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

Author(s):  
David L. Bark ◽  
Andrea N. Para ◽  
David N. Ku

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].

Author(s):  
David L. Bark ◽  
David N. Ku

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.


2019 ◽  
Vol 28 ◽  
pp. S18
Author(s):  
Georgina Bird ◽  
Kathryn Hally ◽  
Anne La Flamme ◽  
Scott Harding ◽  
Peter Larsen

Angiology ◽  
2021 ◽  
pp. 000331972110125
Author(s):  
Atalay Demiray ◽  
Baris Afsar ◽  
Adrian Covic ◽  
Masanari Kuwabara ◽  
Charles J. Ferro ◽  
...  

Increased serum uric acid (SUA) levels have been associated with various pathologic processes such as increased oxidative stress, inflammation, and endothelial dysfunction. Thus, it is not surprising that increased SUA is associated with various adverse outcomes including cardiovascular (CV) diseases. Recent epidemiological evidence suggests that increased SUA may be related to acute myocardial infarction (AMI). Accumulating data also showed that elevated UA has pathophysiological role in the development of AMI. However, there are also studies showing that SUA is not related to the risk of AMI. In this narrative review, we summarized the recent literature data regarding SUA and AMI after providing some background information for the association between UA and coronary artery disease. Future studies will show whether decreasing SUA levels is beneficial for outcomes related to AMI and the optimum SUA levels for best outcomes in CV diseases.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T Kawai ◽  
D Nakatani ◽  
T Yamada ◽  
T Watanabe ◽  
T Morita ◽  
...  

Abstract Background Diuretics has been reported to have a potential for an activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system, leading to a possibility of poor clinical outcome in patients with cardiovascular disease. However, few data are available on clinical impact of diuretics on long-term outcome in patients with acute myocardial infarction (AMI) based on plasma volume status. Methods To address the issue, a total of 3,416 survived patients with AMI who were registered to a large database of the Osaka Acute Coronary Insufficiency Study (OACIS) were studied. Plasma volume status was assessed with the estimated plasma volume status (ePVS) that was calculated at discharge as follows: actual PV = (1 − hematocrit) × [a + (b × body weight)] (a=1530 in males and a=864 in females, b=41.0 in males and b=47.9 in females); ideal PV = c × body weight (c=39 in males and c=40 in females), and ePVS = [(actual PV − ideal PV)/ideal PV] × 100 (%). Multivariable Cox regression analysis and propensity score matching were performed to account for imbalances in covariates. The endpoint was all-cause of death (ACD) within 5 years. Results During a median follow-up period of 855±656 days, 193 patients had ACD. In whole population, there was no significant difference in long-term mortality risk between patients with and without diuretics in both multivariate cox regression model and propensity score matching population. When patients were divided into 2 groups according to ePVS with a median value of 4.2%, 46 and 147 patients had ACD in groups with low ePVS and high ePVS, respectively. Multivariate Cox analysis showed that use of diuretics was independently associated with an increased risk of ACD in low ePVS group, (HR: 2.63, 95% confidence interval [CI]: 1.22–5.63, p=0.01), but not in high ePVS group (HR: 0.70, 95% CI: 0.44–1.10, p=0.12). These observations were consistent in the propensity-score matched cohorts; the 5-year mortality rate was significantly higher in patients with diuretics than those without among low ePVS group (4.7% vs 1.7%, p=0.041), but not among high ePVS group (8.0% vs 10.3%, p=0.247). Conclusion Prescription of diuretics at discharge was associated with increased risk of 5-year mortality in patients with AMI without PV expansion, but not with PV expansion. The role of diuretics on long-term mortality may differ in plasma volume status. Therefore, prescription of diuretics after AMI may be considered based on plasma volume status. Funding Acknowledgement Type of funding source: None


Sign in / Sign up

Export Citation Format

Share Document