Gross specimen: thromb of the left ventricle of the heart, thromb in the aorta, spherical blood clot of the left auricle, cardiovascular accident, ischemic infarction of the spleen, cyst of the cerebrum, ischemic infarction of the cerebrum (grey softening of the brain), metastases of cancer of the stomach in the liver.
Microscopic specimen: blood clot in the artery, organization of blood clot, fatty embolism of the pulmonary capillaries, ischemic infarction of the kidney, metastasis of cancer in the liver.
Thrombosis refers to the formation within a vascular lumen of a thrombus, defined as an aggregate of coagulated blood containing platelets, fibrin, and entrapped cellular elements. A thrombus is by definition adherent to the vascular endothelium and should be distinguished from a simple blood clot, which reflects only the activation of the coagulation cascade and can form in vitro or in situ in the postmortem state. Similarly, a thrombus is different from a hematoma, which results from hemorrhage and subsequent clotting outside the vascular system.
Thrombosis in the Arterial System.Pathogenesis: The most common cause of arterial thrombosis is atherosclerosis, and the most important vessels involved are the coronary, cerebral, mesenteric, renal arteries and the arteries of the lower extremities. Uncommonly, arterial thrombosis occurs in other disorders, including inflammation of the arteries (arteritis), trauma, and diseases of the blood. Thrombi are common inaneurysms (localized dilatations of the lumen) of the aorta and its major branches, in which the distortion of blood flow, combined with intrinsic vascular disease, promotes thrombosis.
The pathogenesis of arterial thrombosis involves principally three factors:
Damage to the endothelium, usually by atherosclerosis, disturbs the anticoagulant properties of the vessel wall and serves as the nidus for platelet aggregation and fibrin formation.
Alterations in blood flow, whether from turbulence in an aneurysm or at the sites of arterial bifurcation, or slowing in narrowed arteries, tend to favour thrombosis.
Increased coagulability of the blood, as seen in polycythemia vera, or after the use of oral contraceptives, is associated with an increased risk of thrombosis.
Pathology: Initially, an arterial thrombus, which is belied to the vessel wall, is soft, friable, and dark red, with fine alternating bands of yellowish platelets and fibrin, the so-called lines of Zahn. Once formed, arterial thrombi have several outcomes.
Lysis of an arterial thrombus may occur, owing to the potent thrombolytic activity of the blood.
Propagation of a thrombus (i.e., an increase in its size) may occur, because the thrombus serves as the focus for further thrombosis. Organization refers to the eventual invasion of connective tissue elements, which causes it to become firm and grayish white.
Canalization is the process by which new lumina lined by endothelial cells form in an organized thrombus. The functional significance of this change is often questionable.
The organized structure of a thrombus reflects a tight interaction between platelets and fibrin and differs in appearance from a postmortem clot or one formed in vitro. The lines of Zahn stabilize the thrombus formed during life, whereas the postmortem clot has a more gelatinous structure. Postmortem clots occur in stagnant blood in which gravity fractionates the erythrocytes. The part of the clot that contains many red blood cells is called currant jelly. The overlying clot, which represents coagulated plasma without red blood cells, is called chicken fat because of its color and consistency.
Clinical Features:Arterial thrombosis is the most common cause of death in Western industrialized countries. Since most arterial thrombi occlude the vessel, they often lead to ischemic necrosis of the tissue supplied by the artery—that is, an infarction. Thus, thrombosis of the coronary or cerebral artery results in myocardial infarcttion (heart attack) or cerebral infarction (stroke). Other end arteries that are affected by atherosclerosis and often suffer from thrombosis include the mesenteric arteries (intestinal infarction), renal arteries (kidney infarctions), and arteries of the leg (gangrene).
Thrombosis in the heart.As in the arterial system, endocardial injury and changes in blood flow in the heart are associated with mural thrombosis. The disorders in which mural thrombosis occurs include the following:
Myocardial infarction: Adherent mural thrombi form in the cavity of the left ventricle over the areas of myocardial infarction, owing to damaged endocardium and alterations in blood flow associated with an adynamic segment of the myocardium.
Atrial fibrillation: A disorder of atrial rhythm (atrial fibrillation) leads to slower blood flow in the left atrium, a situation that predisposes to the formation of mural thrombi in that location.
Cardiomyopathy: Primary diseases of the myocardium are associated with mural thrombi in the left ventricle. The reasons are poorly understood but presumably relate to endocardial injury and altered hemodynamics associated with poor myocardial contractility.
Endocarditis: Small thrombi, termed vegetations, may also develop on cardiac valves, usually mitral or aortic, that are damaged by a bacterial infection (bacterial endocarditis). Occasionally, in the absence of valve infection, vegetations form on the mitral or tricuspid valve injured by systemic lupus erythematosis (Libman-Sacks endocarditis). In chronic wasting states, such as occur with terminal cancer, large, fri-able vegetations may appear on the cardiac valves, possibly reflecting a hypercoagulable state.
The major complication of thrombi in any location in the heart is the detachment of fragments and their transport to distant sites (embolization), where they lodge and occlude arterial vessels.