It is likely that the risk of cardiovascular events from pharmaceuticals as COX-2 inhibitors can be reduced significantly by standard pharmaceutical and lifestyle preventative measures

Abstract

Based on the principles of the altered homeostatic theory, a case will be made that the risk of cardiovascular (CV) events from pharmaceuticals as COX-2 inhibitors (coxibs) and sympatho-mimetic drugs can be reduced significantly by using standard pharmaceutical and lifestyle preventative measures as statins, exercise, a proper diet, and weight and stress reduction. The standard method of preventing CV events from coxibs, the prototypical pharmaceuticals which induce CV events, is not overly helpful; this method is based essentially on limitation of coxibs to low risk individuals, and to low dose and short term usage. Use of standard preventative measures apparently had not been considered because coxib-induced CV events are regarded as "special" as they are attributed to thromboxane. "Regular" CV events are attributed basically to dyslipidemia, and standard preventative measures are designed to improve dyslipidemia; therefore, it probably has been assumed that standard therapy for "regular" CV events would not be applicable to coxib-induced infarctions. In contrast, the altered homeostatic theory treats pharmaceuticals which induce CV events as "regular" risk factors which induce "regular" CV events. Therefore, "regular" preventative measures as exercise and statins should reduce the incidence of pharmaceutical-induced CV events. The critical issue is the mechanism of CV events. Thrombosis is the accepted and vasoconstriction (spasm of resistance vessels) is a proposed mechanism for CV events, and thrombosis and/or vasoconstriction (thrombosis/vasoconstriction) is regarded as the direct mechanism of CV events. Multiple and diverse "regular" risk factors express thrombosis/vasoconstriction, and multiple and diverse pharmaceutical and lifestyle preventative measures express anti-thrombosis/vasodilation. Risk and preventative factors are considered to operate in a dynamic balance; dominance of thrombosis/vasoconstriction favors development of CV events, and dominance of anti-thrombosis/vasodilation favors prevention of CV events. Thromboxane, and thus coxibs, and sympatho-mimetic drugs also express thrombosis/vasoconstriction; it is this expression which makes pharmaceuticals "regular" risk factors which induce "regular" CV events. It is assumed that all pharmaceuticals which induce CV events express thrombosis/vasoconstriction; thrombosis/vasoconstriction is the obvious mechanism for CV events from any source, and expression of thrombosis/vasoconstriction by multiple and diverse "regular" risk factors is supportive. Just as standard pharmaceutical and lifestyle preventative agent significantly reduce the risk of "regular" CV events, such measures should significantly reduce the risk of pharmaceuticals which favor CV events; protection is effected by shifting the overall balance between thrombosis/vasoconstriction and anti-thrombosis/vasodilation beneficially towards dominance of anti-thrombosis/vasodilation.