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J Am Coll Cardiol, 2001; 37:76-80
© 2001 by the American College of Cardiology Foundation
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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{ddagger}, Cesare Greco, MD* {dagger} {ddagger}, Enrico Mangieri, MD* {dagger} {ddagger}, Giovanni Scibilia, MD* {dagger} {ddagger}, Garret A. FitzGerald, MD{dagger} and Francesco Violi, MD*

* Istituto di I Clinica Medica, University La Sapienza, Rome, Italy
{dagger} Center for Experimental Therapeutics, University of Pennsylvania, Philadelphia, Pennsylvania, USA
{ddagger} 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


   Abstract
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 Abstract
Methods
 Results
 Discussion
 References
 
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{alpha}-III, isoprostane F2{alpha}-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{alpha}-III and iPF2{alpha}-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{alpha}-III, 125 ± 12 pg/ml (p < 0.001); iPF2{alpha}-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

Percutaneous transluminal coronary angioplasty (PTCA) is a widely used and effective method to restore coronary flow in patients with symptomatic coronary artery disease (1). It is known that restoration of coronary flow may also adversely affect myocardium by inducing effects such as myocardial stunning and arrhythmogenesis (2,3). Such effects have been well documented in animal studies and are probably mediated by oxygen free radicals (OFR) (4). In these models, OFR scavenging agents reduce the severity of myocardial injury (5–8). However, how these models relate to human studies is still uncertain. Some studies have shown the formation of OFR after PTCA in humans (9,10). Others, however, have not found an increase in the levels of lipid products during PTCA (11).

Isoprostanes (iPs) are prostaglandin isomers formed by free radical-catalyzed oxidation of arachidonic acid esterified in membrane phospholipids (12). They represent chemically stable end products of lipid peroxidation that circulate in plasma and are excreted in urine (13). Measurement of iPs may be a sensitive and specific index of oxidant stress in vivo. Levels of iPs are increased in animal models of OFR-mediated injury as well as in humans in diverse settings in which OFR-mediated tissue damage is strongly implicated (14–16). Recently, it has been reported that iPs generation is increased in syndromes of coronary reperfusion (17). Moreover, iPs are significantly increased in urine of patients undergoing acute PTCA for myocardial infarction, whereas only a slight increase was observed in patients undergoing elective PTCA (18). However, it is still not known whether iPs are increased in vivo locally in the coronary arteries during PTCA.

A peculiar characteristic of these isoeicosanoids is that they also possess biological activities. Thus, a member of the F2-iPs family, 8-iso prostaglandin F2{alpha}, now known as iPF2{alpha}-III (19), is a potent mitogen for smooth muscle cells, causes vasoconstriction in bovine and porcine coronary arteries and increases platelet activation and adhesion (20–23).

Because of the potential importance of iPs as markers of oxidant stress in vivo and as biological active compounds on the vasculature, and in view of the PTCA-related sequelae such as coronary vasospasm, we monitored the coronary sinus levels of two distinct iPs within the framework of elective PTCA.


   Methods
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Results
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Patients.   Twelve consecutive subjects (mean age 57 years; range 45 to 70 years) were enrolled with the following characteristics: 1) stable angina pectoris with an exercise treadmill test positive for ischemia within the preceding six months; 2) single-vessel coronary artery defined as >70% stenosis in left anterior descending coronary artery deemed approachable by PTCA on previous diagnostic coronary angiography; 3) lack of angiographic features suggestive of an "active" lesion (defined as a lesion with an intracoronary filling defect suggestive of stenosis-related thrombus); and 4) no conduction defects on the electrocardiogram (ECG). All patients were taking aspirin (160 mg/day) for at least four weeks before the procedure, and ticlopidine (500 mg/day) for at least 48 h before the procedure. Other medications for the treatment of angina pectoris (calcium channel blockers, beta-blockers and nitrates) were continued. As controls, four patients (all men, mean age 58 years; range 46 to 70 years) undergoing cardiac catheterization for valvular heart disease with no coronary lesions were also studied. The study was approved by the ethical committee of the hospital board, and all patients signed an informed consent.

PTCA and sample acquisition.   All 12 patients underwent PTCA via a femoral approach. Briefly, they were premedicated with diazepam and diphenhyldramine. Heparin (5,000 IU) was given as a bolus at the beginning of the procedure and additional boluses were injected if necessary to maintain an activated coagulation time ≥250 s. Diagnostic coronary angiography was performed using a nonionic contrast media (Omnipaque, Nycomed Imaging AS). Five contrast injections in different X-ray projections were used for the left coronary artery and two contrast injections for the right coronary artery (total 42 ml of nonionic contrast media). At the end of the diagnostic procedure, a 6F NIH catheter was positioned in the distal coronary sinus via the right internal jugular vein, and a 7F Judkins guide catheter was positioned in the ostium of the left main coronary artery to start the PTCA. For each patient, basal contemporary samples were obtained at this time from the coronary sinus and from the left main coronary artery. After flushing with saline and discarding 5 ml of blood, from each catheter a 10-ml sample was withdrawn into a second syringe containing heparin (500 IU/ml) and EDTA (2 mmol/liter). The EDTA was used to prevent the artifactual generation of eicosanoids during the sampling procedure.

Next, the intracoronary wire was positioned distally in the left anterior descending artery, and the balloon catheter was advanced across the stenosis and inflated for 120 s at the nominal balloon inflating pressure. Immediately upon balloon deflation, after flushing with saline and discarding 5 ml of blood, a 10-ml blood sample was taken from the coronary sinus catheter as was done with the first sample. There were no acute vessel closures and no patients experienced complicating myocardial infarction, or significant bleeding. There were no stent implantations. Coronary angiography was then performed to ensure a satisfactory angioplasty result.

Patients undergoing diagnostic coronary angiography before valvular replacement operation were studied as controls. Blood samples were taken from the coronary sinus and the left main coronary artery after the performance of coronary angiography. No complications related to the procedure occurred.

Analyses were performed without knowledge of the location within the coronary artery from which the blood originated.

Biochemical analysis.   Blood samples were centrifuged at 3,000 rpm for 10 min. Plasma was collected and added with 10 µg [2H8]-arachidonic acid in order to detect any artifactual formation of the isoprostanes of interest, then stored at –80°C. Samples were shipped in dry ice and received within 24 h. Artifactual generation of iPs was monitored by measuring formation of [2H8]-iPF2{alpha}-III or [2H8]-iPF2{alpha}-VI. All of the gas chromatography/mass spectrometry (GC/MS) analyses were performed on a Fisons MD-800 mass spectrometer interfaced with a Fisons 800 GC and an AS-800 autosampler as previously described (15–18,24). The mass spectrometer was operated in the negative ion chemical ionization mode using ammonia as the moderating gas (15–18,24). Standard validation criteria as well as interassay and intra-assay variability for all the following methodology described have been reported elsewhere (24–26). The iPF2{alpha}-III was analyzed as pentafluorylbenzyl ester (PFB)/ter-butyldimethylsilyl ether derivative (15–18,24,25), while iPF2{alpha}-VI was analyzed as PFB/trimethylsilyl ether derivative (24,25). TxA2, measured as its stable hydrolysis product TxB2, was analyzed as the PFB/trimethylsilyl ether derivative as previously described (24,26,27).

Statistical analysis.   All data are expressed as mean ± SEM. Data were compared by use of appropriate t-test for paired data, and by a one-way analysis of variance. Simple regression analysis was performed to analyze the relation between iPF2{alpha}-III and iPF2{alpha}-VI. Differences were considered significant at a value of p < 0.05.


   Results
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 Methods
 Results
Discussion
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Twelve patients underwent elective PTCA. The clinical characteristics of the population study are described in Table 1. Ten patients had a history of cigarette smoking, two had high blood pressure, eight had total plasma cholesterol levels greater than 200 mg/dl, and four had type II diabetes mellitus. No complications were encountered during PTCA. Angiography of the target coronary artery immediately after postdeflation sample acquisition showed no significant residual stenosis with normal contrast runoff.


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  		Table 1 Clinical Characteristics of the Patients Undergoing PTCA

 
Table 2 reports on the levels of TxB2, iPF2{alpha}-III and iPF2{alpha}-VI at baseline in patients undergoing PTCA. Samples taken from the coronary sinus before the balloon inflation had TxB2 values below the detection limit of the assay (Table 2). Levels of iPF2{alpha}-III and iPF2{alpha}-VI were 40 ± 9 and 115 ± 10 pg/ml, respectively (Table 2). By measuring [2H8]-iPF2{alpha}-III or [2H8]-iPF2{alpha}-VI levels in each sample (data not shown), no artifactual generation of iPs was detected. To assess whether the site of the sampling in the coronary artery was important for the baseline values observed, additional samples were taken from the left coronary artery. No significant difference in iPs and TxB2 levels was observed between samples taken from the coronary sinus or the left coronary artery (Table 2). In contrast, all of the post-PTCA samples taken from the coronary sinus showed increased amounts (mean ± SEM) of both iPF2{alpha}-III (125 ± 12 pg/ml, p < 0.001) and iPF2{alpha}-VI (295 ± 20 pg/ml, p < 0.001) (Fig. 1). No increase in TxB2 was detected in any of the subjects after PTCA, indicating that aspirin had completely suppressed platelet cyclooxygenase enzyme activity in these patients. A significant correlation existed between the levels of the two iPs (r = 0.68, p < 0.05).


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  		Table 2 Levels of TxB2, iPF2{alpha}-III and iPF2{alpha}-VI in the Coronary Sinus and in the Left Main Coronary Artery Before PTCA

 


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  		Figure 1 Coronary sinus levels of iPF2{alpha}-III (A) and iPF2{alpha}-VI (B) before and after elective PTCA (n = 12). *p < 0.001.

 
To assess the potential contribution of the catheter per se during angiography, we monitored the coronary levels of iPs in four patients undergoing cardiac catheterization for valvular heart disease. At the end of the diagnostic procedure, two samples from these patients were collected, one in the coronary sinus and one in the left main coronary artery, as was done for the cohort of PTCA patients. Levels of the two iPs were similar to the levels observed in the patients undergoing PTCA at baseline before balloon inflation (Table 3).


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  		Table 3 Levels of iPF2{alpha}-III and iPF2{alpha}-VI in Patients Undergoing Diagnostic Coronary Angiography (n = 4)

 

   Discussion
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 Abstract
 Methods
 Results
 Discussion
References
 
Isoprostanes and PTCA.   The iPs are prostaglandin isomers formed by a free radical catalyzed attack of phospholipid-containing arachidonic acid in situ in membranes (28). They are stable end products of lipid peroxidation that offer advantages over other indices of lipid peroxidation used thus far. They are formed in vivo, possess potent biological activities, circulate in plasma and are excreted in urine (12,13). We and other investigators have demonstrated that iPs are sensitive and specific markers of lipid peroxidation and oxidative stress in vivo (14–17,29). Recently, it has been reported that systemic increase of iPs in patients undergoing acute PTCA for myocardial infarction has been reported (17,18). The present investigation extends these findings, as no data are available on the iPs levels in the coronary vessels during this procedure. In this study we demonstrate for the first time that angioplasty is associated with an increase in iPs levels in the coronary sinus. Samples taken before balloon inflation revealed only discrete levels of iPF2{alpha}-III and iPF2{alpha}-VI in the coronary circulation. In contrast, samples taken after PTCA at the coronary sinus contained significantly increased levels of both types of iPs, which were highly correlated. The specific role of balloon inflation during PTCA in inducing this increase was further supported by the iPs levels found in control patients undergoing diagnostic coronary angiography. In fact, these patients at the end of coronary angiography had iPs levels in the left main coronary artery and in the coronary sinus comparable to baseline values of patients before undergoing PTCA. However, we cannot exclude the theoretical possibility of a "stress" related to the performance of PTCA, which caused a systemic rise in iPs levels, as we did not take a sample from the left coronary ostium after balloon deflation.

Percutaneous transluminal coronary angioplasty is a well-established method of restoring coronary flow in patients with symptomatic coronary artery disease (1), and it can be considered as an in vivo model of ischemia-reperfusion injury. The increased level of the two iPs in patients undergoing elective PTCA is consistent with the hypothesis that generation of these compounds reflects a common OFR-dependent pathway as a result of ischemia-reperfusion chemistry.

Eicosanoids and PTCA.   Several studies have provided evidence for increased formation of eicosanoids during PTCA. For example, thromboxane generation by activated platelet during PTCA is at least in part considered responsible for the vasoconstriction (30,31). However, in a significant number of patients, aspirin, at a dosage that inhibits TxB2 formation, does not prevent PTCA-induced vasospasm (32). Similarly, restenosis after PTCA has not been shown to be influenced by aspirin (33,34). These data suggest that mediators not inhibited by aspirin may also play a role in some of the complications of PTCA. The finding that PTCA triggers an increase in coronary sinus isoprostane levels, whose actions are not inhibited by aspirin, provides further insight into the pathophysiology of PTCA-induced vasospasm and may have important implications in patients undergoing interventions that produce coronary vascular injury. Interestingly, intracoronary administration of iPF2{alpha}-III has been shown to cause in vitro vasoconstriction in porcine and bovine coronary arteries with an EC50 of 0.5 and 1 µmol/liter, respectively (21). These concentrations are similar to the intracoronary levels of iPF2{alpha}-III that we found after PTCA. Thus, the constriction often observed in the distal segment of the instrumented vessel might be due to the formation and translocation "downstream" of this vasoactive prostaglandin isomer formed as result of oxidative stress.

Furthermore, PTCA-induced plaque rupture with the exposure of cellular constituents it is known to increase in vivo platelet activation and adhesion, which may play a role in some of the sequelae of this procedure. It has been reported that iPF2{alpha}-III increases in vitro platelet activation and adhesion with a EC50 similar to the one reported above, and that both effects are prevented by thromboxane receptor antagonist but not by aspirin (22,23). Thus, we suggest that this isoeicosanoid should be added to the complex list of biologically active compounds formed after PTCA.

Conclusions.   The present investigation demonstrates for the first time an increase in iPs generation, markers of in vivo lipid peroxidation and oxidative stress, in the coronary sinus of patients after elective PTCA. Considering that their formation and biological activities are aspirin-insensitive and that the coronary sinus levels reached after PTCA are close to the ones that provoke coronary artery constriction in animals and increase human platelet activation and adhesion, we conclude that iPs could play a role in the untoward events of this procedure such as vasospasm. Further studies to assess the mechanism of PTCA-induced release of iPs as well as the impact of pharmacological interventions are warranted.


   Footnotes
 
Financial support was supported in part by CNR grant 96-03098.04 (to Dr. L. Iuliano) and by MURST grant 60%–1997 (to Dr. F. Violi).


   References
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L. Fontana, C. Giagulli, L. Cominacini, A. F. Pasini, P. Minuz, A. Lechi, A. Sala, and C. Laudanna
{beta}2 Integrin-Dependent Neutrophil Adhesion Induced by Minimally Modified Low-Density Lipoproteins Is Mainly Mediated by F2-Isoprostanes
Circulation, November 5, 2002; 106(19): 2434 - 2441.
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 J Am Coll CardiolHome page
M. G. Andreassi, N. Botto, A. Rizza, M. G. Colombo, C. Palmieri, S. Berti, S. Manfredi, S. Masetti, A. Clerico, and A. Biagini
Deoxyribonucleic acid damage in human lymphocytes after percutaneous transluminal coronary angioplasty
J. Am. Coll. Cardiol., September 4, 2002; 40(5): 862 - 868.
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 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
J. D. Krier, M. Rodriguez-Porcel, P. J. M. Best, J. C. Romero, A. Lerman, and L. O. Lerman
Vascular responses in vivo to 8-epi PGF2alpha in normal and hypercholesterolemic pigs
Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2002; 283(2): R303 - R308.
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 J Am Coll CardiolHome page
J.-L. Cracowski, S. Marliere, and G. Bessard
Vasomotor effects and pathophysiologic relevance of F2-isoprostane formation in vascular diseases
J. Am. Coll. Cardiol., February 6, 2002; 39(3): 554 - 554.
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 Proc. Natl. Acad. Sci. USAHome page
C. Napoli, G. Aldini, J. L. Wallace, F. de Nigris, R. Maffei, P. Abete, D. Bonaduce, G. Condorelli, F. Rengo, V. Sica, et al.
Efficacy and age-related effects of nitric oxide-releasing aspirin on experimental restenosis
PNAS, February 5, 2002; 99(3): 1689 - 1694.
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