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Matrix metalloproteinase inhibition with PG-116800 failed to reduce LV remodeling or improve clinical outcomes after MI.

T HAS BEEN SHOWN IN SEVERAL 1-6 BUT not all studies 7-9 that job strain, a combination of high psychological demands and low decision latitude, 10 increases the risk of a first coronary heart disease (CHD) event. However, the association of job strain with the risk of recurrent CHD events after a first myocardial infarction (MI) has been documented in only 2 prospective studies whose findings were inconsistent. 11,12 Two major limitations of these previous studies were that they did not assess the duration of psychosocial work exposure 11-13 and were conducted with a limited number of participants (n=62, 11 n=200 12). Our study was undertaken to determine whether job strain increases the risk of recurrent CHD events when the duration of psychosocial work exposure is taken into account in a large cohort who returned to work after a first recent MI. METHODS Patients and Data Collection A total of 1191 patients younger than 60 years were recruited from 30 hospitals in the province of Quebec, Canada, between November 1995 and October 1997. Eligible patients had a first acute MI, held a paid job in the 12 months before their MI, and planned to return to work at least 10 hours per week within 18 months after their MI. The ethics board of each hospital approved the study. Written informed consent was obtained before hospital discharge. The final study population included 972 patients (FIGURE 1). Medical information regarding the acute MI and past medical history was documented during the first hospitalization. Participants were interviewed 3 times by telephone: at baseline in 1996-1998, an average of 6 weeks after their return to work, 2.2 years later in 1998-2000, and after 6.9 years in 2003-2005. Validated questionnaires for the first 2 inter-See also p 1693 and Patient Page.

Fibrinopeptide A, platelet factor 4, /3-thromboglobulin, thromboxane B2, and 6-ketoprostaglandin F la were estimated by radioimmunoassay on venous plasma samples taken within 48 hr of admission from 16 consecutive patients with unstable angina and 15 patients with stable angina matched for clinical variables. The ratio of circulating platelet aggregates, platelet aggregation to increasing concentrations of ADP (0.455 to 1.82 yg/ml), and platelet thromboxane B2 production in vitro were also tested. The two groups of patients were statistically similar in terms of sex distribution, age, presence of risk factors, use of medication, extent of coronary artery disease and history of previous myocardial infarction. Mean plasma levels of fibrinopeptide A were 2.7 ± 0.4 ng/ml (geometric means ± SEM, range 1.5 to 5.5) in patients with stable angina vs 5.5 ± 1.8 ng/ml (range 2.4 to 32; p < .001) in those with unstable angina. In the latter group, after 6 to 8 days, fibrinopeptide A levels decreased to 3.6 + 0.5 ng/ml (range 1.5 to 9.3; p < .04 vs admission). All other variables measured were statistically identical in the two groups. We conclude that plasma fibrinopeptide A levels, as opposed to platelet factors, discriminate between patients with unstable and stable angina, indicating an activation of the coagulation system in unstable angina. Circulation 75, No. 1, 156-162, 1987. THE DIAGNOSIS of unstable angina is based on the clinical features of an accelerating pattern of ischemic chest pain. The diagnosis is usually corroborated by demonstrating ST-T changes on the electrocardiogram and the presence of coronary artery obstructive lesions on the angiogram. Although the pathophysiologic mechanisms are still unclear, recent studies have demonstrated a rapid progression of atherosclerosis in this syndrome' and a high prevalence of coronary artery thrombi.24 Fibrinopeptide A (FPA) is a very sensitive and specific marker of thrombin generation in vivo or activation of the coagulation system.7 It is elevated in plasma of patients with various thromboembolic disorders,8 and recent studies have documented a marked increase in patients with evolving myocardial infarction.9-11 The purpose of this study was to determine the plasma levels of FPA in patients hospitalized for unstable angina in order to help clarify the pathophysiologic From the

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