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Chapter 27 Thrombosis and antithrombotic therapy / 363
Thrombi are solid masses or plugs formed in the
circulation from blood constituents. Platelets and
fibrin form the basic structure. Their clinical signifi -
cance results from ischaemia from local vascular
obstruction or distant embolization. Th rombi are
involved in the pathogenesis of myocardial infarc-
tion, cerebrovascular disease, peripheral arterial
disease, deep vein thrombosis (DVT) and pulmo-
nary embolism (PE).
Thrombosis, both arterial and venous, is more
common as age increases and is frequently associ-
ated with risk factors (e.g. surgery or pregnancy).
The term thrombophilia is used to describe inher-
ited or acquired disorders of the haemostatic mech-
anism that predispose to thrombosis.
Arterial t hrombosis Figure 27.1 Arteriogram showing saddle embolus at
the aortic bifurcation (dotted arrow) and embolus in
the left common iliac artery (solid arrow).
Pathogenesis
Atherosclerosis of the arterial wall, plaque rupture
and endothelial injury expose blood to subendothe-
lial collagen and tissue factor. This initiates the for-
mation of a platelet nidus on which platelets adhere Table 27.1 Risk factors for arterial
thrombosis (atherosclerosis).
and aggregate.
Platelet deposition and thrombus formation are
Positive family history
important in the pathogenesis of atherosclerosis.
Platelet - derived growth factor stimulates the migra- Male sex
tion and proliferation of smooth muscle cells Hyperlipidaemia
and fibroblasts in the arterial intima. Regrowth of
Hypertension
endothelium and repair at the site of arterial damage
and incorporated thrombus result in thickening of Diabetes mellitus
the vessel wall.
Gout
As well as blocking arteries locally, emboli of
platelets and fibrin may break away from the Polycythaemia
primary thrombus to occlude distal arteries. Hyperhomocysteinaemia
Examples are carotid artery thrombi leading to cere-
Cigarette smoking
bral thrombosis and transient ischaemic attacks
and heart valve and chamber thrombi leading to ECG abnormalities
systemic emboli and infarcts (Fig. 27.1 ). Elevated CRP, IL6, fi brinogen, lipoprotein -
associated phospholipase A 2
Clinical r isk f actors Lupus anticoagulant
The risk factors for arterial thrombosis are related Collagen vascular diseases
to the development of atherosclerosis and are listed Beh ç et ’ s disease
in Table 27.1 . Th e identification of patients at risk
is largely based on clinical assessment. A number of
CRP, C - reactive protein; ECG, electrocardiogram.
epidemiological studies have resulted in the con-