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Distinct Mechanism Between Arterial

vs Venous Thrombosis:
Impact for Clinical Manifestations
M Taufik Ismail, MD, FIHA
Arterial vs Venous Thrombosis

Arterial thrombosis (AMI) Venous thrombosis (VTE)

• Endothelial dysfunction ➔ • Mostly intact endothelial

atherosclerotic plaque ➔
rupture ➔ platelet
aggregation ➔ thrombus
• Rich in platelet • Rich in fibrin & RBC, and
platelet activation
• High shear flow • Slow shear flow

(Koupenova et al., 2016)

(Koupenova et al., 2016)
Arterial thrombosis

Thrombus in STEMI (562 patients)

• White thrombi: 31% of cases; and red thrombi, 69%
• White thrombi ➔ smaller vessels and lower ischemic times.
• White thrombi were smaller and associated with fibrin infiltration,
whereas red thrombi were associated with red blood cell infiltration.
• Red thrombi were associated with large filling defects, white thrombi
➔ hazy lesions

(Quadros et al. 2012)

(Quadros et al. 2012)
(Quadros et al. 2012)
Venous thrombi
VTE Pathophysiology

• Begins at the valves or venous sinuses

• Antithrombotic proteins (thrombomodulin) and endothelial
protein C receptor (EPCR) are regionally expressed on the
valves and are sensitive to hypoxia and inflammation.
• Hypoxia ➔ upregulation of procoagulants such as tissue
factor on endothelium and P-selectin (an adhesion
molecule) also on endothelium leading to recruitment of
leukocytes or monocyte derived leukocyte microparticles
also containing tissue factor
• These conditions + acute inflammation ➔ thrombus
(Behravesh et al., 2017)
(Butnik & Brill, 2018)

• Factor V Leiden mutation

• Inability of activated protein C to degrade and inactivate
factor V.
• mutations in prothrombin and fibrinogen and mutations in
proteins mediating anticoagulation.
• Mutations in antithrombin, protein C and protein S.
• Non-O blood types
• Genetic mutation:
• alanine to cytosine mutation (A1298C) in the
methylenetetrahydrofolate reductase (MTHFR) gene
• The 4G/5G polymorphism in the plasminogen activator inhibitor (PAI-
(Koupenova et al., 2016)
(Butnik & Brill, 2018)
Continuity of Arterial and Venous Trombosis

• Venous and arterial thrombotic disorders have long been

viewed as separate pathophysiological entities.
• Arterial thrombosis ➔ platelet activation; venous
thrombosis ➔ activation of the clotting system
• However, there is evidence that this dichotomy is likely to be
an oversimplification.
• Accordingly, anticoagulant drugs are highly effective for
prevention of arterial embolism related to AF, and for
prevention and treatment of CAD
• Likewise, platelets play an inevitable role in the formation of
thrombi in the venous system, and antiplatelet agents have
been shown to be effective for prevention of VTE.

• Prandoni et al (2003) odds ratio (OR) for carotid plaques in patients

with unprovoked as compared to secondary DVT and controls was
found to be 2.4.
• Hong et al (2005) found a higher prevalence of coronary artery
calcium, as assessed by CT, in patients with unprovoked VTE than in
matched control individuals.
• Glynn et al (2009) reported that VTE rosuvastatin treatment
decreased the prevalence of VTE in the JUPITER trial
• Duran et al (2010) reported that aortic elastic properties were
impaired and aortic stiffness was increased in patients with VTE
• CAVI was increased in patients with VTE.

(Aykan et al, 2016)


• Arterial thrombosis mostly involve plaque rupture and

trombotic formation
• Venous thrombosis appeared in contact endothelium
• There are continuity between arterial and venous occlusion
-Matur Nuwun-
• A retrospective subgroup analysis of the Heart and Estrogen
Replacement Study (HERS): the use of statins ➔ 50% risk reduction
of VTE
• This beneficial effect of statins may be due to decreased thrombus
formation mediated:
• anti-inflammatory activity,
• suppression of the prothrombotic and endothelial-altering properties of
circulating lipids and
• improvement of the rheological properties of the blood.
• alter elements of the coagulation cascade consistent with an antithrombotic
• In this study: long-term aspirin therapy decreased the risk of VTE in
women with established CAD
(Grady et al, 2000)
(Butnik & Brill, 2018)
risk factor pathogenetic mechanism reference
older age increased oxidative stress Prandoni et al – 8
increased BMI metabolic deterioration Nurses Health Study – 9
hypertension haemodynamic stress Nurses Health Study – 9
metabolic deterioration

smoking damage of vessel wall Nurses Health Study – 9

oxidative stress

hypercholesterolemia impairment of regulation of Voya et al – 10

coagulation Spbieszcyk at el - 4
Libby and Simon - 5
increased viscosity
and erythrocyte aggregation