Related Experiment Video
Updated: Aug 18, 2026

Improvement of a Closed Chest Porcine Myocardial Infarction Model by Standardization of Tissue and Blood Sampling Procedures
Published on: March 12, 2018
[Blood rheological effects in ischemic heart disease treated with antianginal and thrombolytic agents]
Insights
This study investigated how antianginal and thrombolytic drugs affect blood viscosity and platelet activity in ischemic heart disease patients. Several agents, including aspirin/propranolol and verapamil, demonstrated significant platelet disaggregation, suggesting a role for hemorheological mechanisms in treatment efficacy.
Area of Science:
- Cardiology
- Hematology
- Pharmacology
Background:
- Ischemic heart disease (IHD) involves complex hemorheological alterations.
- Understanding drug effects on blood viscosity and platelet function is crucial for IHD management.
Purpose of the Study:
- To investigate the impact of various antianginal and thrombolytic agents on blood viscosity, erythrocyte aggregation, and platelet behavior in IHD patients.
- To elucidate the role of hemorheological mechanisms in the therapeutic effects of these cardiovascular drugs.
Main Methods:
- Study included 161 patients with different forms of IHD.
- Assessed changes in blood viscosity, erythrocyte aggregation, and thrombocyte parameters during treatment.
- Evaluated effects of nitroglycerin, Sustac, micristin (aspirin/propranolol), verapamil, dipyridamol, trental, nonachlazin, sodium nitroprusside, and streptokinase (avelisine).
Main Results:
- Nitroglycerin and Sustac showed no significant hemorheological changes.
- Micristin and verapamil exhibited notable platelet disaggregational effects.
- Dipyridamol, trental, and nonachlazin improved erythrocyte function, reducing blood viscosity.
- Sodium nitroprusside transiently decreased platelet aggregation and blood viscosity.
- Streptokinase in acute myocardial infarction led to defibrinization, reduced aggregation, and lower blood viscosity.
Conclusions:
- Hemorheological mechanisms appear to play a significant role in the antianginal efficacy of the studied drugs.
- Different drug classes exert distinct effects on blood rheology and platelet activity.
- These findings highlight the importance of considering hemorheological profiles in cardiovascular drug selection and therapy.
Abstract:
In 161 patients with different forms of ischaemic heart disease the authors studied changes of the blood viscosity, erythrocyte aggregation and of thrombocytes during treatment with modern antianginal and the thrombolytic agents. Treatment with nitroglycerin in tablets and Sustac revealed no statistically significant differences in the changes of the haemorheological parameters. The mainly thrombocyte disaggregational effect was shown by micristin (aspirin/propranolol in the daily dose of over 120 mg) and verapamil (the daily dose over 160 mg). The use of dipyridamol, trental and nonachlazin was accompanied both by the decrease of functional activity of thrombocytes and by the decrease of the blood viscosity as a result of improvement of the functional properties of erythrocytes. Sodium nitroprusside depressed shortly the aggregation of platelets and decreased the blood viscosity at the expense of the decrease of the haematocrit. The use of streptokinase (avelisine) in patients with acute myocardial infarction was accompanied by defibrinisation of the blood, by marked decrease of the aggregation facility of formed elements of the blood and its viscosity. The results suggest that the haemorheological mechanisms participate in the antianginal effect of the drugs studied.
Related Concept Videos
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Ischemic Heart Disease: Overview
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...
Myocarditis I: Introduction
Myocarditis III: Medical Management
Coronary Artery Disease V: Interprofessional Care
Angina IV: Management

