[Fibrinolytic system in patients with myocardial infarction and other coronary disease risk factors].

PURPOSE

To evaluate the fibrinolytic system function in survivors of acute myocardial infarction (AMI) and to appreciate the differences between patients with history of diabetes and/or dyslipaemia and those without such history.

PATIENTS AND METHODS

A series comprised of 101 patients (83 men and 18 women) surviving six months after AMI and with mean age of 61.7 +/- 8.5 years was studied. Previous history of type II diabetes mellitus was present in 22 cases, while 42 others had some type of dyslipaemia (16, hypertriglyceridaemia; 15, hypercholesterolaemia; 11 both). Of the patients with diabetes mellitus, 14 had also dyslipaemia (5, hypertriglyceridaemia; 6, hypercholesterolaemia; 3, both conditions). The rates of plasminogen-activator inhibitor (PAI-1), fibrinogen, plasminogen, and alpha-2-antiplasmin, along with the venous occlusion test to determine tissular plasminogen activator (t-PA), both functional and antigenic, before and after venous occlusion, were tested in all cases. The studies were performed at the moment of AMI and 6 months later.

RESULTS

PAI-1 concentration during AMI in the patients with some concurrent lipid anomaly showed significant differences with respect to the patients without any such associated disease (p < 0.001). The patients with history of dyslipaemia had significant increase of PAI-1 (p < 0.001) with respect to those without such history. Those patients with associated diabetes showed significantly increased PAI-1 concentration with regard to those without it, both in the acute phase and 6 months later (p < 0.05); significant increase was also found when comparing the patients with diabetes and dyslipaemia with those ones with only diabetes or dyslipaemia (p < 0.05). A significant increase of PAI-1 level (p < 0.001) was found in the 6-month study in the dyslipaemia patients with respect to non-dyslipaemic, and similar findings appeared with respect to diabetics and non-diabetics (p < 0.05). The 14 patients with both disorders showed increased values when compared with those having only one associated impairment (p < 0.05). When comparing the PAI-1 rates at AMI and 6 months later in the patients with dyslipaemia or diabetes, statistically significant decrease could be noted (p < 0.05 and p < 0.01, respectively). Before venous occlusion, t-PA was significantly increased in diabetic or dyslipaemic patients (p < 0.05) and in the patients with both conditions (p < 0.01).

CONCLUSIONS

Patients with AMI and abnormalities of the lipidic or glycaemic metabolism have fibrinolytic dysfunction on the basis of an increase of the main inhibitor of the fibrinolytic system and a decreased release of tissular plasminogen activator. Those patients with both metabolic abnormalities have a deeper fibrinolytic hypofunction, with higher PAI-1 concentration.