Low level of tissue plasminogen activator activity in non‐diabetic patients with a first myocardial infarction

• Published in: Journal of Internal Medicine
• Main Authors: LUNDBLAD, D., DINESEN, B., RAUTIO, A., RØDER, M. E., ELIASSON, M.
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 2005
• Subjects: Northern Sweden
• Online Access: http://dx.doi.org/10.1111/j.1365-2796.2005.01507.x; https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1365-2796.2005.01507.x; https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2796.2005.01507.x

Abstract. Objective. To explore the role of tissue plasminogen activator (tPA) activity and plasminogen activator inhibitor type 1 (PAI‐1) in survivors of a first myocardial infarction (MI). Insulin and proinsulin were analysed as potential risk factors. Design. Case–control study in northern Sweden. Subjects. A total of 115 patients under 65 years of age with a first MI were enrolled and recalled for further examination 3 months later. Twenty‐seven patients were excluded, 17 with known diabetes and 10 who did not come to the follow‐up, giving a final number of 88 patients, 73 men and 15 women. Patients were age‐ and sex matched with control subjects drawn from the local cohort in the MONICA population survey 1994. Main outcome measures. We compared MI patients and controls using univariate and multiple regression analyses including odds ratios (OR). Results. PAI‐1 activity, fibrinogen, postload insulin and ‐proinsulin were significantly higher and tPA activity significantly lower in MI patients in the univariate analysis. In a multiple regression analysis, including also age, sex and cardiovascular risk factors, these parameters were divided in quartiles. The lowest quartile of tPA activity was significantly associated with MI (OR = 19.1; CI 3.0–123) together with the highest quartiles of fibrinogen (OR = 25; CI 5.2–120) but other variables were not. Conclusion. Low tPA activity, i.e. low fibrinolytic activity, characterized nondiabetic subjects after a first MI which is not explained by concomitant disturbances in metabolic and anthropometric variables.