[In Process Citation]

Abstract

The confirmation of ischaemic disease of the heart increases the probability of death due to cardiovascular causes to more than 80%. The overcoming of myocardial infarction increases, according to the past AHA data, the risk of the origin of a new coronary episode 5 or 7 fold. The necessity of decreasing this risk in the frame of secondary prevention is therefore very urgent. The first assumption of success in secondary prevention resides in optimal therapy in the acute phase of myocardial infarction. The thrombolytic therapy is accompanied by risks of re-perfusion lesion implying from the increased production of free oxygen radical, activation of leukocytes, intracellular calcium overload at a current deficit in potassium and magnesium, the defects of coronary microcirculation, increased sympathetic activities general disturbances of energetic reserves in myocardium. Very significantly is an early stratification of patients after MI to those indicated to intervention / in case that the mass of ischaemic myocardium exceeds 20%, or if EF is below 40%, and to patients who regarding the low risk are manageable by conservative procedure. Both groups profit from the modification of classical risk factors (hypertension, smoking, hypercholesterolaemia). The values of cholesterol measured within the acute phase of myocardial infarction are not indicative, very often they are low. Finally, also in the later period with so-called adequate values of the total cholesterol, the patient after overcoming IM is increasingly under threat. The aim of secondary prevention is to reduce the chief pathogen, namely LDL cholesterol below 2.6 mmol/l, the level of HDL cholesterol on the opposite should be above 1.0 mmol/l. It is necessary to re-emphasize that the bioactive capacity is borne but by the oxidated form of LDL. Oxidative stress has a direct negative effect on vascular endothelium, and haemocoagulation potential, it participates in the metabolic X syndrome (insulin resistance, hyperinsulinaemia, defects in glucose tolerance, hypertriglyceridaemia, hypertension). (Ref. 41.)