Beta-blockers, plasma lipids, and coronary heart disease

High plasma cholesterol concentration is an important coronary heart disease risk factor, particularly in subjects less than 50 years old. Cholesterol is transported mainly by low (LDLs) and high (HDLs) density lipoproteins. High plasma levels of HDL and its apolipoprotein (A-I) are associated with low coronary heart disease risk, and the reverse is true for LDL and its apolipoprotein (B). Plasma levels of very low density lipoproteins (VLDLs) are probably not an independent risk factor, and the situation for plasma triglycerides is unclear. beta-Blockers have no significant effects on plasma concentrations of either total or LDL cholesterol, but HDL plasma concentration is reduced by about 10%, particularly by nonselective beta-blockers. Plasma triglyceride and VLDL concentrations are both raised by beta-blockade. Despite these plasma lipid changes, beta-blockers, by decreasing myocardial oxygen requirements, exhibit marked anti-ischemic properties. beta-Blockers without intrinsic sympathomimetic activity effect a 30% decrease in death from myocardial infarction (MI) in the years after an acute MI. Primary prevention of MI by beta-blockade in hypertensive persons has been well debated and probably exists (although to a lesser extent than secondary prevention) in men, particularly for nonsmokers (for nonselective beta-blockers), and despite any plasma lipid changes. beta-Blockade can inhibit the preatheromatous and atheromatous changes induced by catecholamines in the coronary arteries of animals. beta-blockers may also reduce or slow the following processes: 1) endothelial permeability to lipoproteins; 2) acylcholesterol acyltransferase activity within the arterial wall, thereby preventing cholesterol esterification and deposition in foam cells; 3) LDL precipitation with arterial wall proteoglycans; 4) calcium influx into atheromatous areas; 5) preatheromatous increased endothelial turnover; 6) heart rate; 7) blood velocity and flow disturbances; 8) atheromatous plaque rupture and consequent coronary thrombosis; and 9) platelet activity. Thus, beta-blockers may inhibit atheromatous plaque formation and reduce the likelihood of plaque beta-blockers may inhibit atheromatous plaque formation and reduce the likelihood of plaque rupture, clot formation, and coronary thrombosis.