Abstract. Strandberg L-E, Ericsson C-G, O'Konor M-L, Bergstrand L, Lundin P, Rehnqvist N, Tornvall P (Norrta Èlje Hospital, Danderyd Hospital, the Swedish National Board of Health, Karolinska Hospital and the Karolinska Institute, Stockholm, Sweden). Diabetes mellitus is a strong negative prognostic factor in patients with myocardial infarction treated with thrombolytic therapy. J Intern Med 2000; 248: 119± 125.Objectives. To assess the long-term prognostic values of baseline demographic data, occurrence of vectorcardiographic signs of reperfusion, left ventricular function and coronary angiographic features. Design. Longitudinal study of morbidity and mortality. Setting. Coronary care unit at Danderyd Hospital, Stockholm, Sweden. Subjects. A total of 222 patients (mean age 61 years) with a suspected acute myocardial infarction treated with thrombolysis were investigated and followed for 2±5 years (mean 1216 days). Main outcome measures. Death or a new myocardial infarction. Results. Age above 55 years (P , 0.05), a previous diagnosis of diabetes mellitus (P , 0.005), hypertension (P , 0.05), heart failure (P , 0.001) and myocardial infarction (P , 0.05), a previous use of beta-blockers (P , 0.05) and an ejection fraction below 60% (P , 0.01) were predictors for death or a new myocardial infarction in univariate analysis. Sex, a previous history of smoking or angina pectoris, vectorcardiographic signs of reperfusion or degree of coronary artery disease had no prognostic values. In multivariate analysis including age above 55 years, a previous diagnosis of diabetes mellitus, hypertension and myocardial infarction, and an ejection fraction below 60%, only age (P , 0.05), diabetes mellitus (P , 0.01) and ejection fraction (P , 0.05) were predictors for death or a new myocardial infarction. Conclusions. The results of the present study emphasize the importance of diabetes mellitus as a long-term prognostic risk factor in patients with myocardial infarction treated with thrombolysis. Further studies are needed to determine the mechanisms behind this increased risk.

Background: There is a paucity of studies using quantitative coronary angiography (QCA) to determine progression of coronary artery disease (CAD) after an acute coronary event. Furthermore, despite a great interest in effects of inflammation and ‘early’ lipid lowering therapy, no data have been published on the role of plasma C-reactive protein (CRP) and lipoprotein levels in CAD progression after myocardial infarction. Methods: Seventy-two patients with myocardial infarction treated with thrombolysis, but not with statins, were investigated with QCA during admission and after 6 months. Plasma CRP concentrations were measured by a high sensitive method 2 days after the acute event, and plasma high-sensitive CRP and lipoprotein levels were determined 3 months after myocardial infarction. Results: Overall, there was no significant progression of CAD, but when stenoses were grouped into those reducing the lumen diameter greater or less than 50%, progression was seen in stenoses originally <50%, whereas regression was seen in stenoses >50%. No consistent associations were seen between plasma CRP, lipoprotein lipid or lipoprotein(a) levels and CAD. Conclusions: Progression of stenoses <50% might be of clinical importance since these stenoses are more prone to rupture. Furthermore, the lack of associations between change in minimum lumen diameter and plasma CRP and lipoprotein concentrations suggests that positive effects on CAD progression of early treatment with anti-inflammatory or lipid-lowering drug therapy may not be expected in this subset of patients.