不稳定型心绞痛患者TIMI危险评分与冠状动脉病变严重程度相关

目的探讨心肌梗死溶栓（TIMI）危险积分与不稳定型心绞痛（UA）患者冠状动脉病变严重程度的相关性。方法对102例UA患者分别进行TIMI危险积分评估和冠状动脉造影,以TIMI评分差异分组,分析不同TIMI危险积分与冠脉狭窄程度、病变血管范围、病变性质的相关性。结果TIMI危险积分与冠脉狭窄程度、病变血管范围、病变性质积分均有良好的相关性,TIMI危险积分越高,冠脉病变越重。结论TIMI危险积分可以用来评价UA患者当前冠脉病变的严重程度。     

Continuous multilead ST-monitoring identifies patients with unstable coronary artery disease who benefit from extended antithrombotic treatment.

AIMS: Prolongation of anticoagulant treatment might reduce subsequent cardiac events in patients with unstable coronary artery disease. Multilead ST-segment monitoring identifies patients with a high risk of adverse outcome. The aim was to assess the value of multilead ST-monitoring in prospectively identifying patients who respond to extended anticoagulant treatment with low-molecular weight heparin when treated by a primarily non-invasive strategy. METHODS AND RESULTS: In this substudy of the FRISC II trial, ST-monitoring with a continuous 12-lead ECG or vectorcardiography was performed for 24 h in 629 patients with unstable coronary artery disease randomized to receive either the low-molecular weight heparin dalteparin, or placebo for 3 months after at least 5 days' dalteparin treatment in all patients. Ischaemic episodes were detected in 34% during ST-monitoring. In the group with ischaemic episodes, the extended dalteparin treatment was associated with a lower rate of death, myocardial infarction, or revascularization (35.2% vs 53.4%, relative risk reduction: 34%, P=0.01). In patients without ischaemic episodes, long-term dalteparin treatment had no effect. CONCLUSIONS: In patients with unstable coronary artery disease treated primarily with a non-invasive strategy, ischaemic episodes revealed while on multilead ST-monitoring identifies patients who benefit most from extended treatment with anticoagulants.     

A critical review of clinical trials for low-molecular-weight heparin therapy in unstable coronary artery disease.

Unstable angina and non-ST-segment elevation myocardial infarction (MI) are collectively referred to as unstable coronary artery disease (UCAD). They are conditions that share a common pathophysiology and represent frequently encountered, potentially life-threatening clinical manifestations of advanced atherosclerosis. Therefore, treatment of UCAD is a major focus for practicing clinicians, and although pharmacologic agents have been developed that impact on patient outcome, recent data suggest that a further reduction in ischemic complications is possible. Acute-phase treatment with aspirin is associated with a significant reduction in death and nonfatal MI in patients with UCAD. This benefit is enhanced by the addition of unfractionated heparin (UFH) to the treatment strategy; however, UFH requires careful monitoring and titration. In contrast, low-molecular-weight heparins (LMWHs), produced by chemical or enzymatic depolymerization of UFH, yield a predictable and consistent pharmacokinetic profile and anticoagulant response, making them an attractive treatment alternative to UFH in patients with UCAD. The optimal duration of treatment with LMWH is an important question influenced by the observation that reactivation of coagulation occurs following the early and abrupt discontinuation of heparin treatment. Early trials, such as FRISC and FRIC, demonstrated the benefit of acute therapy with dalteparin sodium; however, the results of extended treatment with dalteparin were inconclusive. The extended phase of these studies included relatively low-risk patients, and a once-daily, relatively low-dose strategy was employed. The findings derived from the FRISC II trial, which used a twice-daily dose of dalteparin, suggest a benefit for at least 60 days with extended treatment in high-risk patients with UCAD. Although an early-invasive treatment strategy is particularly beneficial, patients in whom early revascularization is not possible should be considered for extended treatment with dalteparin for up to 45 days, especially those awaiting percutaneous coronary intervention. Extended treatment with dalteparin therefore provides a protective "bridge" to enhance the outcome of patients with UCAD awaiting revascularization.     

Very early risk stratification by electrocardiogram at rest in men with suspected unstable coronary heart disease

Abstract. Objectives. To determine the possibility of very early prognostic stratification based on electrocardiograms (ECGs) at rest and/or cardiac enzyme levels after an episode of suspected unstable coronary heart disease. Design and setting. Men with suspected unstable angina or non-Q-wave myocardial infarction were studied in the coronary care units of eight hospitals. The ECGs at rest and creatinine kinase were followed. Subjects. In total 911 men were followed for 12 months. Of 8136 consecutively admitted, 3365 fulfilled the inclusion criteria. Excluded were 2454 patients, mainly because of a larger myocardial damage, signs of myocardial dysfunction, other serious cardiac or non-cardiac disease or an ECG not possible to interprete regarding ST-T-segment changes in the precordial leads. Main outcome measures. End-points at follow-up were cardiac death, myocardial infarction and severe (class III or IV) angina. Results. Compared to patients with normal a ECG who had an 8% 1-year risk of myocardial infarction or death, the risk with isolated negative T waves was 14% (P < 0.05), ST elevation 16% (P < 0.05), ST depression 18% (P < 0.01) and the combination of ST elevation and ST depression 26% (P < 0.001). The only finding related to future severe angina was ST depression. The risk of cardiac events was comparably elevated in patients with anterior or inferior site of ECG changes. Cardiac enzyme levels had no predictive value regarding future events. Conclusions. Electrocardiograms at rest obtained during the initial days of hospitalization provide very early and valuble prognostic information in men admitted with suspected unstable coronary heart disease.     

Influence of prolonged dalteparin treatment on coagulation, fibrinolysis and inflammation in unstable coronary artery disease

BACKGROUND. Unstable coronary artery disease (CAD) is a multi-factorial disease involving thrombotic and inflammatory processes. Short-term low molecular weight (LMW) heparin treatment reduces coagulation activity and clinical events. We investigated the influence of prolonged treatment on coagulation, fibrinolysis and inflammation. METHODS AND RESULTS. Serial blood samples were obtained from 555 of 2,267 unstable CAD patients in the FRISC II study. Patients were treated with the LMW heparin dalteparin 120 IU kg(-1) s.c. twice daily for 5-7 days and randomized to placebo (n=285) or gender and weight-adjusted doses of dalteparin (5,000 or 7,500 IU) twice daily (n=270) for 3 months. Dalteparin persistently depressed coagulation activity with, when compared with placebo, lower median levels of factor VIIa (63 IU mL(-1) vs. 84 IU mL(-1)), prothrombin fragment 1 + 2 (0.86 nmol L(-1) vs. 1.09 nmol L(-1)) and D-dimer (21 microg L(-1) vs. 43 microug L(-1)) after 3 months, all P<0.01. Reactivation of coagulation activity was observed after cessation of both short-term and prolonged dalteparin treatment. Higher levels of tPA/PAI-1 complex (11.7 microg L(-1) vs. 6.5 microg L(-1), P<0.001) and von Willebrand factor (162% vs. 136%, P<0.001) were found during prolonged dalteparin treatment. Interleukin-6, C-reactive protein and fibrinogen levels were unaffected by dalteparin treatment. CONCLUSIONS. Three months dalteparin treatment resulted in a sustained and pronounced reduction of coagulation activity, which corresponds to the observed reduction in death and myocardial infarction during the initial 6 weeks in the FRISC II study. The persistently elevated levels of tPA/PAI-1 complex and von Willebrand factor might reflect effects on platelets and endothelial cells and thus contribute to the gradually decreased efficacy by prolonged dalteparin treatment in unstable CAD.     

Increased fibrinogen levels are associated with persistentChlamydia pneumoniaeinfection in unstable coronary artery disease

Aim Increased levels of acute phase proteins, e.g. fibrinogen, arerelated to a poor outcome in unstable coronary artery disease,but the cause of inflammation is unknown. We therefore investigatedthe prevalence of persistent Chlamydia pneumoniae infection,and its relationship to inflammation in this condition. Methods and Results In 256 patients participating in the FRISC trial, evaluatingthe effects of dalteparin (a low molecular weight heparin) inunstable angina or non-Q wave myocardial infarction, Chlamydiapneumoniae IgA antibody titres and levels of fibrinogen, C-reactiveprotein and troponin T were determined at inclusion. IncreasedC. pneumoniae IgA antibody titres were significantly more commonin the patients (36%) than in a reference popu-lation of similarage (19%); P<0·001. Raised titres were associatedwith male gender, increasing age, smoking, and elevated concentrationsof fibrinogen, C-reactive protein and troponin T. The associationbetween persistent C. pneumoniae infection and increased fibrinogenlevels was independent of other risk factors evaluated in multivariateanalysis (P=0·009). Conclusion Persistent C. pneumoniae infection is common in unstable coronaryartery disease. The independent association between increasedC. pneumoniae IgA antibody titres and fibrinogen levels indicatesthat chronic infection could be of importance for disease activity.     

Cost-effectiveness of an invasive strategy in unstable coronary artery disease; results from the FRISC II invasive trial. The Fast Revascularisation during InStability in Coronary artery disease.

AIMS: The utilization and timing of revascularization in unstable coronary artery disease varies, which could have important consequences for patients and for treatment costs. The FRISC II invasive trial compared an early invasive strategy vs a non-invasive strategy with respect to the composite end-point of death and myocardial infarction as well as costs. METHODS AND RESULTS: A total of 2457 patients, median age 66 years, comprising 70% men, were randomized. We prospectively recorded the patients' use of the health service. The results were analysed in a societal perspective. There was a significant 1.7% absolute reduction in deaths and a 3.7% absolute reduction in deaths and myocardial infarctions in the invasive compared to the non-invasive group after 12 months. During the initial hospitalization a patient in the invasive group spent on average 3.9 more days in hospital than a patient in the non-invasive group. Opposite results were found for rehospitalizations. The difference in mean total costs is SEK 23 876 (P<0.001). The incermental cost-effective ratio for choosing the invasive instead of the non-invasive strategy is SEK 1 404 000 per avoided death and SEK 645 000 per avoided death or myocardial infarction. CONCLUSION: The high cost at the beginning of the invasive strategy is substantial. The clinical results of the FRISC II study provided evidence that the invasive strategy reduces the rate of death and myocardial infarction in patients with unstable coronary artery disease. For policy discussions concerning whether or not to implement the invasive strategy, these positive results should be balanced against the cost-consequences of the strategy.     

Brugada phenocopy in a patient with unstable angina and three-vessel coronary artery disease

A 52-year-old male was admitted with unstable angina and three-vessel coronary artery disease. Electrocardiography (ECG) changes consistent with type-1 Brugada ECG pattern were noted during admission. The patient was asymptomatic for syncope and had no family history of sudden cardiac death, ICD implantation, and Brugada syndrome. After coronary by-pass graft the Brugada ECG pattern resolved, and ajmaline test did not elicit type-1 ECG pattern, confirming the suspicion of Brugada phenocopy.     

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

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

D-二聚体定量检测对判定不稳定性心绞痛血栓成分的临床意义

目的 :探讨 D-二聚体检测在判定不稳定性心绞痛 （UAP）血栓成分的价值及临床意义。方法 :选择住院按亚型诊断、分组的 UAP患者 5 6例 ,急性心肌梗死 （AMI）患者 16例 ,稳定性心绞痛 （SAP）患者 2 3例 ,采用胶体金方法动态检测患者静脉血中的 D-二聚体含量。结果 :UAP亚组中 D-二聚体含量 :初发型 0 .73± 0 .31mg/ L ;恶化型 1.0 8± 0 .36 mg/ L ;混合型 0 .49± 0 .10 mg/ L ;梗死后 0 .76± 0 .2 1mg/ L ;AMI组 1.83± 0 .6 4m g/ L。与 SAP组 D-二聚体含量 0 .38± 0 .16 m g/ L比较 ,均存在显著差异 （P<0 .0 5 ）。恶化组、AMI组与 SAP组比较 ,差异最为显著 （P<0 .0 1）。结论 :D-二聚体定量检测是判定 U AP血栓形成、血栓成分相对特异的敏感指标。     

The role of cardiac Troponin-I (cTnI) in risk stratification of patients with unstable coronary artery disease

In patients with chest pain at rest but no ST-segment elevation on the electrocardiogram, the diagnoses of unstable angina and non-Q-wave myocardial infarction (MI) are usually considered together because they cannot be differentiated clinically or angiographically. Since the extent of myocardial necrosis is an important determinant of the risk of death, it is important to identify serum markers with which to predict prognosis, in order to initiate appropriate medical treatment and/or invasive procedures in these patients. Cardiac troponin-I (cTnI), one of the subunits of the troponin regulatory complex, binds to actin and inhibits interactions between actin and myosin. The presence of elevated cTnI in serum is a significant prognostic indicator in patients with unstable angina and non-Q wave MI. Its independent prognostic potential persists even after adjustment for independent baseline variables known to be significantly associated with an increased risk of cardiac events. The use of cTnI in the triage of patients with unstable coronary disease may identify those at greater risk for adverse cardiac events.     

Early symptom-limited exercise test for risk stratification in post menopausal women with unstable coronary artery disease. FRISC study group. Fragmin during Instability in Coronary Artery Disease.

AIMS: The exercise test is considered less reliable in women than in men both for diagnostic and prognostic purposes. The value, however, of the exercise test might vary with the population that is examined, the way the test is performed and which exercise test variables are taken into consideration in the analysis. The aim of the study was to evaluate an early symptom-limited exercise test as a tool for risk stratification in women with unstable coronary artery disease admitted to the coronary care unit. METHODS AND RESULTS: Of the 543 women in the FRISC I study, 395 stabilized on medical treatment and performed a symptom-limited exercise test 5-8 days after inclusion. Sixteen patients with a cardiac event before the scheduled exercise test were excluded. During the 6 months follow-up 17% of the women who did not perform the exercise test and 9% of the 395 women who did, died or had a myocardial infarction (P<0.01). Multivariate stepwise logistic regression analysis was performed to assess the value of clinical variables and findings at the predischarge exercise test to predict cardiac events. Based on the exercise test results three risk groups were identified with an event rate of 19%, 9% and 1%, respectively. The exercise test was better than any of the tested clinical variables in predicting cardiac events. CONCLUSION: Women with unstable coronary artery disease who do not stabilize within a few days have a high event rate early during follow-up. For women who are medically stabilized, considering not only variables like ST depression and chest pain but also parameters reflecting the cardiac performance such as maximal workload and increase in rate-pressure product, an early symptom-limited exercise test is a good predictor of future cardiac events.     

Lactate metabolism as a prognostic index in unstable angina

Fifty patients evaluated because of unstable angina were followed up for a mean period of 63.7 months. Analysis of transmyocardial lactate metabolism was performed in all patients in addition to coronary angiography and ventriculography. All patients had at least one coronary lesion of great than 75%. Although technically feasible, aortocoronary bypass surgery was not performed on initial hospitalization and all patients were treated medically. Patients were divided into two groups on the basis of lactate metabolism; group A lactate production great than 15%, group B lactate production less than 15% or lactate extraction. There was no difference in left ventricular end-diastolic pressure or ejection fraction between the two groups. A coronary score index was higher in group A than group B (5.45 +/- 2.2 vs 3.13 +/- 1.2) (p less than 0.05). The incidence of myocardial infarction was higher in group A than group B in hospital (44.4% vs. 4.3%, p less than 0.05), and long term (70.3% vs. 17.3%, p less than 0.05). Mortality was higher in group A than group B in hospital (25.9% vs. 0%, p less than 0.05) and long term (66.7% vs. 13%, p less than 0.05). Analysis of lactate metabolism thus provides a prognostic index in unstable angina which complements information obtained by coronary angiography and ventriculography.     

An integrated clinical approach to predicting the benefit of tirofiban in non-ST elevation acute coronary syndromes. Application of the TIMI Risk Score for UA/NSTEMI in PRISM-PLUS.

AIMS: We evaluated the TIMI Risk Score for Unstable Angina and Non-ST Elevation Myocardial Infarction for predicting clinical outcomes and the efficacy of tirofiban in non-ST elevation acute coronary syndromes. METHODS AND RESULTS: Developed in TIMI 11B, the risk score is calculated as the sum of seven presenting characteristics (age > or =65 years, > or =3 cardiac risk factors, documented coronary disease, recent severe angina, ST deviation > or =0.5 mm, elevated cardiac markers, prior aspirin use). The risk score was validated in the PRISM-PLUS database (n=1915) and tested for interaction with the efficacy of tirofiban+heparin vs heparin alone. The risk score revealed an increasing gradient of risk for death, myocardial infarction or recurrent ischaemia at 14 days ranging from 7.7-30.5% (P<0.001). Dichotomized at the median, patients with a score > or =4 derived a greater relative risk reduction with tirofiban (P((Interaction))=0.025). Among patients with normal creatine kinase myocardial bands, the risk score showed a 3.5-fold gradient of risk (P<0.001) and identified a population that derived significant benefit from tirofiban (RR 0.73, P=0.027). CONCLUSION: The TIMI Risk Score is a simple clinical tool for risk assessment that may aid in the early identification of patients who should be considered for treatment with potent antiplatelet therapy.     

Black-white differences in severity of coronary artery disease among individuals with acute coronary syndromes

Objective: To determine whether the extent of coronary obstructive disease is similar among black and white patients with acute coronary syndromes.
Design: Retrospective chart review.
Patients: We used administrative discharge data to identify white and black male patients, 30 years of age or older, who were discharged between October 1, 1989 and September 30, 1995 from 1 of 6 Department of Veterans Affairs (VA) hospitals with a primary diagnosis of acute myocardial infarction (AMI) or unstable angina (UnA) and who underwent coronary angiography during the admission. We excluded patients if they did not meet standard clinical criteria for AMI or UnA or if they had had prior percutaneous transluminal coronary angioplasty or coronary artery bypass grafting.
Measurements and Main Results: Physician reviewers classified the degree of coronary obstruction from blinded coronary angiography reports. Obstruction was considered significant if there was at least 50% obstruction of the left main coronary artery, or if there was 70% obstruction in 1 of the 3 major epicardial vessels or their main branches. Of the 628 eligible patients, 300 (48%) had AMI. Among patients with AMI, blacks were more likely than whites to have no significant coronary obstructions (28/145, or 19%, vs 10/155 or 7%, P = .001). Similarly, among patients with UnA, 33% (56/168) of blacks but just 17% (27/160) of whites had no significant stenoses ( P = .012). There were no racial differences in severity of coronary disease among veterans with at least 1 significant obstruction. Racial differences in coronary obstructions remained after correcting for coronary disease risk factors and characteristics of the AMI.
Conclusions: Black veterans who present with acute coronary insufficiency are less likely than whites to have significant coronary obstruction. Current understanding of coronary disease does not provide an explanation for these differences.     

Screening of ruptured plaques in patients with coronary artery disease by intravascular ultrasound

AIM: To visualise the characteristics of ruptured plaques by intravascular ultrasound (IVUS) and to correlate plaque characteristics with clinical symptoms to establish a quantitative index of plaque vulnerability. METHODS: 144 consecutive patients with angina were examined using IVUS. Ruptured plaques, characterised by a plaque cavity and a tear on the thin fibrous cap, were identified in 31 patients (group A), of whom 23 (74%) presented with unstable angina. Plaque rupture was confirmed by injecting contrast medium filling the plaque cavity during IVUS examination. Of the patients without plaque rupture (group B, n = 108), only 19 (18%) had unstable angina. RESULTS: No significant differences were found between groups A and B in relation to plaque and vessel area (p > 0.05). Mean (SD) per cent stenosis in group A was less than in group B, at 56.2 (16.5)% v 67.9 (13.4)%; p < 0.001. Area of the emptied plaque cavity in group A (4.1 (3.2) mm2) was larger than the echolucent zone in group B (1.32 (0.79) mm2) (p < 0.001). The plaque cavity to plaque ratio in group A (38.5 (17.1)%) was larger than the echolucent area to plaque ratio in group B (11.2 (8.9)%) (p < 0.001). The thickness of the fibrous cap in group A was less than in group B, at 0.47 (0.20) mm v 0.96 (0.94) mm; p < 0.001. CONCLUSIONS: Plaques seem to be prone to rupture when the echolucent area is larger than 4.1 (3.2) mm2, when the echolucent area to plaque ratio is greater than 38.5 (17.1)%, and when the fibrous cap is thinner than 0.7 mm. IVUS can identify plaque rupture and vulnerable plaques. This may influence patient management and treatment.     

Lipoprotein(a) is related to the extent of lesions in the coronary vasculature and to unstable coronary syndromes

BACKGROUND: Lp(a) is a highly atherogenic particle with a prothrombotic effect. Until now its relation to the extent and severity of the atheromatic lesions had not been established by standard procedures. HYPOTHESIS: This study examined the correlation of Lp(a) to the extent and severity of coronary artery disease (CAD) and its relation to unstable clinical events (not including sudden death). METHODS: In 202 patients undergoing coronary angiography, plasma lipids were measured with the usual procedures and Lp(a) with the enzyme-linked immunosorbent assay. The extent of CAD was expressed in the number of diseased vessels and its severity in terms of the severity coefficient and the obstruction coefficient. RESULTS: A very strong relationship between LP(a) and the number of diseased vessels (p = 0.0007) signifying diffuse atherosclerosis, but no relation with the severity of the lesions. was found. However, it was the only lipid that correlated significantly with the number of totally occluded vessels (p = 0.0003). The thrombogenic ability of Lp(a) was manifested by increased incidence of myocardial infarction and unstable angina episodes in patients with elevated Lp(a) (p = 0.0157). CONCLUSION: Elevated Lp(a) predisposes to the extent of CAD and total occlusions but not to the severity of lesions. Patients with increased Lp(a) levels and unstable angina are at increased danger of suffering myocardial infarction. Thus, Lp(a) may predispose to plaque destabilization and thrombosis of noncritical lesions.     

Ambulatory ST-recording has no additional value to exercise test for identification of severe coronary lesions after an episode of unstable coronary artery disease in men

One month after an episode of unstable coronary artery disease, 95 male patients performed coronary angiography, 48 hours ambulatory ST-recording and also an exercise test. ST-depression occurred in 29.5% during the ST-recording and in 44.2% during the exercise test (p<0.05). In patients with ST-depression at ambulatory monitoring, 79% demonstrated the same finding at the exercise test. A high risk response at the exercise test — defined as either ST-depression in 3 leads, ST-depression in 1–2 leads with a maximal work load below the 60th percentile or a maximal work load below the 30th percentile regardless of the ECG reaction — occurred in 56.8%. Severe coronary lesions — defined as three vessel disease, left main stenosis or proximal left anterior descending artery stenosis as part of two vessel disease — was observed in 46.3%. Patents with a high risk exercise test response and patients with ST-depression during ST-recording had severe coronary lesions in 67% and 64% respectively. However, a high risk exercise test response occurred in 82%, while ST-depression at ambulatory monitoring was observed only in 41% of the patients with severe coronary lesions (p < 0.001). Thus, ambulatory ST-recording one month after an episode of unstable coronary artery disease in men adds no further information to a symptom limited exercise test in order to identify patients with severe coronary lesions.     

Risk stratification in unstable coronary artery disease: Additive value of troponin T determinations and pre-discharge exercise tests

In 963 patients, participating in a randomized study of lowmolecular weight heparin in unstable coronary artery diseaseand followed for 5 months, troponin T was determined. In the766 patients with a pre-discharge exercise test both troponinT level and exercise test response were independent predictorsof prognosis. Cardiac death or myocardial infarction occurredin 5, 9 and 13% of the patients with a maximal troponin T levelof <0·06 (n=154), 0·06–02 (n=175) and0·2 µg . 1^–1 (n=437), respectively. Basedon exercise tolerance and occurrence of ST depression, patientswith a low (n=361), intermediate (n=325) and high risk (n=80)exercise test response were identified. In these, death or myocardialinfarction occurred in 5, 13 and 29%, respectively. The combinationof troponin T and the exercise test response allowed an evenbetter categorization into low (n=84), intermediate (n=406)and high (n=276) risk groups with 1, 7 and 20% death or myocardialinfarction, respectively. Among those 197 patients unable toperform an exercise test the incidence was 3, 16 and 27% inpatients with troponin T <0·06, 0·06–0·2and 0·2 µg . 1^–1, respectively. Thus, troponin T determinations and pre-discharge exercise testsalone and combined are valuable for risk assessment in unstablecoronary artery disease.     

High prevalence of gastroesophageal reflux in patients with clinical unstable angina and known coronary artery disease

Objectives: Esophageal disease may mimic acute anginal pain. However, the prevalence of gastroesophageal reflux in the acute setting of patients with clinically unstable angina (UA) pectoris is not known. The aim of this study was to determine the co‐existence of coronary artery disease (CAD) and gastroesophageal reflux in UA, and to study the feasibility of esophageal investigation in the chest pain unit. Design: 22 patients with clinical UA and confirmed CAD were monitored by continuous vector cardiography and pH‐measurement during 24?h of observation. Symptoms of chest pain and episodes of ischemia and reflux were recorded. Results: 11 patients (50%) showed abnormal gastroesophageal reflux and another three (14%) had an increased number of reflux episodes. pH‐measurements and esophageal manometry were well tolerated. Few chest pain episodes were recorded during the study period, and no association between chest pain, reflux, and ischemia could be shown. Conclusion: Esophageal reflux is common in patients with UA and established CAD. As reflux‐related chest pain may imitate angina pectoris, it is clinically important that gastroesophageal examination in patients with UA seems to be feasible and well tolerated in the ‘acute setting’.