Effect of long-term beta-blockade with alprenolol on platelet function and fibrinolytic activity in patients with coronary heart disease

Abstract

In 14 patients with coronary heart disease the effect of long-term treatment (mean 16 months, range 12-33) with alprenolol on platelet function and fibrinolytic activity was studied. While on the beta-blocker and two weeks after gradual withdrawal of it, the patients performed a bicycle-ergometer test and blood samples were obtained before and following exercise. Pre-exercise fibrinolytic activity, assessed by the euglobulin clot lysis time, was 183 +/- 27 min (mean +/- SEM) while on alprenolol as compared to 111 +/- 18 min (p less than 0.01) after its withdrawal. Activation of fibrinolysis following exercise was not significantly influenced by alprenolol. In patients treated with alprenolol, the pre-exercise threshold level of ADP, producing platelet aggregation was 3.3 muM (geometric mean) and 5.1 muM after stopping treatment (p less than or equal to 0.05). In patients receiving the beta-blocker, the ADP- threshold value dropped from 3.3 muM before exercise to 2.3 muM immediately after exercise (not significant). The corresponding values after withdrawal of alprenolol were 5.1 muM and 2.7 muM (p less than or equal to 0.02). Adrenaline - stimulated aggregation was not significantly influenced by alprenolol. Serotonin release from platelets following maximal ADP- and adrenaline stimuli was not significantly changed by exercise in patients on beta-blockade. After stopping treatment, ADP-induced serotonin release was 22 +/- 4.1% before and 15 +/- 4.7% after exercise (p less than 0.02). the corresponding values using the adrenaline stimulus were 29 +/- 5.7% and 17 +/- 4.7% (p less than 0.05). It is suggested that during physical stress alprenolol may protect platelets against aggregatory stimuli.

Migraine: Possible Role of Shear‐Induced Platelet Aggregation With Serotonin Release

“…Because some of them are hydrophilic and do not cross the blood–brain barrier, 131,132 a direct effect on central neural mechanisms seems unlikely. Many β ‐blockers decrease platelet aggregability (propranolol, 133 metoprolol, 134 pindolol, 134 practolol, 135 esmolol, 136 carvedilol, 137 alprenolol, 138 atenolol 133 ), probably by increased PGI 2 formation in the arterial wall 135 . Also, the prophylactic effect of calcium antagonists might be associated with their well‐known antiplatelet effect 139 .…”

Tissue‐Specific Analysis of Pharmacological Pathways

“…We performed prospective validation on 22 predicted compounds that have not been used as anticoagulants, and found that their coagulation activity is significantly lower than the negative controls. Among the 22 compounds, several have been reported to affect coagulation in previous research, such as labetalol and alprenolol . Four newly predicted compounds with lowest coagulation activity share a mutual target protein, ADRB2.…”

The long-term effects of metoprolol and epanolol on tissue-type plasminogen activator and plasminogen activator inhibitor 1 in patients with ischaemic heart disease

“…In the one previous study [14] examining the effect of fl-adrenoceptor blockade on fibrinolysis in patients with ischaemic heart disease, which predated assays of t-PA and PAI-1, alprenolol (a nonselective beta blocker with ISA) prolonged euglobulin clot lysis time at rest but did not influence the response to exercise. Metoprolol caused no change in PAI-1 in 10 normal subjects [15], but in 15 hypertensive patients it caused a decrease [16].…”