Related Experiment Videos
The role of sympathetic activity in atherogenesis: effects of beta-blockade
B Ablad1, J A Björkman, D Gustafsson
1Hässle Cardiovascular Research Laboratories, Mölndal, Sweden.
Insights
Certain beta-blockers, like metoprolol, may slow atherosclerosis development. Clinical trials show reduced cardiovascular events, suggesting a protective effect against plaque buildup and complications.
Area of Science:
- Cardiology
- Pharmacology
- Pathology
Background:
- Clinical and experimental data suggest beta-adrenoreceptor antagonists possess antiatherosclerotic properties.
- Long-term metoprolol use reduced mortality and cardiovascular morbidity in hypertensive and post-myocardial infarction patients.
Purpose of the Study:
- To investigate the potential antiatherosclerotic effects of beta-blockers.
- To explore the mechanisms behind the observed cardiovascular benefits of beta-blockade.
Main Methods:
- Analysis of clinical trials (primary and secondary prevention) involving metoprolol.
- Review of animal studies demonstrating beta-blocker effects on atherosclerosis in rabbits and monkeys.
- Examination of biochemical and hemodynamic factors influenced by beta-blockers.
Main Results:
- Metoprolol significantly reduced atherosclerotic plaque development in rabbits without altering blood lipids.
- Propranolol prevented stress-induced atherosclerosis and endothelial injury in animal models.
- Beta-blockers may reduce arterial cholesterol accumulation via increased prostacyclin and altered low-density lipoprotein metabolism, alongside hemodynamic improvements.
Conclusions:
- Beta-blockers exhibit antiatherosclerotic properties, contributing to reduced cardiovascular complications.
- Mechanisms include biochemical changes (prostacyclin, LDL metabolism) and hemodynamic effects (reduced wall stress).
- Further research into beta-blocker's role in atherosclerosis management is warranted.
Abstract:
Clinical and experimental evidence points to potential antiatherosclerotic effects of certain beta-adrenoreceptor antagonists. Long-term treatment with metoprolol resulted in significant reductions of total and cardiovascular mortality or morbidity due to decreased incidence of coronary and cerebrovascular complications both in a primary prevention trial in hypertensive patients and in a secondary prevention trial in patients surviving myocardial infarction. The observations suggest that a retardation of atherosclerosis development might have contributed to the reduced incidence of cardiovascular complications. An antiatherosclerotic effect of beta-blockers has been directly demonstrated in animal studies. In cholesterol-fed rabbits, metoprolol significantly reduced the development of atherosclerotic plaques in the aortic intima in the absence of any changes in blood lipids. Similar findings were reported for propranolol, which prevented psychosocial stress-induced atherosclerosis of the coronary artery in monkeys. Furthermore, beta-blockers have been shown to prevent stress-induced endothelial injury and platelet accumulation to intima at atherosclerotic predilection sites in animal models. These antiatherogenic effects may be due to biochemical and hemodynamic factors. Two biochemical effects of beta-blockade may lead to reduced cholesterol accumulation in arterial intima at unchanged serum cholesterol levels. One is a beta-blocker-induced increase of prostacyclin biosynthesis, and the other a metabolic change of low-density lipoprotein, reducing its potential for deposition in the arterial wall. The antiatherogenic effect of these factors may be reinforced by beta-blocker-induced hemodynamic changes leading to reductions of arterial flow aberrations and pressure-related wall stress.