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Incidence, Range, and Clinical Effect of Hemoglobin ChangesWithin 24 Hours After Transradial Coronary Stenting

Olivier F. Bertrand, MD, PhD*, Éric Larose, DVM, MD, Josep Rodés-Cabau, MD,Stéphane Rinfret, MD, SM, Jean-Pierre Déry, MD, MSc, Rodrigo Bagur, MD, Onil Gleeton, MD,

Can M. Nguyen, MD, Guy Proulx, MD, Robert De Larochellière, MD, Paul Poirier, MD, PhD,Olivier Costerousse, PhD, and Louis Roy, MD

Anemia and major bleeding are independent predictors of outcomes after acute coronarysyndromes and percutaneous coronary intervention (PCI). Although the transradial ap-proach reduces the incidence of bleeding, the hemoglobin changes after transradial PCIhave not been defined. We serially assessed the hemoglobin values before and aftertransradial PCI and evaluated the effect of hemoglobin changes on outcomes. In the EArlyDischarge After Transradial Stenting of CoronarY Arteries (EASY) trial, 1,348 patientsunderwent transradial PCI. All patients received aspirin, clopidogrel, and a bolus ofabciximab before PCI. The hemoglobin values were assessed immediately before and 4 to6 hours and 12 to 24 hours after PCI. The major adverse cardiac events (death, myocardialinfarction, and target vessel revascularization) were assessed <3 years after PCI. Accord-ing to the World Health Organization classification, 206 patients (15%) had anemia beforePCI and 410 (30%) developed anemia within 24 hours after PCI. A mean hemoglobindecrease of 0.6 � 1.0 g/dl occurred within 24 hours after PCI. At 30 days, the major adversecardiac events were significantly increased when the hemoglobin decrease within 24 hoursafter PCI was >3 g/dl (p � 0.0002). Patients with anemia within 24 hours after PCI hadsignificantly more major adverse cardiac events at 30 days, 6 months, 1 year, and 3 yearsthan patients without anemia (log-rank p � 0.0044). After adjustment for differences in thebaseline characteristics, anemia within 24 hours after PCI remained an independentpredictor of major averse cardiac events at 3 years (hazard ratio 1.30, 95% confidenceinterval 1.01 to 1.67, p � 0.045). In conclusion, within 24 hours after transradial PCI withmaximal antiplatelet therapy, only a mild hemoglobin decrease was observed. The choiceof a hemoglobin decrease >3 g/dl after PCI as a cutoff value for current definitions of majorbleeding in modern PCI trials appears reasonable. Measures to prevent anemia and bloodloss during PCI remain to be further studied. © 2010 Elsevier Inc. All rights reserved.

(Am J Cardiol 2010;106:155–161)

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Transradial percutaneous coronary intervention (PCI) isssociated with a lower risk of access site complications andleeding than with the femoral approach.1 The clinical ef-ect of bleeding after PCI has been increasingly recognized.

ajor bleeding after PCI is a strong independent predictorf mortality after femoral and transradial PCI.2–4 However,ver the years, the definitions of major and minor bleedingave evolved with different cutoffs for the hemoglobin de-rease.5 Recent efforts have led to the development of effectivend new antithrombotic strategies such as fondaparinux be-ore PCI and bivalirudin during PCI to maintain ischemicrotection and reduce the incidence of access site and non-

Quebec Heart-Lung Institute, Quebec, Quebec, Canada. Manuscripteceived Feb 17, 2010; manuscript received and accepted March 4, 2010.

This study was designed as investigator-initiated trial and funded bynrestricted grants from Eli-Lilly, Indianapolis, Indiana, Bristol-Myers-quibb (New York, New York)/Sanofi-Aventis (Paris, France), Régie Ré-ionale de Québec (Québec City, Québec, Canada), and Corporation de’Institut de cardiologie de Québec (Québec City, Québec, Canada).

*Corresponding author: Tel: (418) 656-8711; fax: (418) 656-4544.

TE-mail address: olivier.bertrand@crhl.ulaval.ca (O.F. Bertrand).

002-9149/10/$ – see front matter © 2010 Elsevier Inc. All rights reserved.oi:10.1016/j.amjcard.2010.03.013

ccess site bleeding complications, at least with the femoralpproach.6–8 Anemia in acute coronary syndromes and afteroronary artery bypass grafting (CABG) confers a worserognosis. However, few data have been reported on theemoglobin or hematocrit changes after PCI using the fem-ral approach, and no data have been published for theransradial approach.9 –14 We assessed the incidence,ange, and clinical effects of hemoglobin changes afterransradial coronary stenting and maximal antiplateletherapy in the EArly Discharge After Transradial Sten-ing of CoronarY Arteries (EASY) trial (Clinicaltrial.ov identifier no. NCT00169819).

ethods

The details of the EASY trial have been previouslyescribed.15 Owing to the study design, a contraindicationor same-day discharge such as ST-segment elevation myo-ardial infarction (MI) within 72 hours and history of leftentricular ejection fraction of �30% or a contraindicationor abciximab administration were the exclusion criteria.

he Health Canada and Laval Hospital ethics review board

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pproved the protocol. All patients provided written in-ormed consent for participation in the trial.

The study was a randomized, controlled, open-labeltudy comparing same-day home discharge and bolus-onlyf abciximab (n � 504) with overnight hospitalization andbolus dose followed by a 12-hour infusion of abciximab

n � 501) after uncomplicated transradial coronary stenting.n the case of angiographic or clinical complications, theatients were excluded from same-day discharge after PCInd received the abciximab bolus and infusion (n � 343).16

bciximab was administered as a 0.25 mg/kg bolus before

able 1aseline characteristics

haracteristic

ge (years)eniabetes mellitusrevious myocardial infarctionrevious percutaneous coronary interventioncute coronary syndromerevious coronary artery bypass surgerylycoprotein IIb/IIIa inhibitors before percutaneous coronaryintervention

nemia before percutaneous coronary interventionlatelet count (109/L)ematocrit (%)reatinine clearance (ml/min)eight (kg)

able 2rocedural characteristics

haracteristic Anemia 24 Hours After PCI p Value

Yes(n � 410; 30%)

No(n � 938; 70%)

umber of vessels1 227 (55%) 573 (61%) 0.0732 136 (33%) 287 (31%)3 47 (11%) 78 (8.3%)umber of sites dilated1 245 (60%) 598 (64%) 0.172 115 (28%) 255 (27%)�3 50 (12%) 85 (9.0%)�1 B2/C lesion 277 (68%) 517 (55%) �0.0001argest catheter sheath

used5Fr 160 (39%) 468 (50%) 0.00026Fr 244 (60%) 466 (50%)7Fr 6 (1.5%) 4 (0.4%)inal activated clotting

time (s)310 � 65 311 � 66 0.83

ompromised/suboccludedbranch

20 (4.9%) 36 (3.8%) 0.38

hrombolysis InMyocardialInfarction flow �3after stenting

9 (2.2%) 18 (1.9%) 0.83

rocedure duration (min) 55 � 30 46 � 23 �0.0001

he first balloon angioplasty and infusion was given for a p

otal of 12 hours at 0.125 �g/kg/min to a maximum of 10g/min. All patients were pretreated with aspirin and clo-idogrel before diagnostic angiography. After radial orlnar sheath insertion, a bolus of 70 U/kg heparin wasiven intravenously with a target final activated clottingime of 300 seconds.17 The vascular sheaths were re-oved at the end of the procedure, and a bracelet (He-ostop, Zoom, Piedmont, Quebec, Canada) remained in

lace until hemostasis was completed, usually within 2ours. Cardiac biomarkers and complete blood countsere evaluated on blood samples collected immediatelyefore the procedure, shortly after PCI (4 to 6 hours), andhe next day (12 to 24 hours). Study personnel inter-iewed all patients the day after PCI and at 30 days, 180ays, and 1 and 3 years after PCI.

The major cardiac adverse event (MACE) rate, includingeath, MI, and target vessel revascularization was calcu-ated at 30 days and 6, 12, and 36 months after the index

igure 1. Hemoglobin decrease 24 hours after PCI according to hemoglo-in baseline value. Solid line indicates regression line; short dashes, 95%onfidence interval of regression line; long dashes, 95% prediction intervalf regression line.

Anemia 24 Hours After PCI p Value

Yes� 410; 30%)

No(n � 938; 70%)

64 � 11 59 � 10 �0.0001278 (68%) 772 (82%) �0.000196 (23%) 137 (15%) �0.0001

193 (47%) 406 (43%) 0.2176 (19%) 185 (20%) 0.65

293 (71%) 610 (65%) 0.02335 (8.5%) 50 (5.3%) 0.02931 (7.6%) 36 (3.8%) 0.0060

167 (41%) 39 (4.2%) �0.0001245 � 64 236 � 57 0.0188.0 � 3.5 42.5 � 3.3 �0.000181 � 29 96 � 41 �0.000177 � 17 83 � 16 �0.0001

(n

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rocedure. The end point adjudications and classifications at

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157Coronary Artery Disease/Hemoglobin Changes and Transradial PCI

ll points were made by a clinical events committee whoas unaware of the study groups. Revascularization, includ-

ng repeat PCI or CABG, was also assessed. For non–Q-ave MIs, periprocedural MIs were classified when anyost-PCI creatine kinase MB value was �3 times the upperimit of normal (i.e., 30 �g/ml at our laboratory). Afterospital discharge, non–Q-wave MIs were classified usinghe American College of Cardiology/European Society ofardiology nomenclature (i.e., using any troponin-I or tro-onin-T-value or creatine kinase/creatine kinase-MB valuesreater than the upper limits of normal.18 Major bleedingpisodes were categorized using the Randomized Evalua-ion in PCI Linking Angiomax to Reduced Clinical events-2REPLACE-2) trial classification.19 Anemia was catego-ized using the World Health Organization criteria (i.e.,emoglobin �13 g/dl for men and hemoglobin �12 g/dl foromen).14 All blood samples were analyzed in the same

igure 2. Range of hemoglobin decrease after PCI. Proportion of hemo-lobin decrease among patients at 24 hours after PCI.

igure 3. Incidence of MACE according to hemoglobin decrease. MACEates at 30 days 1 year, and 3 years of follow-up, according to hemoglobinecrease 24 hours after PCI.

ore laboratory. At 3 years of follow-up, vital status data p

ere complete for 100%, and the MACE rate for 99.2% ofhe study population.20

Categorical variables are presented as numbers andercentages and continuous variables as the mean � SD.he baseline and procedural characteristics were com-ared using Fischer’s exact test or chi-square test forategorical variables and Student’s t test for continuousariables. Potential predictors of anemia at 24 hoursfter PCI were selected with stepwise, backward, andorward procedures with logistic regression analyses.urvival curves were constructed using Kaplan-Meier

echniques, and comparisons between anemic and non-nemic patients after PCI were done using the log-rankest. The Cox proportional hazard model was used tossess the relative risks of anemia 24 hours after PCI onlinical outcomes for �3 years. Stepwise selection wassed to identify potential predictors, which were enterednto the model at p �0.20 and retained at p �0.10.

igure 4. Anemia before and after PCI. Hemoglobin levels at baselinebefore PCI), 4 to 6 hours, and 24 hours after PCI in patients according tonemia status.

Figure 5. Independent predictors of anemia at 24 hours after PCI.

Values �0.05 were considered significant. Statistical

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ests were performed using JMP, version 7.0 (SAS Insti-ute, Cary, North Carolina).

esults

Of the 1,348 patients enrolled in the trial, 206 (15%)resented with anemia before PCI and 410 (30%) met theorld Health Organization criteria for anemia within 24

ours after PCI (Tables 1 and 2). Significantly more womenad anemia than men both before (23% vs 13%, p �0.0001)nd after PCI (44% vs 26%, p �0.0001). Overall, a meanemoglobin decrease of 0.6 � 1.0 g/dl occurred within 24ours after PCI (Figure 1). The hematocrit decreased from1.1% to 38.1% at 4 to 6 hours after PCI and to 39.0% theext day. As shown in Figure 2, 27% had no hemoglobinecrease and 41% had �1 g/dl, 24% a decrease of 1 to 2/dl, 7% a decrease of 2 to 3 g/dl, and 1.3% a decrease of3 g/dl. Considering the incidence of MACE according to

he hemoglobin decrease, a clear cutoff was seen with aignificant increase in MACE at 30 days when the hemo-lobin decrease was �3 g/dl (Figure 3). This effect pro-ressively vanished during follow-up.

Patients with anemia at 24 hours after PCI had a gradualemoglobin decrease at 4 to 6 hours after PCI and 24 hours

igure 6. MACE according to anemia status 24 hours after PCI. MACE raours after PCI.

fter PCI. In contrast, nonanemic patients had only a tran- h

ient hemoglobin decrease at 4 to 6 hours after PCI, whichad almost completely recovered at 24 hours (Figure 4). Ofhe independent predictors of anemia at 24 hours, anemiaefore PCI was the strongest independent factor (odds ratio3.5, 95% confidence interval 9.17 to 20.41, p �0.0001;igure 5). Patients with anemia within 24 hours after PCI

0 days, 1 year, and 3 years of follow-up, according to anemia status at 24

igure 7. Event-free survival curves. Kaplan-Meier analysis of MACEtratified according to presence or absence of anemia 24 hours after PCI.

tes at 3

ad significantly more MACE at 30 days, 6 months, 1 year,

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159Coronary Artery Disease/Hemoglobin Changes and Transradial PCI

nd 3 years than did patients without (Figures 6 and 7).lthough mortality did not significantly differ between theatients with and without anemia within 24 hours after PCI,atients with anemia had significantly more MI and targetessel revascularization than did patients without anemia atll intervals (Figure 6). Furthermore, although no differenceas found in the rates of repeat PCI at 1 year (9% vs 7%,� 0.28) or at 3 years (14% vs 13%, p � 0.67) in patientsith and without anemia within 24 hours after PCI, signif-

cantly more CABG had occurred at 1 year (5% vs 2%, p �.0086) and 3 years (6% vs 3%, p � 0.0023) in the groupf patients with anemia after PCI. On multivariate analysis,nemia within 24 hours after PCI remained an independentredictor of MACE �3 years after PCI (Table 3).

iscussion

Our unique findings can be summarized as follows: 24ours after transradial PCI and maximal antiplatelet ther-py, the mean hemoglobin decrease (0.6 � 1.0 g/dl) wasinimal, the incidence of 30-day MACE significantly in-

reased when the hemoglobin decrease was �3 g/dl, anemiaas a frequent finding with a significant preponderance inomen, and anemia remained a negative independent pre-ictor of MACE for �3 years after PCI.

Although numerous definitions of major and minorleeding have been proposed in acute MI and PCI trials,urprisingly few reports have studied hemoglobin and/orematocrit decreases after PCI. In a study of 177 patientsndergoing uncomplicated balloon angioplasty, mainly witheparin-based anticoagulation, Jauch et al21 found that theemoglobin decreased 1 to 2 g/dl (depending on the base-ine hemoglobin values) between the baseline and 24-hourercutaneous transluminal coronary angioplasty assess-ent. Patients were treated by femoral approach with 8Fr

heath size. Other studies using standard femoral approachave found a hematocrit decrease of 5% to 15% after per-utaneous transluminal coronary angioplasty and 21%fter coronary stenting, in part because of hemodilutionith dextran.9,22–24 From our results, transradial PCI

able 3nivariate and multivariate predictors of major adverse cardiovascular ev

ariable

HR

iabetes mellitus 1.46iseased vessels �2 1.73reated lesions �3 1.981 Lesion B2/C 1.49ajor bleeding* 4.15

ercutaneous coronary intervention duration �1 hour 1.99nemia 24 hours after percutaneous coronary intervention 1.43ompromised/suboccluded branch 2.31hrombolysis In Myocardial Infarction flow �3 after

stenting2.83

Only variables significantly associated with MACE on univariate anaultivariate model.* According to Randomized Evaluation in PCI Linking Angiomax to R— � not retained by forward-backward stepwise selection of variables

eems to limit the periprocedural hemoglobin decrease, t

ecause the mean decrease the day after the procedureas limited, with 68% of patients having no hemoglobinecrease or �1 g/dl.

Initially, the Thrombolysis In Myocardial Infarction clas-ification defined major bleeding as overt bleeding with aemoglobin decrease of �5 g/dl.25 More recent definitions,uch as from the REPLACE-2 or ACUITY, have used aower threshold by including overt bleeding with �3 g/dl orny hemoglobin decrease of �4 g/dl without an overtource.8,19 The definitions used for the Clopidogrel in Un-table angina to prevent Recurrent Events (CURE), Orga-ization for the Assessment of Strategies for Ischemic Syn-romes (OASIS), or SafeTy and Efficacy of Enoxaparin inCI patients, an internationaL randomized EvaluationSTEEPLE) trials also used a threshold of 3 g/dl but re-uired an overt bleeding episode.7,26 With current tech-iques and recent antithrombotic regimens, the incidence ofajor bleeding has considerably decreased; however, its

egative effect has been increasingly recognized. Using aransradial approach, we found an incidence of 1.4% forajor bleeding in the EASY trial using the REPLACE-2

riteria and 0.5% using the Thrombolysis In Myocardialnfarction major criteria.2 In the present analysis, we foundhat a hemoglobin decrease of �3 g/dl was associated withsignificant increase of early and late MACE compared tolower hemoglobin decrease. However, the hemoglobin

ecrease was not an independent predictor of events. Over-ll, this suggests that a cutoff of �3 g/dl to define majorleeding in modern PCI trials is justified.

Anemia is a well-recognized independent predictor ofortality and adverse outcomes in patients with heart

ailure and acute coronary syndromes and before CABGr PCI.10 –12,14 The mechanisms are likely complex butnvolve organ hypoxia owing to decreased oxygen deliv-ry and a reduced coronary flow reserve.12 The preva-ence of anemia before PCI has been reported in 20% to0% of patients in several observational and randomizedrials.10 –12,14,27 The lower prevalence in the present studyight have simply reflected different selected popula-

ACE) at 3 years

ivariate Analysis Multivariate Analysis

CI) p Value HR (95% CI) p Value

1.93) 0.012 —2.20) �0.0001 1.52 (1.18–1.96) 0.00132.70) 0.0001 1.52 (1.06–2.12) 0.0241.93) 0.0018 —7.38) 0.0003 2.52 (1.20–4.71) 0.0162.54) �0.0001 —1.83) 0.0054 1.30 (1.01–1.67) 0.0483.48) 0.0008 2.09 (1.31–3.16) 0.00284.83) 0.0024 2.30 (1.20–3.98) 0.014

e shown; multivariate hazard ratios are given for variables included in

Clinical events-2 criteria.ted with MACE; CI � Confidence interval; HR � hazard ratio.

ents (M

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aseline anemia had more co-morbidities than patientsithout baseline anemia. After adjustment for the base-

ine and procedural differences, anemia before transradialCI was not retained as an independent predictor of thearly or late incidence of death or MACE. Evaluatingemoglobin values early (i.e. 4 to 6 hours after PCI) cane confounded by iatrogenic hemodilution, which fre-uently occurs periprocedurally. In our multivariateodel, anemia within 24 hours after PCI remained an

ndependent predictor of MACE at 3 years of follow-up,lthough major bleeding was the strongest independentredictor.

It should be emphasized, however, that in our study,nemia at 24 hours after PCI was not a predictor of early orate death. This is in sharp contrast to previous stud-es.11,12,14,28 This could be a consequence of the limitationf blood loss associated with the transradial approach oresult from the limited number of early and late deaths in theresent study. However, the incidence of nonfatal ischemicvents was associated with anemia after PCI. Baseline ane-ia has also been reported to be associated with ischemic

vents in some studies but not others.10,14 Additional anal-sis of studies using the femoral approach and assessingnemia after PCI are required to better understand the po-ential relation between anemia and ischemic events. It wastriking that women are more prone to hemoglobin de-reases and anemia after PCI than men. Although the causesre likely multifactorial, we should pay particular attentiono this group of patients. In this trial, we previously reportedhat female gender was the only independent predictor ofccess site hematoma.29

The limitations of the present study include that it waspost hoc analysis; therefore, our findings should pri-arily be viewed as hypothesis generating. Owing to the

tudy design, some patients at greater risk of bleedingere excluded. This could have resulted in an underes-

imation of the true incidence of post-PCI anemia andimited the generalizability of our results. Our resultsight not be applicable to PCI performed using the

emoral approach and/or with different antithromboticegimens. The hemoglobin changes were assessed at 4 to

and 12 to 24 hours after PCI; however, it remainsossible that a later assessment would show an evenreater incidence of anemia.

cknowledgment: O. F. Bertrand, E. Larose, S. Rinfret,nd P. Poirier, are research scholars of the Quebec Foun-ation for Health Research (FRSQ).

1. Jolly SS, Amlani S, Hamon M, Yusuf S, Mehta SR. Radial versusfemoral access for coronary angiography or intervention and the im-pact on major bleeding and ischemic events: a systematic review andmeta-analysis of randomized trials. Am Heart J 2009;157:132–140.

2. Bertrand OF, Larose E, Rodes-Cabau J, Gleeton O, Taillon I, Roy L,Poirier P, Costerousse O, Larochelliere RD. Incidence, predictors, andclinical impact of bleeding after transradial coronary stenting andmaximal antiplatelet therapy. Am Heart J 2009;157:164–169.

3. Feit F, Voeltz MD, Attubato MJ, Lincoff AM, Chew DP, Bittl JA,Topol EJ, Manoukian SV. Predictors and impact of major hemorrhageon mortality following percutaneous coronary intervention from the

REPLACE-2 trial. Am J Cardiol 2007;100:1364–1369.

4. Manoukian SV, Feit F, Mehran R, Voeltz MD, Ebrahimi R, Hamon M,Dangas GD, Lincoff AM, White HD, Moses JW, King SB III, OhmanEM, Stone GW. Impact of major bleeding on 30-day mortality andclinical outcomes in patients with acute coronary syndromes: an anal-ysis from the ACUITY trial. J Am Coll Cardiol 2007;49:1362–1368.

5. Steinhubl SR, Kastrati A, Berger PB. Variation in the definitions ofbleeding in clinical trials of patients with acute coronary syndromesand undergoing percutaneous coronary interventions and its impacton the apparent safety of antithrombotic drugs. Am Heart J 2007;154:3–11.

6. Hamon M, Rasmussen LH, Manoukian SV, Cequier A, Lincoff MA,Rupprecht HJ, Gersh BJ, Mann T, Bertrand ME, Mehran R, StoneGW. Choice of arterial access site and outcomes in patients with acutecoronary syndromes managed with an early invasive strategy: theACUITY trial. EuroIntervention 2009;5:115–120.

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