Patient population

The participants in this study were recruited from the RICO survey, a French regional survey of AMI. Details on the survey have been published previously . Our study cohort consisted of all primary and rescue PCI procedures, in the 12 hours after symptom onset, using the Export ^® catheter between the 1 January 2009 and 31 December 2009. We then performed a retrospective analysis for patients who met the criteria to select the study population, meaning that all patients with a baseline TIMI flow greater than 1 or those who underwent a PCI procedure without the Export ^® catheter were excluded. Three-hundred and eighty eligible patients admitted for ST-segment elevation myocardial infarction were excluded from the analysis. The main criterion for evaluation was successful thrombectomy, defined as a visible atherothrombotic clot in the filtered, aspirated material (group T+). Otherwise, thrombectomy was deemed to have failed (group T−). Myocardial infarction was diagnosed according to European Society of Cardiology and American College of Cardiology criteria .

Data collection

The following patient characteristics were collected prospectively: age, sex and cardiovascular risk factors (history of or treated hypertension, known history of diabetes, treated hypercholesterolaemia, current smoker [defined as active cigarette smoking within the 3 months prior to this admission]). Anthropometric parameters (i.e., body mass index in kg/m ² ) were measured within 48 hours of admission. Haemodynamic parameters on admission (heart rate, systolic and diastolic blood pressures) and Killip class were also gathered. Ischaemic time was determined by the delay between symptom onset and crossing the lesion with the floppy guide wire. Patients were diagnosed with ST-segment elevation myocardial infarction when they had new or presumed new ST-segment elevation greater than 1 mm seen in any location or new left bundle branch block on the index or subsequent electrocardiogram. Left ventricular ejection fraction was measured by echocardiography at 3 ± 1 days after admission using the Simpson method. The Global Registry of Acute Coronary Events in-hospital to 6-month risk score was calculated with the published variables. Data on chronic and acute treatments administered within 48 hours of admission to hospital were also collected. Coronary angiograms were reviewed by two experienced interventionists not involved with the procedure. Data on the following items were collected: infarct wall location; final TIMI 3 flow; number of diseased vessels; characteristics of the culprit artery and multivessel disease; presence of thrombus or calcifications; eccentric nature of the lesion; presence of 0, 1, ≥ 2 angles of 70° before the lesion; lesion level (ostial, proximal, middle, distal, bifurcation); diameter of the artery at the level of the culprit lesion; lesion type according the American Heart Association classification (A, B1, B2 or C); and distal embolization or no-reflow. Stent thrombosis was defined as follows: evidence of any myocardial infarction, with angiographic confirmation of in-stent thrombus or unexplained death within 30 days after the procedure. Interobserver and intraobserver coefficients of variation assessed in 15 non-selected patients were 5% and 4%, respectively.

This study complied with the Declaration of Helsinki, was approved by the ethics committee of University Hospital of Dijon, and each patient gave written consent before participation.

Laboratory analysis

Blood samples to assess NT-pro-BNP, C-reactive protein, glucose and creatinine concentrations were taken on admission. Median time from symptom onset to blood sampling was 190 min (85–498). Blood samples to assess NT-pro-BNP concentrations were collected in EDTA-containing tubes and stored at –20 °C before analysis (< 3 days). Plasma NT-pro-BNP was determined by enzyme-linked immunosorbent assay using Elecsys NT-pro-BNP sandwich immunoassay on Elecsys 2010 (Roche Diagnostics). The inter- and intra-assay coefficients of variation were both less than 3.1%. The sensitivity of the assay was found to be 0.6 pg/L. Cross-reactivity with other natriuretic peptides, atrial natriuretic peptide and C-type natriuretic peptide was less than 0.01%. C-reactive protein was measured on Dimension Xpand (Dade Behring, Newark, NE) and creatinine on a Vittos 950 analyzer (Ortho Clinical Diagnostics Rochester, NY). Serum creatinine clearance was estimated using the Cockcroft–Gault formula . Peak plasma creatine kinase was assessed by sampling every 8 hours during the first 2 days after admission (Dimension Vista Intelligent Lab System, Siemens).

Procedural treatment

For all patients, the first procedural step was the passing of a floppy, steerable guide wire through the target lesion. The usual pharmacological treatments were used before and during PCI, including intracoronary nitrates, aspirin (500-mg loading dose), either weight-adjusted unfractionated heparin or heparin (5000 IU), and clopidogrel (300- or 600-mg loading dose). The glycoprotein IIb/IIIa inhibitor abciximab was used at the interventionist’s discretion. Administration of a high-dose (50 μg) intracoronary bolus of adenosine was used in most patients with AMI in whom a primary PCI was performed. Stents implanted were either bare metal or drug eluting. Standard therapies after PCI according to current guidelines were continued at hospital discharge, including aspirin (> 81 mg) and clopidogrel (75 mg).

Statistical analysis

The dichotomous data are expressed as numbers (%) and the continuous data are expressed as medians (25th to 75th percentiles). Comparisons between the groups were performed either with the unpaired Student’s t test, or with the non-parametric Mann–Whitney U-test as appropriate. The Chi ² test was used for qualitative variables and Fisher’s exact test for small numbers of patients. Logistic regression was performed using the backward stepwise technique to determine the independent predictors of successful thrombectomy. Results are expressed as odds ratios (ORs) with 95% confidence intervals (CIs). All variables listed in Tables 1 and 2 were tested by univariate analysis and only the variables with a P < 0.10 were examined in the multivariable models. The criteria used for the backward logistic regression were the following: entry in the model with a threshold at 0.05 and exit of the model with a threshold at 0.10. A P -value < 0.05 was considered statistically significant and two-sided tests were used. All the analyses were performed using the SPSS 13.0 software package (SPSS Inc, Illinois, USA).

Table 1

Clinical data, medical history and treatments on admission ( n = 180).

	Group T−	Group T+	P
	( n = 25)	( n = 155)
Men	20 (80)	125 (69)	0.84
Age (years)	74 (57–83)	61 (53–74)	0.015
BMI (kg/m 2 )	27 (24–29)	27 (25–30)	0.81
Hypertension	17 (68)	64 (41)	0.023
Hypercholesterolaemia	11 (44)	59 (38)	0.73
Diabetes mellitus	3 (12)	13 (8)	0.83
Family history of coronary artery disease	7 (28)	39 (25)	0.96
Smoker	7 (28)	63 (41)	0.33
History of TIA or stroke	2 (8)	4 (3)	0.42
Heart rate (beats/min)	78 (65–91)	74 (61–85)	0.18
Systolic blood pressure (mmHg)	148 (130–160)	135 (120–149)	0.031
Diastolic blood pressure (mmHg)	85 (70–100)	80 (70–92)	0.39
ST-elevation myocardial infarction	19 (76)	122 (79)	0.97
Anterior location	12 (48)	56 (36)	0.36
Left ventricular ejection fraction (%)	45 (32–55)	50 (40–60)	0.039
Lysis	2 (8)	25 (16)	0.45
Ischaemic time (min)	226 (136–570)	210 (137–596)	0.996
Cardiogenic shock	1 (4)	6 (4)	0.60
GRACE risk score	156 (130–172)	139 (118–159)	0.094
Cardiovascular death at 30 days	4 (16)	8 (5)	0.11
Biological data
Peak creatine kinase (UI/l)	1301 (948–2535)	1511 (463–2963)	0.99
Creatinine clearance (mL/min)	66.10 (43.80–87.40)	81.00 (60.25–104.80)	0.019
Total cholesterol (g/l)	2.01 (1.61–2.44)	2.03 (1.75–2.25)	0.95
Low-density lipoprotein cholesterol (g/L)	1.37 (1.08–1.61)	1.31 (1.08–1.53)	0.87
High-density lipoprotein cholesterol (g/L)	0.45 (0.38–0.56)	0.45 (0.38–0.53)	0.62
Triglycerides (g/L)	0.91 (0.72–1.53)	1.28 (0.90–1.82)	0.13
C-reactive protein (mg/L)	2.99 (2.90–7.25)	4.56 (2.90–10.60)	0.15
Glycaemia on admission (mmol/L)	7.04 (5.98–9.00)	7.07 (5.90–9.09)	0.92
NT-pro-BNP (pg/mL)	638 (138–2864)	606 (96–1394)	0.39
Chronic treatment
Aspirin	2 (8)	11 (7)	0.80
Clopidogrel	2 (8)	7 (5)	0.81
Statin	8 (32)	25 (16)	0.10
Vitamin K antagonist	4 (16)	5 (3)	0.026
Acute phase
Angiotensin-converting enzyme inhibitor	18 (72)	112 (72)	0.83
Aspirin	24 (96)	150 (97)	0.69
Beta-blocker	22 (88)	129 (83)	0.76
Clopidogrel	25 (100)	150 (97)	0.80
Glycoprotein IIb/IIIa inhibitor	20 (80)	108 (70)	0.41
Insulin	8 (32)	29 (19)	0.21
Low-molecular-weight heparin	13 (52)	99 (64)	0.36
Statin	21 (84)	139 (90)	0.62
Unfractionated heparin	11 (44)	52 (34)	0.43

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