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CLINICAL STUDY: INTERVENTIONAL CARDIOLOGY

Angioplasty increases coronary sinus F₂-isoprostane formation: evidence for in vivo oxidative stress during PTCA

Luigi Iuliano, MD^*, Domenico Praticò, MD, Cesare Greco, MD^* , Enrico Mangieri, MD^* , Giovanni Scibilia, MD^* , Garret A. FitzGerald, MD and Francesco Violi, MD^*

^* Istituto di I Clinica Medica, University La Sapienza, Rome, Italy
Center for Experimental Therapeutics, University of Pennsylvania, Philadelphia, Pennsylvania, USA
Instituto di Cardiochirurgia, Servizio di Emodinamica II, University La Sapienza, Rome, Italy

Manuscript received September 30, 1999; revised manuscript received July 11, 2000, accepted September 7, 2000.

Reprint requests and correspondence: Prof. Francesco Violi, Instituto di I Clinica Medica, University La Sapienza, 00185 Rome, Italy
violi{at}uniromal.it

OBJECTIVES

Isoprostanes, stable end-products of oxygen free radical mediated–lipid peroxidation, were measured in the coronary vessels during percutaneous transluminal coronary angioplasty (PTCA) to provide direct evidence for enhanced oxidative stress in a local milieu in vivo.

BACKGROUND

Percutaneous transluminal coronary angioplasty is associated with complications such as myocardial stunning and accelerated restenosis, which at least in part are mediated by oxygen free radicals. Because isoprostanes are markers of oxidant stress and potent vasoactive compounds, the formation of which is not inhibited by aspirin treatment in vivo, it is possible that these mediators are increased locally during PTCA.

METHODS

In 12 coronary artery disease patients who were given aspirin and ticlopidine, blood samples from coronary sinus were taken immediately before and immediately upon balloon deflation during PTCA. Isoprostane F₂-III, isoprostane F₂-VI, and TxB₂ were quantified after extraction and chromatography using a stable dilution isotope gas chromatography/mass spectrometry assay.

RESULTS

Coronary sinus and left main coronary artery levels of iPF₂-III and iPF₂-VI at baseline were (mean ± SEM) 40 ± 9 pg/ml and 115 ± 10 pg/ml, respectively. The TxB₂ levels were undetectable. Following PTCA, isoprostane levels markedly increased (mean ± SEM): iPF₂-III, 125 ± 12 pg/ml (p < 0.001); iPF₂-VI, 295 ± 20 pg/ml (p < 0.001), whereas TxB₂ levels remained undetectable.

CONCLUSIONS

These results indicate that PTCA induces coronary sinus increase in F₂-isoprostane formation, and they also provide direct evidence for enhanced oxidative stress in a local milieu in vivo. Thus, an increased F₂-isoprostane formation could play a role in the pathogenesis of some PTCA-associated untoward events.

Abbreviations and Acronyms   ECG = electrocardiogram   iPs = isoprostanes   OFR = oxygen free radicals   PFB = pentafluorybenzyl   PTCA = percutaneous transluminal coronary angioplasty

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