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Arterial thrombi are frequently occlusive; the most common sites in decreasing order of frequency are the coronary, cerebral, and femoral arteries.They typically consist of a friable meshwork of platelets, fibrin, red cells, and degenerating leukocytes.Although these are usually superimposed on a ruptured atherosclerotic plaque, other vascular injuries (vasculitis, trauma) may be the underlying cause.Under special circumstances, they can also occur in the dural sinuses, portal vein, or hepatic vein.Venous thrombi are firm, are focally attached to thevessel wall, and contain lines of Zahn, features that help distinguish them from postmortem clots (see later).The veins of the lower extremities are most commonly involved (90% of cases); however, upper extremities, periprostatic plexus, or the ovarian and periuterine veins can also develop venous thrombi.Venous thrombosis (phlebothrombosis) is almost invari- ably occlusive, with the thrombus forming a long luminal cast.Postmortem clots can sometimes be mistaken for ante- mortem venous thrombi.

Arterial thrombi are frequently occlusive; the most common sites in decreasing order of frequency are the coronary, cerebral, and femoral arteries.They typically consist of a friable meshwork of platelets, fibrin, red cells, and degenerating leukocytes.Although these are usually superimposed on a ruptured atherosclerotic plaque, other vascular injuries (vasculitis, trauma) may be the underlying cause.
Venous thrombosis (phlebothrombosis) is almost invari- ably occlusive, with the thrombus forming a long luminal cast. Because these thrombi form in the sluggish venous circulation, they tend to contain more enmeshed red cells (and relatively few platelets) and are therefore known as red thrombi or stasis thrombi. Venous thrombi are firm, are focally attached to thevessel wall, and contain lines of Zahn, features that help distinguish them from postmortem clots (see later).The veins of the lower extremities are most commonly involved (90% of cases); however, upper extremities, periprostatic plexus, or the ovarian and periuterine veins can also develop venous thrombi. Under special circumstances, they can also occur in the dural sinuses, portal vein, or hepatic vein.
Postmortem clots can sometimes be mistaken for ante- mortem venous thrombi. However, clots that form after death are gelatinous and have a dark-red dependent portion where red cells have settled by gravity and a yellow “chicken fat” upper portion, and are usually not attached to the underlying vessel wall.
Thrombi on heart valves are called vegetations, which may be infected or sterile. Blood-borne bacteria or fungi can adhere to previously damaged valves (e.g., due to rheumatic heart disease) or may cause valve damage directly; in either case, endothelial injury and disturbed blood flow can induce the formation of large thrombotic masses (infective endocarditis; Chapter 12). Sterile vegetations can also develop on noninfected valves in persons with hypercoagulable states, so-called nonbacterial thrombotic endocarditis (Chapter 12). Less commonly, sterile verrucous endocarditis (Libman-Sacks endocarditis) can occur in the setting of systemic lupus erythematosus