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The beta-blockers were introduced into medicine for the treatment of angina pectoris, [1] but their most extensive use has been in hypertension. Millions of patients have been treated with them [...]

Calcium antagonists and [beta] blockers may retard or inhibit atherogenesis. This study investigated whether nifedipine or propranolol influences coronary atherosclerosis in humans. In selected patients with effort angina and prove coronary artery disease, the cineangiographic pattern after 2-year therapy with nifedipine (group 1, 39 patients), propranolol (group 2, 36 patients) or isosorbide dinitrate (group 3, 38 patients) was compared to that before treatment. The disease evolved to a different extent in the 3 groups. Patients with evidence of progression of old narrowings and appearance of new narrowings were significantly fewer in group 1 (31% and 10%) than in group 2 (53% and 34%) and group 3 (47% and 29%). The number of stenoses withe evidence of progression was significantly smaller after nifedipine (14), and larger after propanolol (39) compared with group 3 (24). Thus, nifedipine seemed more protective than the other 2 drugs against coronary atherosclerosis. The coronary risk factors were normal in the nifedipine group and remained so with treatment, suggesting that they were dissociated from influences on atherosclerosis. The evolution, as judged by the number of narrowings with progression, appeared significantly (p [is less than]0.01) worse with propranolol than with isosorbide dinitrate. Propranolol caused unfavorable modifications of serum lipids; there was a 28% increase in total triglycerides and a 25% decrease in high density lipoprotein cholesterol at 12 months in group 2. (Am J Cardiol 1989;64:433-439), The use of beta blockers and calcium antagonists (agents that are used in the control of blood pressure) has been found to prevent or slow the progress of atherogenesis, the formation of plaque along the walls of the arteries. The effectiveness of three drugs was examined: nifedipine (a calcium inhibitor), propranolol (a beta-block), and isosorbide dinitrate (a nitroglycerin derivative which opens passages of heart). One hundred thirteen patients with angina pectoris, a severe chest pain, and atherogenesis were matched for age and extent of disease. These individuals were then divided into three groups of approximately the same number, each group receiving treatment with one of these drugs over a two-year period. The group taking isosorbide dinitrate served as the control. Measurements were taken to determine how or if the disease had progressed. The group that took nifedipine was found to have less progression of atherogenesis where the arteries had previously become narrowed, and fewer incidents of new narrowings were observed. A lower incidence of progression of stenosis was recorded in this group as well, when compared with the group that took propranolol. The propranolol group not only compared poorly to the first group, but was found to have a 28 percent higher total triglyceride count and a 35 percent lower count of high density lipids (HDL) when measurements were made 12 months into the study. Clearly, nifedipine proved to be the superior treatment for atherogenesis. It was less clear if propranolol was merely less effective than the isosorbide dinitrate or if propranolol actually aggravated the existing condition. Further research into consequences of the increase in triglycerides and the decrease in HDLs which accompanied the use of propranolol was recommended.