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[In Process Citation]
Bada1
1III.interna klinika LFUK, Bratislava, Slovakia.
Insights
Secondary prevention is crucial after heart attack to reduce cardiovascular death risk. Optimal therapy, risk factor modification, and targeted cholesterol management (LDL < 2.6 mmol/l, HDL > 1.0 mmol/l) are key to improving outcomes.
Area of Science:
- Cardiology
- Preventive Medicine
- Biochemistry
Background:
- Ischaemic heart disease significantly elevates cardiovascular mortality risk, with myocardial infarction survivors facing a 5-7 fold increased risk of new coronary events.
- Secondary prevention strategies are urgently needed to mitigate this heightened risk.
- Optimal acute phase management of myocardial infarction is the cornerstone of successful secondary prevention.
Purpose of the Study:
- To emphasize the critical need for secondary prevention in patients with ischaemic heart disease.
- To highlight the importance of early patient stratification and risk factor modification.
- To define target lipid profiles for secondary prevention post-myocardial infarction.
Main Methods:
- Early stratification of myocardial infarction patients into intervention-indicated and conservative management groups based on ischaemic mass and ejection fraction (EF).
- Modification of classical cardiovascular risk factors including hypertension, smoking, and hypercholesterolaemia.
- Monitoring and management of lipid profiles, specifically targeting low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels.
Main Results:
- Thrombolytic therapy, while essential, carries risks such as reperfusion injury due to free radical production and leukocyte activation.
- Early stratification allows for tailored treatment, with intervention recommended for ischaemic myocardium >20% or EF <40%.
- Effective secondary prevention requires lowering LDL cholesterol to <2.6 mmol/l and increasing HDL cholesterol to >1.0 mmol/l, addressing the detrimental effects of oxidised LDL.
Conclusions:
- Successful secondary prevention hinges on optimal acute phase management and early risk stratification of myocardial infarction patients.
- Aggressive modification of risk factors, including achieving specific LDL and HDL cholesterol targets, is vital.
- Oxidative stress and its role in endothelial dysfunction and metabolic syndrome underscore the complexity of managing cardiovascular risk post-myocardial infarction.
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.)