Thrombotic Tendencies in Excess Catecholamine States

Abstract

Catecholamines are neurotransmitters distributed throughout the body including adrenal glands, chromaffin tissues and other tissues innervated by post ganglionic adrenergic neurons. The rate of release of medullary hormones is responsible for the control of serum catecholamines. Thrombogenicity of catecholamines are due various mechanisms including hypercoagulable states, endothelial damage, blood stasis and platelet aggregation. Oxidative stress generated by catecholamine excess causes coronary spasm, ultrastructural cell damage and arrhythmias. Elevated plasminogen activator inhibitor-1 during catecholamine excess causes hypercoagulability by hypofi-brinosis. During stress, Catecholamines released in procoagulant environment causes vasoconstriction in adrenal veins resulting in venous thrombosis. Catecholamines generate moderately elevated levels of platelet count which enhances the risk of thrombosis. Hypercoagulability results in formation of coronary thrombus, rupture of atherosclerotic plaque and plaque progression due to gradual fibrinogen accumulation in the vessel walls. High levels of circulating catecholamines produce elevated levels thrombomodulin, the biomarkers of endothelial cell damage. In patients with hypertension in catecholamine excess, resistance to blood flow and damage to the integrity of blood vessels lead to atherosclerosis. A case report has been discussed which suggests an association of thrombotic tendency and catecholamine excess.