Background Inflammation within vulnerable coronary plaques maycause unstable angina by promoting rupture and erosion. In unstableangina, activated leukocytes may be found in peripheral andcoronary-sinus blood, but it is unclear whether they are selectivelyactivated in the vascular bed of the culprit stenosis.
Methods We measured the content neutrophil myeloperoxidase contentin the cardiac and femoral circulations in five groups of patients:two groups with unstable angina and stenosis in either the leftanterior descending coronary artery (24 patients) or the rightcoronary artery (9 patients); 13 with chronic stable angina;13 with variant angina and recurrent ischemia; and 6 controls.Blood samples were taken from the aorta, the femoral vein, andthe great cardiac vein, which selectively drains blood fromthe left but not the right coronary artery.
Results The neutrophil myeloperoxidase content of aortic bloodwas similar in both groups of patients with unstable angina(–3.9 and –5.5, with negative values representingdepletion of the enzyme due to neutrophil activation) and significantlylower than in the other three groups (P<0.05). Independentlyof the site of the stenosis, the neutrophil myeloperoxidasecontent in blood from the great cardiac vein was significantlydecreased in both groups of patients with unstable angina (–6.4in those with a left coronary lesion and –6.6 in thosewith a right coronary lesion), but not in patients with stableangina and multiple stenoses, patients with variant angina andrecurrent ischemia, or controls. There was also a significanttranscoronary reduction in myeloperoxidase content in both groupswith unstable angina.
Conclusions The widespread activation of neutrophils acrossthe coronary vascular bed in patients with unstable angina,regardless of the location of the culprit stenosis, challengesthe concept of a single vulnerable plaque in unstable coronarysyndromes.
The hypothesis that inflammation of a vulnerable plaque is responsiblefor the development of acute coronary syndromes1,2,3,4,5 isstimulating a variety of techniques for the detection and stabilizationof vulnerable plaques.6,7,8,9,10 Yet, it is unclear whetherthe inflammatory process is confined to a single vulnerableplaque or whether it is more widespread in the coronary vasculature.
The possibility of widespread inflammation of the coronary arterialbed is suggested by the recent report of multiple complex coronaryplaques in patients with acute myocardial infarction11 and byprevious postmortem findings of multiple fresh thrombi in patientswith unstable angina12 and of multiple fissured, thrombosedplaques.13,14 A widespread acute inflammatory process in thecoronary arterial bed would have important implications fora clearer understanding of the pathogenesis, and eventuallyfor the treatment and prevention, of acute coronary syndromes.By "widespread," we mean involvement of more than one majorcoronary artery. By measuring leukocyte expression of CD11band CD18 in aortic and coronary-sinus blood, Mazzone et al.15and de Servi et al.16 demonstrated a transcoronary inflammatoryactivation of monocytes and neutrophils in patients with unstableangina. Such activation was not detectable in aortic blood.Unfortunately, these authors did not assess the correlationbetween activation and the location of the culprit coronarystenosis responsible for the angina.15,16 Marked activationof neutrophils was also detected in the peripheral blood ofpatients with unstable angina, but not in those with stableangina or in controls. Activation was detected by measuringthe neutrophil myeloperoxidase content, which is an index ofmore advanced inflammatory activation than that identified bymeasuring CD11b and CD18 expression.17,18
We ascertained whether the activation of neutrophils, presumablydue to inflammation, in patients with unstable angina was confinedto the vascular bed perfused by the vessel with the culpritcoronary stenosis, or whether it also involved the vascularbed of angiographically normal or nearly normal arteries. Weselected patients with coronary stenoses of either the leftanterior descending or the right coronary artery. We simultaneouslymeasured the neutrophil myeloperoxidase content in blood fromthe aorta, the femoral vein, and the great cardiac vein, whichselectively drains blood from the left anterior descending coronaryartery but not the right coronary artery.19 Patients with stableangina and stenosis of the left anterior descending coronaryartery, patients with variant angina and recurrent ischemiaof the left anterior descending coronary artery, and patientswithout coronary disease (controls) were also studied.
Methods
Patients
We studied a total of 65 patients, divided into five groups.Two of the groups consisted of the 33 patients who had Braunwaldclass IIIB unstable angina. Coronary angiography showed thatthe coronary stenosis responsible for the angina (the culpritstenosis) was in the left anterior descending coronary arteryin 24 of these patients (the first group), and in the rightcoronary artery in the other 9 patients (the second group).The remaining three groups were made up of 13 patients withchronic stable angina and stenosis in the left anterior descendingcoronary artery; 13 patients with active variant angina andrecurrent spasm in the left anterior descending coronary artery,which was documented by testing with ergonovine; and 6 controlpatients with mild mitral stenosis, atrial septal defect, orsupraventricular tachycardia and a normal coronary angiogram.
Patients with a recent myocardial infarction (within three months),prior coronary interventions, an occluded coronary vessel, aculprit coronary stenosis in the circumflex branch, or intercurrentinfective or inflammatory disorders were excluded from the study.No patients were taking antiinflammatory agents other than aspirin(up to 100 mg daily).
The protocol was approved by the ethics committee of the CatholicUniversity of Rome, and all patients gave written informed consent.
Protocol
Serum levels of C-reactive protein were measured on admissionand used as a marker of systemic inflammation. Cardiac catheterizationwas performed within a mean (±SD) of 2±1 days.Before the injection of a contrast agent, all patients underwentsampling of blood from the right femoral vein and simultaneoussampling of blood from the aorta and great cardiac vein forthe measurement of neutrophil myeloperoxidase. In both groupsof patients with unstable angina, in order to demonstrate thatthe great cardiac vein selectively drained blood from the leftanterior descending but not from the right coronary artery,the blood oxygen saturation in the great cardiac vein was determinedbefore and after the injection of 1.0 mg of isosorbide dinitrateinto the left anterior descending or the right coronary artery,according to the location of the culprit stenosis. The venous–arterialdifferences in neutrophil and leukocyte counts through the coronaryand peripheral circulations were also determined.
The myeloperoxidase content was determined by using a hematologicanalyzer (Bayer H*1), which measures the differential leukocytecount as well as the cell count by automated flow cytochemistry,as previously described.17 The H*1 computer software calculatesa myeloperoxidase index of the mean myeloperoxidase contentin the neutrophil population. In healthy subjects, this indexis close to 0. Positive values characterize neutrophils richin myeloperoxidase, and negative values characterize neutrophilsdepleted of myeloperoxidase as a consequence of their activation.A lower myeloperoxidase index in blood from the great cardiacvein or the femoral vein, as compared with the aorta, was takenas an index of neutrophil activation through the coronary orfemoral vascular bed. C-reactive protein levels were measuredby a high-sensitivity, latex-enhanced immunonephelometric assay(Dade Behring BN II analyzer).20 The working range of the assaywas 0.175 to 1100 mg per liter, and the coefficient of variationwas less than 5 percent.
Statistical Analysis
Because the myeloperoxidase index did not have a normal distribution,nonparametric tests were used: the Mann–Whitney test andthe Kruskal–Wallis test with multiple-comparison procedures(Dunn's method) for comparisons between groups, and the Friedmantest and the Wilcoxon test with the Bonferroni correction forcomparisons within groups. Correlations were determined withuse of Spearman's rank-correlation coefficient.21 The leukocyteand neutrophil counts had a normal distribution and were evaluatedby analysis of variance for repeated measures with the Bonferronicorrection. Chi-square statistics were used for categoricalvariables. A P value of less than 0.05 (two-tailed) was consideredto indicate statistical significance. Data are reported as mediansand ranges or as means ±SD, as appropriate.
Results
The demographic, clinical, and angiographic characteristicsof the patients are reported in Table 1 and Table 2. Anginalsymptoms before coronary angiography were similar in patientswho had unstable angina with a left coronary lesion, those whohad unstable angina with a right coronary lesion, and thosewho had variant angina (Table 1).
The blood oxygen saturation in the great cardiac vein markedlyincreased after injection of isosorbide dinitrate (1 mg) intothe left anterior descending coronary artery of patients whohad unstable angina with a left coronary lesion, but not afterinjection into the right coronary artery of patients who hadunstable angina with a right coronary lesion (P=0.001 by two-wayanalysis of variance). The median change in the blood oxygensaturation as a result of the isosorbide dinitrate injectiondiffered significantly between the two groups (52.4 percentvs. 12.2 percent, P=0.04), indicating that positioning the catheterin the great cardiac vein allowed for selective sampling ofthe blood draining from the vascular bed of the left anteriordescending coronary artery. The leukocyte and neutrophil countsin the aorta, great cardiac vein, and femoral vein were similar;no differences were observed among groups (Table 1). Among patientswho had unstable angina with a right coronary lesion, the territoryof the left anterior descending coronary artery had no wallirregularities in three patients, wall irregularities alonein three patients, and stenosis of 30 to 50 percent of the luminaldiameter in the remaining three patients. Therefore, the atheroscleroticinvolvement was much smaller than that observed in patientswho had unstable angina with a left coronary lesion and thosewho had chronic stable angina (Table 2).22
Neutrophil Activation in the Systemic Circulation
The median aortic myeloperoxidase indexes did not differ significantlybetween patients who had unstable angina with a left coronarylesion (–3.9) and those who had unstable angina with aright coronary lesion (–5.5, P=0.21), but they were significantlylower than those observed in patients with stable angina (+0.1),patients with variant angina (+0.1), and controls (–0.8)(P<0.05 for all comparisons). The ranges for all values arereported in Table 1 and illustrated in Figure 1.
Figure 1. Neutrophil Activation, as Indicated by the Change in the Myeloperoxidase Index in Blood from the Femoral Vein, Aorta, and Great Cardiac Vein.
Patients with angina had stenosis of either the left anterior descending coronary artery or the right coronary artery. Data are presented as medians, with 25th and 75th percentiles (boxes) and 10th and 90th percentiles (I bars). Significantly lower values for myeloperoxidase in the aorta and the femoral vein were observed in both patients with unstable angina with a left coronary lesion and those with unstable angina with a right coronary lesion than in the other groups. In patients with unstable angina, but not in patients in any of the other groups, a further decrease in myeloperoxidase content was observed in blood from the great cardiac vein, not only when the neutrophils traversed the coronary vascular bed perfused by the culprit stenosis and thus subjected to recurrent ischemia (unstable angina with a left coronary lesion), but also when there was no coronary stenosis or any plausible cause of ischemia in the vascular bed draining into the great cardiac vein (unstable angina with a right coronary lesion). No neutrophil activation was detectable through the femoral circulation in any of the five groups studied. The asterisk indicates P<0.05 for the comparisons of the groups with unstable angina with a left coronary lesion and unstable angina with a right coronary lesion with the group with chronic stable angina, the group with variant angina, and controls. The dagger indicates P<0.01 for the comparisons of the groups with unstable angina with a left coronary lesion and unstable angina with a right coronary lesion with the group with chronic stable angina, the group with variant angina, and controls.
Neutrophil Activation through the Coronary and Femoral Circulations
In patients who had unstable angina with either a left or aright coronary lesion, a significant transcoronary decreasein the neutrophil myeloperoxidase index was observed. The medianvalues in blood from the aorta and the great cardiac vein were–3.9 and –6.4, respectively, for those with a left-coronary-arterylesion (P<0.001) and –5.5 and –6.6 for thosewith a right-coronary-artery lesion (P=0.003). Conversely, nostatistically significant transcoronary decrease in neutrophilmyeloperoxidase content was observed in any of the other threegroups; the myeloperoxidase values in blood from the great cardiacvein were +0.6 in patients with stable angina, –0.4 inthose with variant angina, and –0.2 in controls (P<0.01for all the comparisons of patients with stable angina, patientswith variant angina, and controls with both patients with unstableangina with a left coronary lesion and those with unstable anginawith a right coronary lesion) (Table 1 and Figure 1). No significantdifferences between the neutrophil myeloperoxidase contentsof aortic and femoral venous blood were observed in any of thefive groups (Table 1 and Figure 1).
The change in neutrophil myeloperoxidase content across thecoronary circulation was significantly greater in both patientswith unstable angina with a left coronary lesion and those withunstable angina with a right coronary lesion than in those withstable angina, those with variant angina, and controls (Table 1and Figure 2). The change in neutrophil myeloperoxidase contentacross the coronary circulation was significantly greater thanthe difference in neutrophil myeloperoxidase content betweenaortic and femoral venous blood in both patients with unstableangina with a left coronary lesion and those with unstable anginawith a right coronary lesion, but not in any of the other threegroups (Table 1 and Figure 2).
Figure 2. Venous–Arterial Differences in Myeloperoxidase Content across the Femoral and Coronary Vascular Beds.
Data are presented as medians, with 25th and 75 percentiles (boxes) and 10th and 90th percentiles (I bars). The difference in myeloperoxidase content across the coronary circulation was significantly greater in both patients with unstable angina with a left coronary lesion and those with unstable angina with a right coronary lesion than in patients with chronic stable angina, patients with variant angina, and control patients. The difference in myeloperoxidase content across the coronary vascular bed was significantly greater than that across the femoral vascular bed in both patients with unstable angina with a left coronary lesion and those with unstable angina with a right coronary lesion, but not in any of the other three groups. The asterisk indicates P<0.05 for the comparison of the group with unstable angina with a left coronary lesion and unstable angina with a right coronary lesion with the group with chronic stable angina, the group with variant angina, and controls.
Correlation between Levels of C-Reactive Protein and Myeloperoxidase
The median plasma levels of C-reactive protein were similarin patients with unstable angina with a left coronary lesion(6.5 mg per liter) and those with unstable angina with a rightcoronary lesion (4.5 mg per liter, P=0.76) and were significantlyhigher than the levels in patients with stable angina (2.1 mgper liter), patients with variant angina (1.8 mg per liter),and controls (1.2 mg per liter; P<0.01 for all comparisons)(Table 1).
Overall, in the five groups, a significant correlation was foundbetween systemic levels of C-reactive protein and the aorticneutrophil myeloperoxidase content (r=–0.45, P=0.03),as well as between systemic levels of C-reactive protein andthe neutrophil myeloperoxidase content in blood from the greatcardiac vein (r=–0.41, P=0.01) (Figure 3).
Figure 3. Correlation between Systemic Values for C-Reactive Protein and the Change in the Myeloperoxidase Content in Blood from the Aorta and the Great Cardiac Vein.
C-reactive protein values were significantly and inversely correlated with the myeloperoxidase content of blood from the aorta (Panel A) and the great cardiac vein (Panel B). The diagonal lines are the regression lines.
Discussion
Our findings confirm previous reports that in patients withunstable angina, leukocytes become activated as they traversethe coronary vascular bed,15,16 and that such activation maybe detectable systematically.17,23,24 In addition, we foundno significant increase in neutrophil activation in the greatcardiac vein in controls, in patients with stable angina anddocumented left anterior descending coronary stenosis, or inpatients with active variant angina and recurrent ischemia inthe territory of the left anterior descending coronary artery.Moreover, there was no detectable increase in neutrophil activationthrough the femoral circulation in any of the five groups studied.
In patients with unstable angina, transcoronary neutrophil activationwas not confined to the vascular bed perfused by the arteryin which the culprit stenosis was located and thus subjectedto recurrent ischemia. In fact, neutrophil activation occurredto a similar extent in patients in whom the left anterior descendingcoronary artery was not the site of the culprit stenosis. Patientswith unstable angina and a culprit lesion in the right coronaryartery had only minimal atherosclerotic involvement of the leftanterior descending coronary artery, which was angiographicallynormal in three patients, had only luminal irregularities inthree patients, and had stenosis of less than 50 percent ofthe diameter in three patients.
In animal models, neutrophil activation has been observed after15 minutes of coronary occlusion–reperfusion.25 However,our findings cannot be explained simply on the basis of an ischemia–reperfusionmechanism, in view of the fact that transcardiac neutrophilactivation was not observed in patients with active variantangina, spasm of the left anterior descending artery, and atotal ischemic burden similar to that of patients with unstableangina.
In patients with unstable angina, inflammatory-cell infiltratesare commonly found in most atherosclerotic plaques at postmortemexamination1 and in endarterectomy specimens.2,26 Multiple fissured,thrombosed coronary plaques seem to be a common finding in acutecoronary syndromes. Falk et al. reported 103 fissured, thrombosedplaques in 47 patients,13 and Davies and Thomas reported 111fissured, thrombosed plaques in 76 patients.14 Neither of thesereports discussed the possible clinical significance of thesimultaneous rupture of multiple plaques. Multiple plaques withinflammatory-cell infiltrates and with a high content of proinflammatorycytokines were reported by Arbustini et al.12 Finally, multiplecomplex lesions were reported by Goldstein et al.11 The possibilitythat multiple plaque fissures and thrombi develop simultaneouslyat different sites merely as a result of mechanical stress seemsrather unlikely. It would appear more reasonable to speculatethat a multifocal or widespread inflammatory activation of theendothelium could change the characteristics of the interfacebetween the blood and the vessel walls from anticoagulant andvasodilative to prothrombotic and vasoconstrictive, while atthe same time activating the metalloproteases and collagenasesresponsible for endothelial-cell detachment and lysis of theplaque capsule at the sites where it is weakest.
Whether neutrophils become activated by interacting with thesurface of sparse inflamed plaques or as a result of more widespreadcontact with a diffusely inflamed coronary endothelium is notknown. De Servi et al. detected no activation of monocytes andneutrophils across the culprit coronary stenosis in patientswith unstable angina.16 Conversely, the possibility of widespreadcoronary inflammation is suggested by the reports of alterationsin coronary flow27,28 and [18F]deoxyglucose uptake29 in myocardialterritories perfused by arteries without stenosis or culpritlesions in patients with recent infarctions and in those withunstable angina. Finally, in 10 percent of patients with unstableangina, inflammatory red streaks were observed along nonstenosedcoronary arteries at the time of bypass surgery.30
The reported prevalence of systemically detectable inflammatorymarkers in acute coronary syndromes varies. Serum levels ofC-reactive protein and of proinflammatory cytokines such asinterleukin-6 are elevated in about 70 percent of patients withsevere unstable angina on admission,31,32 in 50 percent of suchpatients at discharge, and in 45 percent of such patients atsix months of follow-up.20 These increased levels are associatedwith recurrent instability and acute infarction. Accordingly,elevated levels of C-reactive protein and interleukin-6 arefound before the appearance of markers of myocardial necrosisin nearly all patients in whom infarction is preceded by unstableangina, but in less than 50 percent of patients with myocardialinfarction not preceded by unstable angina.31,33 Therefore,the triggers of coronary thrombosis and vasoconstriction arenot necessarily the same in all patients with acute coronarysyndromes.
The activation of neutrophils as they traverse the coronarycirculation of patients with unstable angina is a marker ofa widespread inflammatory process occurring in the coronaryvasculature. When the intensity of the inflammatory stimulivaries, such a process may lead to waxing and waning of thrombosisand vasoconstriction. The possibility of widespread coronaryinflammation has important implications for research and therapy.It challenges the widely accepted hypothesis that a single vulnerableplaque is responsible for the development of coronary instability— a hypothesis that is currently stimulating the developmentof techniques for the detection and stabilization of such plaques.
Supported by grants from the National Research Council, Rome(94.00518.PF41), the European Community (PL951505), and theFondazione Internazionale di Ricerca per il Cuore Onlus, Rome.
Source Information
From the Institute of Cardiology (A.B., L.M.B., G.L., F.C.) and the Institute of Hematology (G.D.), Catholic University, Rome; and the Cardiothoracic and Vascular Department, University Vita e Salute, Milan, Italy (A.M.).
Address reprint requests to Dr. Maseri at the Cardiothoracic and Vascular Department, University Vita e Salute, San Raffaele Hospital, Via Olgettina 60, 20132 Milan, Italy, or at maseri.attilio{at}hsr.it.
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