but whether antichlamydial antibodies and the presence of this pathogen in the coronary atherosclerotic tissue are related to prognosis in unstable angina remains unclear. Methods: A total 76 coronary specimens from 45 patients with unstable angina undergoing bypass surgery were subjected to nested polymerase chain reaction (PCR) for C. pneumoniae. Antichlamydial immunoglobulin G (IgG), A (IgA) and M (IgM) were also examined by an enzyme immunoassay. Patients were followed during a 2-year period to determine the incidence of adverse cardiovascular events. Results: DNA of C. pneumoniae was detected in 57 (75%) of 76 atherosclerotic lesions: 39 patients showed a positive PCR result in at least one plaque. Of the 45 patients, 44 (97.7%) showed a positive serological result: IgG was positive in 39 (86.6%) patients, IgM in five (11.1%) patients and IgA in 42 (93.3%). Clinical characteristics and serologic results were similarly distributed in patients with and without infected lesions at enrollment. At least one adverse event occurred in 21 (46.6%) of the 45 patients at 2 years: death in nine (20%), recurrent angina in 12 (26.6%), revascularization in six (13.3%) and myocardial infarction in two (4.4%) patients. The composite endpoint of death, myocardial infarction, recurrent angina and revascularization at 2-year follow-up did not differ according to the PCR or serologic results. Conclusions: The presence of C. pneumoniae in coronary atherosclerotic plaques of patients with unstable angina undergoing coronary bypass grafting does not have prognostic significance. In addition, serology does not allow us to differentiate those patients with plaque infection by C. pneumoniae and also does not provide any prognostic information in these patients.

Elevated concentrations of macrophage colony stimulating factor predict worse in-hospital prognosis in unstable angina

Elevated concentrations of macrophage colony stimulating factor predict worse in-hospital prognosis in unstable angina

Antibodies to chlamydial lipopolysaccharides in unstable angina pectoris

Patients with coronary artery disease frequently have elevated antibody titers against Chlamydia pneumoniae, but whether antichlamydial antibody titers are correlated with prognosis in unstable angina remains unclear. We therefore investigated the sera of 1,096 patients with unstable angina regarding immunoglobulin (Ig) IgG, IgA, and IgM antibody titers against chlamydial lipopolysaccharides (LPS) and the concentrations of C-reactive protein (CRP) and troponin T (TnT). Anti-LPS IgG titers were increased in 45% of patients at enrollment and in 48% of patients at discharge (p <0.0001). Anti-LPS IgA titers were increased in 27% of patients at enrollment and in 33% of patients at discharge (p <0.0001). Patients who subsequently died had significantly lower IgM titers at enrollment than patients without events (p = 0.016). IgG, IgA, or IgM titers did not correlate with concentrations of CRP or TnT. In this large-scale study of patients with unstable angina, we frequently found elevated antichlamydial antibody titers. Patients with low IgM anti-LPS titers were at risk for subsequent death. However, there was no correlation between antichlamydial antibody titers and CRP or TnT.

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. (Am Heart J 2001;141:780-3.)

Depression and 1-Year Prognosis in Unstable Angina

Depression is common after acute myocardial infarction and is associated with an increased risk of mortality for at least 18 months. The prevalence and prognostic impact of depression in patients with unstable angina, who account for a substantial portion of acute coronary syndrome admissions, have not been examined. Interviews were carried out in hospital with 430 patients with unstable angina who did not require coronary artery bypass surgery before hospital discharge. Depression was assessed using the 21-item self-report Beck Depression Inventory and was defined as a score of 10 or higher. The primary outcome was 1-year cardiac death or nonfatal myocardial infarction. The Beck Depression Inventory identified depression in 41.4% of patients. Depressed patients were more likely to experience cardiac death or nonfatal myocardial infarction than other patients (odds ratio, 4.68; 95% confidence interval, 1.94-11.27; P<.001). The impact of depression remained after controlling for other significant prognostic factors, including baseline electrocardiographic evidence of ischemia, left ventricular ejection fraction, and the number of diseased coronary vessels (adjusted odds ratio, 6.73; 95% confidence interval, 2.43-18.64; P<.001). Depression is common following an episode of unstable angina and is associated with an increased risk of major cardiac events during the following year.

Elevated C-Reactive Protein Predicts Prognosis in Unstable Angina

C-reactive protein (CRP) is a marker for inflammation that has been shown to predict increased long-term cardiovascular risk in patients with and

Clinical predictors of in-hospital prognosis in unstable angina: ECLA 3

Objectives Because of recent changes in the treatment of unstable angina, we wanted to reassess the short-term prognostic value of clinical and echocardiographic variables. Methods This was an observational, prospective study that included 1038 nonselected consecutive patients admitted to coronary care units for unstable angina. Results Baseline characteristics were age 60.18 ± 16 years, history of prior myocardial infarction in 336 patients (32%), and a history of previous angina in 817 patients (78.7%). Angina during the 48 hours before admission was observed in 1004 patients (96.7%) and ST-segment changes on admission electrocardiogram occurred in 385 patients (37%). In-hospital treatment consisted of nitrates in 81.4% of patients, aspirin in 88.6%, β-blockers in 71%, intravenous heparin in 34.5%, subcutaneous heparin in 23%, and angioplasty or coronary artery bypass grafting in 25.1%. After admission, angina occurred in 443 patients (40.8%), refractory angina in 223 patients (21.5%), and death or myocardial infarction in 84 patients (8.1%). At admission, the independent predictors of myocardial infarction or death identified by multivariate logistic regression analysis were ST-segment depression (odds ratio [OR] 2.13, 95% confidence interval [CI] 1.23 to 3.68, P =.006), prior angina (OR 2.23, 95% CI 0.98 to 5.05, P =.05), number of episodes of angina within the previous 48 hours (OR 1.63, 95% CI 0.98 to 2.70, P =.05), and history of smoking (OR 0.69, 95% CI 0.56 to 0.85, P =.004). Age greater than 65 years (OR 1.49, 95% CI1.09 to 2.03, P = 0.03) was significantly related to in-hospital death. The area under the receiver operating characteristic curve for application of this model was 0.59. Sensitivity was 80% with a specificity of only 33%. Refractory angina after admission showed a strong relation with an adverse short-term outcome. Conclusions With current therapy, clinical and electrocardiographic variables provide useful information about the short-term outcome of unstable angina. However, this model has low specificity to identify high-risk patients. Future studies about the incremental value of the new serum markers such as troponin T and C-reactive protein to assist in identification of high-risk patients are necessary. (Am Heart J 1999;137:322-31.)

Recent advances in the management of unstable angina and non-Q-wave myocardial infarction

Recent advances in the management of unstable angina and non-Q-wave myocardial infarction

Acute coronary syndromes: unstable angina and non-Q-wave myocardial infarction.

Ischemic heart disease includes a wide spectrum of conditions, ranging from silent ischemia and exertion-induced angina, through unstable angina, to acute MI. Unstable angina occupies the center of this spectrum, causing disability and risk greater than that of chronic stable angina but less than that of acute MI1 (Fig 1⇓). Although non–Q-wave MI for many years was considered prognostically similar to unstable angina, recent longitudinal studies indicate that it is similar to Q-wave infarction2 3 (Fig 2⇓). Figure 1. Cumulative 6-month mortality from ischemic heart disease. Diagnosis on admission to hospital (n=21 761; 1985 to 1992). From Duke Cardiovascular Database. Reproduced with permission from Reference 1. Figure 2. Top, Cumulative 1-year combined death or MI among patients with Q-wave and non–Q-wave MI treated with fibrinolysis. Reproduced with permission from Reference 2. Bottom, Risk of subsequent cardiac events in stable convalescing patients after first non–Q-wave and Q-wave MI. Reproduced with permission from Reference 3. The concept of unstable angina has emerged from observations of frequent symptoms preceding acute MI, followed by prospective documentation that unstable symptoms frequently culminated in acute MI. The syndrome was rapidly accepted as a well-defined clinical entity as specific clinical manifestations, pathophysiological mechanisms, laboratory findings, and treatment became better characterized. Unstable angina is currently one of the leading causes of hospital admission for CAD, and non–Q-wave MI accounts for >30% of admissions for acute MI.1 4 Yet, the diagnosis of unstable angina remains clinical, based on symptom recognition. The physician caring for patients with unstable angina is in a privileged position of recognizing rapidly evolving CAD and being able to intervene to prevent irreversible left ventricular damage and progression of CAD. Unstable angina is classically described as a heterogeneous disease, referring to a wide spectrum of clinical manifestations from stable angina to MI, of disease …

Long-term prognosis in unstable angina. The importance of early risk stratification using continuous ST segment monitoring.

To assess the ability of clinical characteristics, admission ECG and continuous ST segment monitoring in determining long-term prognosis in unstable angina. Two hundred and twelve patients with unstable angina (mean age 59 years), presenting within 24 h of an acute episode of angina were recruited at three hospitals and treated with standardized medical therapy. All patients kept chest pain charts and underwent ST segment monitoring for 48 h. The occurrence of death, myocardial infarction, and need for revascularization was assessed over a median follow-up of 2.6 years. The risk of death of myocardial infarction was greatest in the first 6-8 weeks after admission. Admission ECG ST depression and the presence of transient ischaemia predicted increased risk of subsequent death or myocardial infarction, whereas a normal ECG predicted a good prognosis. In 14 patients, ST segment monitoring provided the only evidence of recurrent ischaemia, and 72% of this group suffered an adverse event. Transient ischaemia and a history of hypertension were the most powerful independent predictors of death or myocardial infarction. Adverse events in unstable angina occur early after admission and can be predicted by clinical and ECG characteristics, and by the presence of transient ischaemia during ST segment monitoring. Risk stratification by these simple assessments can identify patients with unstable angina at high risk.

Depression influences 1-year prognosis in unstable angina

Depression influences 1-year prognosis in unstable angina

Prognostic influence of elevated values of cardiac troponin I in patients with unstable angina.

Elevations of the MB isoform of creatine kinase (CK) and cardiac troponin T seem to confer an adverse prognosis in unstable angina. We examined whether this prognostic influence is also present for cardiac troponin I (cTnI), a new and even more specific marker of myocardial injury. We studied 106 patients with the clinical diagnosis of unstable angina showing chest discomfort at rest within 48 hours of admission, ECG evidence of myocardial ischemia, and normal values of total CK over the initial 16 hours of observation. The primary end point was death or nonfatal myocardial infarction (MI) at 30 days; the secondary end point was the incidence of cardiac events at 1 year. Blood was drawn every 8 hours for 3 days. Thirteen patients were excluded because of increased CK-MB mass concentrations within 16 hours of admission (non-Q-wave MI) and 2 because of inadequate blood sampling. Of the remaining 91 patients, 22 had cTnI elevations on admission (n=7) or after 8 hours (n=15). At 30 days, no deaths (0%) and 4 MIs (5.8%) occurred in the 69 patients with normal cTnI compared with 2 deaths (9.1%) and 4 MIs (18.2%) in the 22 patients with elevated cTnI. The combined incidence of death and nonfatal MI was 5.8% and 27.3%, respectively (P=.02). At 1 year, only 68% of patients with elevated cTnI were free of cardiac events, compared with 90% of those without elevations (P=.01). These data indicate that cTnI is an important prognostic variable in patients with unstable angina. Elevations of cTnI predict an adverse short- and long-term prognosis.