Related Experiment Videos
Hypertension-related coronary thrombosis: prothrombic role of angiotensin II
C R Spillert1, S Sun, M A Miller
1Department of Surgery, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark 07103-2757.
Insights
Hypertension contributes to heart attacks. This study shows angiotensin II accelerates blood clotting, similar to endotoxin, potentially explaining hypertension
Area of Science:
- Cardiovascular Medicine
- Hematology
- Biochemistry
Background:
- Hypertension is a known risk factor for acute myocardial infarction.
- The role of hypercoagulability in thrombosis leading to myocardial infarction is not fully understood.
- A sensitive coagulation test is needed to investigate this link.
Purpose of the Study:
- To determine if angiotensin II accelerates coagulation using a modified recalcification time (MRT) test.
- To investigate the hypercoagulable effects of angiotensin II and Escherichia coli endotoxin.
- To establish a link between hypertension, vasospasm, and myocardial infarction.
Main Methods:
- A modified recalcification time (MRT) test was developed to assess coagulation.
- Citrated human blood aliquots were incubated with saline, E. coli endotoxin, angiotensin II, or a combination.
- Coagulation times were measured and statistically analyzed using Student's t-test.
Main Results:
- Angiotensin II significantly shortened the MRT, indicating accelerated coagulation (P < .05).
- E. coli endotoxin also significantly shortened the MRT (P < .001).
- Combined angiotensin II and endotoxin resulted in the shortest MRT (P < .001).
Conclusions:
- Angiotensin II exhibits a hypercoagulable effect in vitro.
- This hypercoagulability, alongside vasospasm, can explain hypertension's role in acute myocardial infarction.
- The study provides evidence for angiotensin II-induced hypercoagulability, independent of other in vivo mechanisms.
Abstract:
Although hypertension is a major risk factor in acute myocardial infarction, concomitant hypercoagulability causing thrombosis leading to myocardial infarction remains unproven for lack of an appropriate coagulation test. This study was devised to determine whether a modified recalcification time (MRT) test can demonstrate that angiotensin II, a potent vasoconstrictor, also accelerates coagulation to promote thrombosis. The MRT incorporates blood cells and chemical coagulants for maximizing sensitivity. Four groups (A, B, C, and D) of aliquots of citrated human blood were incubated for 2 hours at 37 degrees C after adding to A--20 microL saline, to B--10 micrograms Escherichia coli endotoxin, to C--20 micrograms angiotensin II, and to D--a combination of E coli endotoxin and angiotensin II. The experiment was repeated with nonincubated aliquots. Modified recalcification time values +/- standard deviation in minutes were: A--5.5 +/- 1.5, B--4.6 +/- 1.1, C--4.9 +/- 1.0, and D--3.9 +/- 1.0. Significance (Student's t test) was as follows: B versus A P < .001; C versus A, P < .05; C versus D, P < .001; B versus C, P < .05; and B versus D, P < .001. No significant changes occurred in nonincubated blood. We conclude that angiotensin II has a hypercoagulable effect, as does endotoxin. The hypercoagulability in concert with vasospasm can explain the role of hypertension in acute myocardial infarction. This in vitro study excludes the role of other in vivo mechanisms in the development of angiotensin II-induced hypercoagulability.