THROMBOSIS RESEARCH Printed in the United
Vol. States
6, pp. 209-214, Pergamon Press,
1975 Inc.
PLATELET ADHESIVENESS IN THE ASSESSMENT OF ISCHAEMIC HEART DISEASES*
Sujata Chaudhurif Blood Coagulation Laboratory, Department of Cardiology, All India Institute of Medical Sciences, New Delhi-16
(Received 2.10.1975; in revised form 22.1.1975. Accepted by Editor W.H. Seegers)
ABSTRACT Study of adhesiveness of the platelets in ischaemic heart disease was undertaken. Fasting venous blood samples were collected from four groups of individuals: (1) cases with angina, (2) cases with acute infarction without anticoagulant therapy, (3) post-infarction cases after several months to years after the acute episode, and (4) normal individuals. Preliminary investigation employing arterial and venous blood from the same individual revealed no significant difference in the adhesiveness of platelets at 60 minutes (when rotation was done at the rate of 40 revolutions per minute for arterial blood and 10 revolutions per minute for venous blood). All subsequent determinations were, therefore, done with venous blood. Conclusions from the observations were: (1) Initial platelet counts in ischaemic heart disease group were significantly higher than in the normal group; (2) On rotation, adhesiveness was more marked in ischaemic heart disease group than in the normal group; (3) Adhesiveness in the IHD categories were not significantly different from each other. Higher initial counts and more adhesiveness in the ischaemic heart disease group seemed to point out a basal disturbance in homeostatic balance of qualitatively defective platelets in these potential states of thrombogenesis. If this adhesiveness of platelets had a relationship to the thrombotic episodes, these data suggested that angina cases should be considered as potential cases of acute and subacute myocardial infarction.
* Abstract published in the Proceedings of the XIII International Congress of Hematology held in Munich, 1970. ' Emeritus Scientist, ICMR. 209
210
PLGTELET
ADHESIVENESS
vo1.6,No.3
INTRODUCTION The platelets in the circulating blood, normally not adherent to the normal vascular endothelium, form aggregates on damaged intima as in atherosclerosis. Thus, platelet aggregation may be taken as the initial step in the chain of events which leads to thrombosis (l-3). Mustard et al (4) have shown by in vitro studies that blood clots formed in a glass tube are quite different from a thrombus, but Chandler (5) has demonstrated that blood clots formed in a rotating tube are similar in structure to thrombi formed in flowing blood. O'Brien (6) has shown that ADP induces platelet aggregation and possibly platelet adhesiveness to surfaces. Born and Cross (7) described a method by which the ADP-induced aggregation of platelets could be quantitatively studied. Wright (8) made important observations on increased platelet stickiness in conditions associated with intravascular thrombosis. McDonald and Edgill (9) demonstrated increased platelet adhesiveness in patients with ischaemic heart disease and McDonald (10) suggested that abnormal platelet adhesiveness might precede the development of intravascular clotting as in ischaemic heart disease. Slack et al (11) studied the level of lipoprotein lipase and the degree of platelet stickiness in patients with ischaemic heart disease as compared to controls and suggested the possibility of a deficiency of this enzyme in these patients. As part of an overall study on the pathogenesis of thrombotic diseases, the role of platelet adhesiveness in the genesis of intravascular clotting was investigated. This communication reports the findings in ischaemic heart diseases with and without overt thrombosis.
MATERIALS AND METHODS Study of platelet adhesiveness was undertaken by Wright's (8) method. A rotator machine constructed locally was used in the study. A measured amount of whole blood was taken in siliconized glass bulbs containing sodium citrate (3.8% solution 0.3 ml for 1.7 ml of blood). The bulb was rotated on a turntable and samples removed periodically for platelet counting which was done by the method of Brecher and Cronkite (12). The percentage difference between initial platelet count and after 30 and 60 minutes was taken as degree of platelet adhesiveness and called the adhesive index as described by Wright (8). Since thrombi in ischaemic heart disease occur mainly on the arterial side, simultaneous samples of both arterial and venous blood were withdrawn from the same individuals during cardiac catheterization. A siliconized set up was used. This included 20 cardiac patients free from ischaemic heart disease. Since the circulating blood on the arterial side has higher velocity than on the venous side, different speeds of rotation were worked out in several trials until respective speeds were determined which gave approximately the same results of adhesiveness in both arterial and venous blood. Arterial blood required the rate of 40 revolutions per minute while venous blood required 10. At these speeds, a comparison between adhesiveness in arterial and venous blood from the same normal individual hardly showed any difference after 60 minutes of rotation. Platelet adhesiveness was therefore studied in venous blood only in individuals suffering from ischaemic heart disease of the three types; namely, 16 patients with angina pectoris, 9 with acute myocardial infarction without anticoagulant treatment and 8 post-infarction cases several months to years after the acute episode. Eleven normal persons were also studied.
PLATELET
_
NORMAL
_____
ANGINA ACUTE
.._._.-
211
ADHESIVENESS
M.1
FIG. 1 Drop in platelet counts with time.
2 u
0.6 0.5.
t, i
0.4.
t if
0.3, 0
(t4:&,,,
69
TIME
TABLE I Mean and Standard Deviation of Platelet Adhesiveness in Normals and Ischaemic Diseases of the Heart
Group
Mean + S.D.
Number 30 minutes
A)
Normal
11
B)
Acute MI
C)
Angina
D)
Post-infarction
9 16 a
60 minutes
40.47 + 12.24
52.16 + 9.66
66.28 +
3.88
73.05 + 5.53
59.67 2 12.17
73.42 + 8.42
60.66 +
71.40 + 7.55
8.30
Statistical Evaluation 30 minutes
60 minutes
Groups t value
p value
t value
p value
A&B
6.054
Vol. States
6, pp. 209-214, Pergamon Press,
1975 Inc.
PLATELET ADHESIVENESS IN THE ASSESSMENT OF ISCHAEMIC HEART DISEASES*
Sujata Chaudhurif Blood Coagulation Laboratory, Department of Cardiology, All India Institute of Medical Sciences, New Delhi-16
(Received 2.10.1975; in revised form 22.1.1975. Accepted by Editor W.H. Seegers)
ABSTRACT Study of adhesiveness of the platelets in ischaemic heart disease was undertaken. Fasting venous blood samples were collected from four groups of individuals: (1) cases with angina, (2) cases with acute infarction without anticoagulant therapy, (3) post-infarction cases after several months to years after the acute episode, and (4) normal individuals. Preliminary investigation employing arterial and venous blood from the same individual revealed no significant difference in the adhesiveness of platelets at 60 minutes (when rotation was done at the rate of 40 revolutions per minute for arterial blood and 10 revolutions per minute for venous blood). All subsequent determinations were, therefore, done with venous blood. Conclusions from the observations were: (1) Initial platelet counts in ischaemic heart disease group were significantly higher than in the normal group; (2) On rotation, adhesiveness was more marked in ischaemic heart disease group than in the normal group; (3) Adhesiveness in the IHD categories were not significantly different from each other. Higher initial counts and more adhesiveness in the ischaemic heart disease group seemed to point out a basal disturbance in homeostatic balance of qualitatively defective platelets in these potential states of thrombogenesis. If this adhesiveness of platelets had a relationship to the thrombotic episodes, these data suggested that angina cases should be considered as potential cases of acute and subacute myocardial infarction.
* Abstract published in the Proceedings of the XIII International Congress of Hematology held in Munich, 1970. ' Emeritus Scientist, ICMR. 209
210
PLGTELET
ADHESIVENESS
vo1.6,No.3
INTRODUCTION The platelets in the circulating blood, normally not adherent to the normal vascular endothelium, form aggregates on damaged intima as in atherosclerosis. Thus, platelet aggregation may be taken as the initial step in the chain of events which leads to thrombosis (l-3). Mustard et al (4) have shown by in vitro studies that blood clots formed in a glass tube are quite different from a thrombus, but Chandler (5) has demonstrated that blood clots formed in a rotating tube are similar in structure to thrombi formed in flowing blood. O'Brien (6) has shown that ADP induces platelet aggregation and possibly platelet adhesiveness to surfaces. Born and Cross (7) described a method by which the ADP-induced aggregation of platelets could be quantitatively studied. Wright (8) made important observations on increased platelet stickiness in conditions associated with intravascular thrombosis. McDonald and Edgill (9) demonstrated increased platelet adhesiveness in patients with ischaemic heart disease and McDonald (10) suggested that abnormal platelet adhesiveness might precede the development of intravascular clotting as in ischaemic heart disease. Slack et al (11) studied the level of lipoprotein lipase and the degree of platelet stickiness in patients with ischaemic heart disease as compared to controls and suggested the possibility of a deficiency of this enzyme in these patients. As part of an overall study on the pathogenesis of thrombotic diseases, the role of platelet adhesiveness in the genesis of intravascular clotting was investigated. This communication reports the findings in ischaemic heart diseases with and without overt thrombosis.
MATERIALS AND METHODS Study of platelet adhesiveness was undertaken by Wright's (8) method. A rotator machine constructed locally was used in the study. A measured amount of whole blood was taken in siliconized glass bulbs containing sodium citrate (3.8% solution 0.3 ml for 1.7 ml of blood). The bulb was rotated on a turntable and samples removed periodically for platelet counting which was done by the method of Brecher and Cronkite (12). The percentage difference between initial platelet count and after 30 and 60 minutes was taken as degree of platelet adhesiveness and called the adhesive index as described by Wright (8). Since thrombi in ischaemic heart disease occur mainly on the arterial side, simultaneous samples of both arterial and venous blood were withdrawn from the same individuals during cardiac catheterization. A siliconized set up was used. This included 20 cardiac patients free from ischaemic heart disease. Since the circulating blood on the arterial side has higher velocity than on the venous side, different speeds of rotation were worked out in several trials until respective speeds were determined which gave approximately the same results of adhesiveness in both arterial and venous blood. Arterial blood required the rate of 40 revolutions per minute while venous blood required 10. At these speeds, a comparison between adhesiveness in arterial and venous blood from the same normal individual hardly showed any difference after 60 minutes of rotation. Platelet adhesiveness was therefore studied in venous blood only in individuals suffering from ischaemic heart disease of the three types; namely, 16 patients with angina pectoris, 9 with acute myocardial infarction without anticoagulant treatment and 8 post-infarction cases several months to years after the acute episode. Eleven normal persons were also studied.
PLATELET
_
NORMAL
_____
ANGINA ACUTE
.._._.-
211
ADHESIVENESS
M.1
FIG. 1 Drop in platelet counts with time.
2 u
0.6 0.5.
t, i
0.4.
t if
0.3, 0
(t4:&,,,
69
TIME
TABLE I Mean and Standard Deviation of Platelet Adhesiveness in Normals and Ischaemic Diseases of the Heart
Group
Mean + S.D.
Number 30 minutes
A)
Normal
11
B)
Acute MI
C)
Angina
D)
Post-infarction
9 16 a
60 minutes
40.47 + 12.24
52.16 + 9.66
66.28 +
3.88
73.05 + 5.53
59.67 2 12.17
73.42 + 8.42
60.66 +
71.40 + 7.55
8.30
Statistical Evaluation 30 minutes
60 minutes
Groups t value
p value
t value
p value
A&B
6.054
