Computational Model of Thrombosis: A Study of Transport as a Determinant of Rapid Platelet Accumulation

2011 ◽  
Author(s):  
David L. Bark ◽  
David N. Ku
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Blood Flow ◽  
Blood Vessel ◽  
Growth Rates ◽  
Heart Attack ◽  
Arterial Thrombosis ◽  
Platelet Adhesion ◽  
Relative Contribution ◽  
Platelet Accumulation

Thrombus is commonly found in the plaque region of atherosclerosis, leading to acute myocardial infarction, known as a heart attack. Arterial thrombosis, which is mostly composed of platelets, can occlude a blood vessel by accumulating enough platelets to block blood flow. Understanding the relative contribution of platelet transport and platelet adhesion to thrombus growth rates is germane to predicting and treating at-risk lesions for thrombus growth.

Thrombus Initiation With Subsequent Growth Measured for Physiological Shear and High Pathological Shear

2011 ◽  
Author(s):  
David L. Bark ◽  
Andrea N. Para ◽  
David N. Ku
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Heart Attack ◽  
Arterial Thrombosis ◽  
Atherosclerotic Disease ◽  
High Shear ◽  
Subsequent Growth ◽  
Low Shear ◽  
Undisturbed Flow

Arterial thrombosis is often found near an atheroma in atherosclerotic disease, which can lead to acute myocardial infarction, i.e. a heart attack. Thrombus typically grows in regions of exposed subendothelium, which can exist when the plaque cap of the atheroma ruptures or erodes. The subendothelium creates an adherent surface to platelets and other thrombus constituents. Furthermore, an atheroma alters the normal physiological hemodynamics, which has been reported to correspond to local thrombus growth, despite equally adherent surfaces in undisturbed flow regions [1,2]. However, there has been some disagreement about which hemodynamics, specifically shear, may play the most influential role of localizing thrombus. Low shear and high shear have both resulted in thrombus growth [1,2]. Shear in the region of an atheroma can get over 100,000 s−1 [3].

scholarly journals Trends in Prehospital Delay in Patients With Acute Myocardial Infarction (from the Worcester Heart Attack Study)

2008 ◽  
Vol 102 (12) ◽  
pp. 1589-1594 ◽  
Author(s):  
Jane S. Saczynski ◽  
Jorge Yarzebski ◽  
Darleen Lessard ◽  
Frederick A. Spencer ◽  
Jerry H. Gurwitz ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Heart Attack ◽  
Prehospital Delay

scholarly journals Effects of Sodium Nitroprusside on Platelet Adhesion, Subsequent Aggregation and Vasoconstriction

1977 ◽  
Author(s):  
H.R. Baumgartner
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Sodium Nitroprusside ◽  
Platelet Adhesion ◽  
Ex Vivo ◽  
Balloon Catheter ◽  
Strong Inhibitor ◽  
Induced Aggregation

Sodium nitroprusside (SNP), a potent vasodilator, has shown beneficial effects in acute myocardial infarction. Since platelets may play an important role in the pathogenesis of myocardial infarction, the effect of SNP on their interaction with rabbit aorta subendothelium was investigated in vivo and under controlled blood flow conditions ex vivo and in vitro.One iliac artery and the abdominal aorta were denuded of endothelium by balloon catheter injury during infusion of glucose, SNP at 6 or 12 μg/kg/min in groups of 12, 6 and 7 rabbits respectively. The aorta and their branches were perfuse-fixed under controlled pressure 10 min after denudation. Morphometric evaluation showed dose-dependent and significant (2p < 0.01 or 0.001) inhibition of platelet spreading, adhesion and aggregation. The latter was abolished at the higher dose of SNP. Denudation and subsequent platelet adhesion caused strong vasoconstriction (2p < 0.001) which was inhibited by SNP (2p < 0.01).By exposure of subendothelium to either citrated blood or native blood in a flow chamber (2000 sec-1 shear rate) strong inhibition of spreading and adhesion-induced aggregation was again demonstrated at 6 and 12 μg/kg/min SNP. In vitro, adhesion-induced aggregation was completely abolished after the addition of SNP to rabbit (at 20 μg/ml) or human blood (2 μg/ml). 1 μg/ml PGE1 was needed to induce a similar inhibitory effect.Thus SNP is a strong inhibitor of platelet function and of injury + platelet induced vasoconstriction. These findings may explain its beneficial effect in acute myocardial infarction.

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