[tadd]

Tobra:
I think you are incorrect about false cardiac connections, there is a mechanistic reason... from here: MMS: Error

Important bit:
Coincident with the approval of rofecoxib and celecoxib in 1999, my colleagues and I reported that both drugs suppressed the formation of prostaglandin I2 in healthy volunteers.2 Prostaglandin I2 had previously been shown to be the predominant cyclooxygenase product in endothelium, inhibiting platelet aggregation, causing vasodilatation, and preventing the proliferation of vascular smooth-muscle cells in vitro. However, it was assumed that prostaglandin I2 was derived mainly from COX-1, the only cyclooxygenase species expressed constitutively in endothelial cells. This assumption later proved incorrect, since studies in mice and humans showed that COX-2 was the dominant source. The individual cardiovascular effects of prostaglandin I2 in vitro contrast with those of thromboxane A2, the major COX-1 product of platelets, which causes platelet aggregation, vasoconstriction, and vascular proliferation.

Whereas aspirin and traditional NSAIDs inhibit both thromboxane A2 and prostaglandin I2, the coxibs leave thromboxane A2 generation unaffected, reflecting the absence of COX-2 in platelets. Increasing laminar shear stress in vitro increases the expression of the gene for COX-2, leading our group to suggest that COX-2 might be hemodynamically induced in endothelial cells in vivo. If so, suppression of the COX-2–dependent formation of prostaglandin I2 by the coxibs might predispose patients to myocardial infarction or thrombotic stroke.

Thus, a single mechanism, depression of prostaglandin I2 formation, might be expected to elevate blood pressure, accelerate atherogenesis, and predispose patients receiving coxibs to an exaggerated thrombotic response to the rupture of an atherosclerotic plaque. The higher a patient's intrinsic risk of cardiovascular disease, the more likely it would be that such a hazard would manifest itself rapidly in the form of a clinical event.

However, my point was that even if there is a possibility of a cardiac event, it should be up to the patient and doctor to decide if that risk is worth it for them.