Abstract

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , Schillaci et al1 raise an interesting possibility—that a drug class (protease inhibitors) can have subtle arterial ill effects, which are not apparent from conventional blood pressure recordings. The authors provide evidence of aortic stiffening (measured as carotid–femoral pulse wave velocity [PWV]), increase in wave reflection from peripheral vessels (measured as aortic augmentation index [AIx]), and impairment of left ventricular subendocardial supply/demand ratio (measured as Buckberg index). Studies to date on arterial stiffening and its implications have concentrated on how age, gender, body height, exercise, lifestyle, and disease affects these properties, and how arterial properties, when deranged by disease, can be improved by drug therapy.2 Such adverse arterial hemodynamic changes with drugs have not been sought before. Before approval of a new drug, government regulatory bodies have required only measurements of cuff brachial systolic and diastolic pressures and assurance that these were not significantly altered. The question arises from the study of Schillaci—is this enough? Is it possible that drug classes may have adverse long-term effects that are not exposed by conventional cuff measurements? The question is relevant to the present concerns on long-term ill effects of COX 2 inhibitors (coxibs), with rofecoxib withdrawn from the market and the subject of legal action in US courts.3 See page 2381 The potential importance of the findings of Schillaci et al on protease inhibitors is unquestioned. These drugs have revolutionised the treatment of AIDS and find routine use in persons who are seropositive to the HIV virus. There were no HIV-positive persons in this study who were not treated with protease inhibitors. Studies of the drugs quoted by Schillaci are in recent issues in the world’s highest impact journals. I will not pursue such important implications to HIV and AIDS, …

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