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(Circulation. 2005;112:941-945.)
© 2005 American Heart Association, Inc.

Editorial

To the Heart of the Matter

Coxibs, Smoking, and Cardiovascular Risk

Matthias Hermann, MD; Henry Krum, MBBS, PhD; Frank Ruschitzka, MD

From the Cardiovascular Center, Cardiology, University Hospital Zürich, Switzerland.

Correspondence to Frank Ruschitzka, MD, FESC, University Hospital Zürich, Cardiology, Ramistrasse 100, CH-8091 Zürich, Switzerland. E-mail frank.ruschitzka@usz.ch

Key Words: Editorials • endothelium • inflammation • platelets • prostaglandins

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
When cyclooxygenase (COX)-2–selective inhibitors (coxibs) first entered the market about 5 years ago, the major concern with regard to cardiovascular side effects related to their potential to increase blood pressure and cause salt and water retention, in a manner similar to conventional (nonselective) nonsteroidal antiinflammatory drugs (NSAIDs). In the short time since, wariness about these side effects has grown into widespread alarm about putative prothrombotic actions and generation of excess major cardiovascular events with these agents.

See p 1024

In September 2004, safety findings of the Adenomatous Polyp Prevention on Vioxx (APPROVe) study indicated an increase in risk for myocardial infarction and stroke among subjects randomized to rofecoxib compared with those randomized to placebo. This study had been designed to examine recurrent colonic polyps rather than cardiovascular disease end points and therefore could only be considered hypothesis generating. Subsequent data from a number of observational studies further implicated the drug’s association with arterial thromboembolic disease. As with APPROVe, no single study generated sufficiently robust attestation by itself, but they provided concordant signals, and the accumulating evidence eventually reached a critical mass.

As the data on rofecoxib emerged, concerns about other COX-2–selective agents on the market also grew. This was based on the assumption of a "class effect" for an increase in risk of cardiovascular disease related to preferential inhibition of prostacyclin over thromboxane and thus a tendency toward prothrombosis.

The results presented by McAdam and colleagues in this issue of Circulation¹ challenge our view with regard to this prostanoid hypothesis . . . [Full Text of this Article]

Related Article:

Contribution of Cyclooxygenase-2 to Elevated Biosynthesis of Thromboxane A₂ and Prostacyclin in Cigarette Smokers

Brendan F. McAdam, Daniel Byrne, Jason D. Morrow, and John A. Oates
Circulation 2005 112: 1024-1029. [Abstract] [Full Text]

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