What is Thromboxane?

Thromboxane is a lipid essential to the body’s production of clots. To stop bleeding, the lipid simultaneously restricts arteries and veins while clumping platelets. Platelets produce thromboxane through conversion of certain prostaglandins. In individuals with high blood pressure and/or high cholesterol, the lipid has a negative effect by restricting arteries and causing arterial plaque buildup. Aspirin inhibits the production of thromboxane, reducing one’s chances of suffering a first or second heart attack.

The primary function of thromboxane is to stop bleeding. When the body experiences a cut, the lipid assists platelets in clumping so that the platelets can eventually form a clot. This process begins when the lipid narrows the arteries leading to the cut site. This action makes the platelets’ job easier by reducing blood pressure and limiting overall blood loss.

The body’s platelets produce thromboxane from arachidonic acid. This process is significant as prostacyclin, a platelet produced lipid that inhibits clot formation, is also created from arachidonic acid. These two lipid compounds normally act in homeostasis within the human body, the balance only changing during and immediately after a bleeding event. In certain instances, though, this balance becomes upset.

When an individual experiences a rise in cholesterol, thromboxane becomes a bane rather than a benefit. When cholesterol levels become unhealthy, the lipid acts by depositing cholesterol on arterial walls. This arterial plaque buildup narrows and hardens arteries, increasing the chances of both heart disease and heart attack. Though nearly anyone can become afflicted with vasoconstriction, a rare medical condition speeds up the process in an unlikely group: young women with no previous coronary disorder.

Prinzmetal’s angina is a form of angina with two unique characteristics. Unlike most forms of angina, pain always presents while the patient is at rest. Also, younger women with normal cholesterol are the most affected. Though thromboxane levels are also normal, a genetic abnormality creates arterial tissue that is more receptive to plaque buildup. Though treatable with nitrate medication, Prinzmetal’s angina is a lifelong condition that requires a patient to maintain a healthy lifestyle.

Individuals at risk for heart attack can lower their levels of thromboxane by taking a daily dose of aspirin. The medication inhibits platelets’ ability to produce the lipid. Taking 40 mg of aspirin a day is the standard daily dose. Individuals wishing to further lower their risk for heart attack should consult their primary care physician before making any other significant lifestyle changes.