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NSAIDs and the Heart

The nonsteroidal anti-inflammatory drugs (NSAIDs) Celebrex and Vioxx have recently come under fire when it was admitted that these drugs could significantly increase the risk of heart attack and stroke. Are these the only NSAIDs capable of increasing this risk though?

Many heart disturbances, including heart attack, result from decreased blood flow to the heart. Common causes of decreased blood flow include arterial plaque formation, blood clots, and narrowing of the arteries from muscular contraction of the blood vessels.

Arterial plaque formation starts with damage to the blood vessel walls. This leads to depositing of cholesterol and calcium on the arterial walls. One of the most common causes of the arterial damage is high blood pressure caused from constriction of blood vessels. Various factors may lead to blood vessel constriction. These include elevated serum calcium, elevated insulin levels in type 2 diabetes, and epinephrine (adrenaline) induced constriction. NSAIDs constrict blood vessels as well, which leads to an elevation of blood pressure. Increased blood pressure may result in narrowing of the arteries from plaque due to resulting arterial damage. This narrowing of the arteries not only increases the risk of heart attack, but also of thrombic and embolytic stroke.

Because NSAIDs constrict blood vessels, these drugs increase the risk of angina, heart arrhythmias, and heart attack in people with already impaired perfusion to the heart. These include individuals with previous angina, or heart attacks, history of congestive heart failure, diabetics, and individuals who tend to put out too much epinephrine, etc.

Further risk comes from the fact that NSAIDs inhibit prostaglandins, including prostacyclin, also known as prostaglandin I2 (PGI2). PGI2 is produced by healthy endothelial cells of blood vessels. The roles of PGI2 are to dilate blood vessels, to increase blood flow, and to inhibit platelet formation and blood clot formation. By dilating blood vessels, blood pressure is reduced, and more blood reaches critical areas, such as the brain and heart. This also lowers the risk of heart disease by reducing arterial damage, which would otherwise lead to plaque formation. By reducing blood clot formation, the risk of heart attack and thrombic stroke are reduced. Both damage to endothelial cells and the use of NSAIDs inhibit PGI2 production, which increases blood clot formation and reduces blood flow. Production of blood clots and reduction of blood flow increase the risk of angina, arrhythmias, and heart attack, as well as transient ishemic attacks, and thrombic stroke.

As we can see, the increased risk of heart attack and stroke are not limited to certain NSAIDs, but rather can occur with all pharmaceutical NSAIDs. And the problem is not a new finding. The blood vessel constricting effects of NSAIDs have been known for decades. Part of the drug approval process includes knowing how the drug works. NSAIDs are known, and have been known, to work by consticting blood vessels. When blood vessels are overdilated by inflamamtory prostaglandins, they become permeable, which leads to leakage of fluids in to the surounding tissues, and resulting inflammation. By consticting blood vessels, NSAIDs prevent blood vessels from leaking. It is well known that the adverse effects of liver and kidney failure by NSAIDs is due to impeded blood flow to these organs due to this constiction of the blood vessels. Other organs, such as the heart, as well as glands are adversely affected by the impeded blood flow in the same manner. Therefore, the only explanation for the increased risk of heart attack and stroke being "discovered" recently would be that the drug companies and FDA knew about the problem all along and just recently decided to make this known fact public.


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