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|This page is dedicated to my dear friend Bill who presumably was first put in a wheel chair by statins and then presumably or most likely died as a result of dual anti platelet therapy which is Aspirin and Plavix together . He died of a hemorrhagic stroke which is the bleeding of a brain vessel. His death in my opinion was most likely Iatrogenic (doctor/drug induced) ironically I now must resort to taking it myself for elevated MPV ,MCV and low salicylate levels from natural foods. For certain I have tried mostly all other natural ways.|
Most below links discourage the use of aspirin for Primary Prevention, primary prevention is when you are taking it to prevent a disease and some links below are pro aspirin for Secondary Prevention only! Secondary Prevention is when you already have a disease and treat it! many links show the pharmacokinetics of aspirin (how it works) Featured Website they seem to have done there homework ~ Repair of the Stomach and Duodenal after ulceration Dr Greger, on Salicylic acid (Aspirin) in Plants
1. http://www.drsinatra.com/is-daily-aspirin-right-for-you/ a
SECTION 3. ASPIRIIN ~ Dual Anti Platelet Therapy is it good for you? what nobody tells us!
|In the early 2000s the endovascular functions of the COX enzymes were unraveled. COX enzymes proved to play important parts in thrombogenesis [ 36 ]. Activated blood platelets produce COX-1-dependent thromboxane TXA2, which acts as a prothrombotic platelet agonist and vasoconstrictor. Nearby endothelial and smooth muscle cells produce COX-2-dependent prostaglandin I2 (PGI2), especially after cell damage has occurred [ 37 ]. PGI2 is an antithrombotic platelet inhibitor and vasodilator and thus modulates the interaction between activated platelets and the endovascular wall. Cell damage, atherosclerotic plaques, and laminar shear forces selectively up-regulate the expression of COX-2 by endothelial cells in an attempt to maintain homoeostasis [ 38 ]. Understanding these mechanisms, one could infer that, in clinical syndromes associated with platelet activation, COX inhibition by any NSAID, but especially by COX- 2-selective NSAIDs, may increase the risk for cardiovascular events [ 37 ]. As their effect is temporary and reversible, only continuous high dosage of nonselective NSAIDs will considerably inhibit COX-1 and COX-2. However, COX-2-selective NSAIDs may, by their irreversible covalent binding of COX-2, strongly impair the synthesis of endothelium derived antithrombotic and vasodilatory prostacyclin while lacking COX-1-inhibiting effects on platelet aggregation, thus tipping the scales of homeostasis in favor of thrombogenesis and vasoconstriction full article|
*Aspirin is still one of the most widely used drugs on the market with 40,000 tons of it being consumed each year around the world! Most people tend to think of over-the-counter medicines as being safe. However, According to the American Gastroenterological Association (AGA), each year the side effects of NSAIDs hospitalize over 100,000 people and kill 16,500 people in the U.S. alone. The most common side effects of aspirin include bleeding ulcers and tinnitus. Use with caution.
Vasoconstriction possibilities? takes minute to load from their library