This article summarizes the design and findings -- both at 3 months and at 1 year follow-up -- of the Fragmin during Instability in Coronary Artery Disease (FRISC) II trial. This multicentre randomized trial compared both an early invasive with an early non-invasive stategy, and prolonged treatment with dalteparin as opposed to placebo, in patients with unstable coronary artery disease. The results show that an early invasive strategy with coronary angiography and, if appropriate, revascularization procedures within 7 days after admission reduces the subsequent rate of mortality and myocardial infarction. The benefits of the invasive treatment were noticeably more marked in patients with any high-risk indicator -- for example, male gender, age above 65 years, previous severe angina, or signs of ischaemia (ST depression on ECG) or of myocardial damage (elevated levels of troponin T). Treatment with dalteparin reduced the risk of death and myocardial infarction in high-risk (i.e. troponin-positive) patients, particularly during the first month of treatment. However, continuation with dalteparin therapy after revascularization procedures conferred no benefit. It is concluded that extended treatment with dalteparin is useful as a bridge to revascularization in this high-risk subgroup of patients with unstable coronary artery disease.
CONTEXT: Randomized trials have established statin treatment as secondary prevention in coronary artery disease, but it is unclear whether early treatment with statins following acute myocardial infarction (AMI) influences survival. OBJECTIVE: To evaluate the association between statin treatment initiated before or at the time of hospital discharge and 1-year mortality after AMI. DESIGN AND SETTING: Prospective cohort study using data from the Swedish Register of Cardiac Intensive Care on patients admitted to the coronary care units of 58 Swedish hospitals in 1995-1998. One-year mortality data were obtained from the Swedish National Cause of Death Register. PATIENTS: Patients with first registry-recorded AMI who were younger than 80 years and who were discharged alive from the hospital, including 5528 who received statins at or before discharge and 14 071 who did not. MAIN OUTCOME MEASURE: Relative risk of 1-year mortality according to statin treatment. RESULTS: At 1 year, unadjusted mortality was 9.3% (1307 deaths) in the no-statin group and 4.0% (219 deaths) in the statin treatment group. In regression analysis adjusting for confounding factors and propensity score for statin use, early statin treatment was associated with a reduction in 1-year mortality (relative risk, 0.75; 95% confidence interval, 0.63-0.89; P =.001) in hospital survivors of AMI. This reduction in mortality was similar among all subgroups based on age, sex, baseline characteristics, previous disease manifestations, and medications. CONCLUSIONS: Early initiation of statin treatment in patients with AMI is associated with reduced 1-year mortality. These results emphasize the importance of implementing the results of randomized statin trials in unselected AMI patients.
On exercise testing after an episode of unstable coronary artery disease (CAD; unstable angina or non-Q-wave myocardial infarction), a proportion of patients show ST-segment depression, indicating myocardial ischaemia, but do not report concomitant symptoms of angina. Treatment of such "silent" ischaemia aims mainly to reduce the risk of subsequent cardiac events. We have studied the effect of low-dose aspirin in patients with myocardial ischaemia defined at the predischarge test as silent (though patients might have had symptomatic ischaemia at other times) or symptomatic. 740 men with unstable CAD aged 70 years or less underwent symptom-limited exercise testing before hospital discharge; 144 showed ST depression without pain and 230 ST depression with simultaneous chest pain. Of the silent ischaemia group, 67 were randomly assigned placebo and 77 aspirin (75 mg daily); the corresponding numbers in the symptomatic group were 125 and 105. Angina symptoms were less common in the silent than in the symptomatic ischaemia group both before inclusion and during follow-up, and a greater proportion of the silent ischaemia group were included because of myocardial infarction. In both ischaemia groups aspirin treatment reduced the risk of subsequent myocardial infarction or death by 3 months' follow-up (silent 4% of aspirin-treated vs 21% of placebo-treated patients, p = 0.004; symptomatic 9% vs 18%, p = 0.05); at 12 months' follow-up a significant benefit of aspirin was still apparent in the silent ischaemia group (9% vs 28%, p = 0.005) but not in the symptomatic group (13% vs 22%, p = 0.109). Low-dose aspirin reduced the risk of subsequent myocardial infarction at least as well in silent as in symptomatic myocardial ischaemia. Since improvement of outlook is the main treatment objective in symptom-free patients, aspirin should be a mainstay of their treatment.
The need of acute coronary care is increasing because of an increase in the incidence of severe angina pectoris, and despite a reduction in that of acute myocardial infarction. Patients with acute myocardial infarction are characterised by continuously increasing age, lower mortality, and shorter hospitalisation. The improvement in acute care is related to increased use of expensive drugs, new diagnostic methods, and an increasing coronary revascularisation rate. However, there is still inequality in the utilisation of cardiac care, and in order to further enhance its quality and equality of utilisation, there is an emphatic need of common registries.
Criteria for the diagnosis of myocardial infarction vary not only from one cardiac intensive care unit (CICU) to another, but also from one study to another. Even the appropriate juncture for ECG, the type of biochemical markers used and blood sampling times vary. Thus, epidemiological studies comparing results over time or between various regions or hospitals tend to be misleading. Reported results are difficult to interpret and to apply to one's own CICU. In order to survey myocardial infarction diagnosis in Sweden and planned future changes, in February-March 1997 a questionnaire was sent to all 82 CICUs in the country. Of the 74 (90%) responders, 72% (53/74) reported formalized printed criteria for myocardial diagnosis to be available at the unit. Eight different biochemical markers of myocardial injury were in use; CK-MB (creatine kinase and its cardio-specific isoenzyme) was the most common, being used at 64% (47/74) of the units; CK and CK-B were used at 32%, and troponin T or I at 53%. Myoglobulin has not been very widely used. If planned changes are carried out, 86% of the units will soon be using CK-MB, and 79% troponin T och I. Cut-off levels of biochemical markers of myocardial infarction varied. Of the 47 units where CK-MB was used, the cut-off level was 10 micrograms/L at 10 (28%) of the units, 15 micrograms/L at 31 (66%) units, and a higher level in a smaller group of units. Cut-off levels for CK-B manifested a similar lack of uniformity. The greatest difference was manifested by troponin levels; of the 28 units using quantitative tests and that cited their cut-off levels, three (11%) used 0.10 microgram/L, 12 (43%) used 0.20 microgram/L, and the remaining 13 (46%) used 0.50 microgram/L. The use of ischaemia monitoring in conjunction with diagnosis and prognosis of myocardial infarction has increased, 72% of the units reporting that they used some form of monitoring, and a further 13% that they planned to introduce it in the near future. Thus, the questionnaire study showed marked differences in myocardial infarction diagnosis to exist in Sweden, although a manifest trend toward increasing uniformity was also seen, and the outlook for the standardisation of diagnostic criteria is good.
AIMS: The aim was to examine the early prognostic value of a combination of a continuous 12-lead ECG and troponin T in patients with chest pain and an ECG non-diagnostic for acute myocardial infarction. METHODS AND RESULTS: ST monitoring was performed and samples for analysis of troponin T were collected from admission for 12 h from 598 patients. After 6 h, the peak value of troponin T in 27% was > or = 0.10 microg.l(- 1), while 15% had had ST episodes, defined as transient ST deviations of at least 0.1 mV. Both a troponin T > or = 0.10 microg. l(-1) and ST episodes predicted worsening outcome. After 30 days, there were 6.8% and 1.4% (P or = 0.10 microg.l(-1), respectively. The corresponding event rates in patients with and without ST episodes were 10% and 1.6% (P
Comment In: Eur Heart J. 2000 Sep;21(17):1403-510952833