Thromboaspiration (TA) has been proposed as an adjunct to primary percutaneous coronary intervention (PCI) in ST-elevation myocardial infarction (STEMI) to reduce thrombus burden. However, its effect on microvascular perfusion remains uncertain, and concerns have been raised about its potential to aggravate microvascular injury. This study aimed to evaluate the impact of TA on microvascular obstruction (MVO) using cardiac magnetic resonance imaging in a large cohort of STEMI patients. We prospectively enrolled 460 STEMI patients treated with primary PCI within 12 hours of symptom onset. TA was performed in 193 patients (42%). Cardiac magnetic resonance was performed at day 6 and 3 months to assess infarct size and MVO. A propensity score-based average treatment effect analysis was used to adjust for baseline differences. Subgroup analyses were conducted according to symptom-to-treatment time, thrombus burden (thrombolysis in myocardial infarction thrombus score), and sex. TA was independently associated with higher MVO incidence (odds ratios [OR] 1.52; 95% confidence intervals [CI]: 1.16 to 1.98; p = 0.0024) and greater MVO extent (standardized mean differences 0.42; 95% CI: 0.02 to 0.72; p = 0.041). The association was particularly significant in patients reperfused beyond 6 hours (OR 3.46; 95% CI: 1.92 to 6.23; p < 0.0001) and those with nonocclusive thrombus (thrombolysis in myocardial infarction thrombus score “1 to 4”) (OR 2.23; 95% CI: 1.29 to 3.85; p = 0.004). Sex-stratified analysis showed increased MVO risk in men (OR 1.52; 95% CI: 1.14 to 2.05; p = 0.005) but not in women. TA during primary PCI was associated with increased occurrence and extent of MVO, particularly in patients with delayed reperfusion or nonocclusive thrombus. These findings reinforce current ESC guidelines against routine TA use and suggest that its application should be restricted to carefully selected patients.
In the acute phase of myocardial infarction, coronary angioplasty is the treatment of choice, improving functional and vital prognosis. Revascularization tools include balloon angioplasty, stenting, antithrombotic therapy, and thromboaspiration (TA).
TA is a technique for aspirating large intracoronary thrombus developed to reduce thrombotic burden during angioplasty and stenting. Among several technical advantages during angioplasty in ST-elevation myocardial infarction (STEMI), it is supposed to provide a better stent apposition to coronary wall and reduced distal thrombotic embolization. By clearing the thrombus from the lesion site, TA may also facilitate optimal stent deployment and expansion. However, two complications may occur: embolization to the systemic circulation leading to a stroke, or distal embolization aggravating myocardial injury through microvascular damage. In terms of microvascular injury, inflating the stent is believed to crush the thrombotic mass between the device and the vessel wall, thereby limiting the risk of distal embolization.
While prior studies suggested an improvement in post-TA coronary flow, large randomized trials and meta-analyses have contradicted these findings, such as TASTE, TAPAS, and TOTAL, which mainly showed the lack of benefit on MACE and an increased risk of stroke. Consequently, the 2017 ESC guidelines (STEMI) and the 2018 ESC/EACTS guidelines (myocardial revascularization) recommended against routine TA in revascularization. Some subgroups, such as those undergoing angioplasty within 6 hours of symptoms, patients on anti-GP IIb/IIIa therapy, or those with a high thrombotic load, may still benefit from the technique.
The thrombotic burden can be assessed using the Thrombolysis in Myocardial Infarction (TIMI) thrombus score (TTS). It is evaluated by coronary angiography, either during a diagnostic angiogram or after engagement of the angioplasty guiding catheter. In cases of an occlusive thrombus, it was determined once coronary flow has been restored following passage of a guidewire. Cardiac magnetic resonance (CMR) is an imaging modality that provides a detailed analysis of myocardial function, perfusion, necrosis, and microvascular obstruction (MVO). Notably, MVO, particularly when extensive, is associated with a higher risk of adverse cardiovascular events following myocardial infarction.
The aim of our study was to compare the effects of TA on coronary microcirculation (specifically MVO) in a large cohort of STEMI patients, as assessed by CMR.
Materials and Methods
Population
This study analyzed a prospective cohort of 460 patients who presented with STEMI (PHRC, N° 2006/0070). Patients were consecutively included from January 2006 to August 2018. Inclusion criteria: STEMI managed with coronary angioplasty within 12 hours of symptom onset; successful angioplasty with stenting; written informed consent. Exclusion criteria: prior myocardial infarction or coronary artery bypass surgery; age <18 years; clinical signs of cardiogenic shock; major comorbidities limiting life expectancy; contraindications for CMR (pacemaker, ferromagnetic body, claustrophobia, or severe renal insufficiency). The study adhered to the Helsinki Declaration principles. All patients provided informed consent before undergoing CMR, and the study protocol was approved by the hospital’s ethics committee.
Procedure of TA
The procedure was performed by an interventional cardiologist. TA was initiated after the lesion crossed by the guidewire. A minimum of two 40 ml syringes was recommended. To avoid systemic embolic risk, selective catheterization beyond the coronary ostia was performed before removing the TA catheter. The guide catheter was also aspirated.
TIMI thrombus score
Thrombus was classified as follows for the purpose of quantitative evaluation: TTS as follows:
The TTS classifies thrombus burden from 1 to 5. Scores “1 to 4” reflect increasing thrombus size without full occlusion, ranging from suspected thrombus to large thrombus >2 vessel diameters. Score “5” indicates complete vessel occlusion. For analysis, scores “1 to 4” were grouped as nonocclusive thrombus, and score “5” as occlusive.
CMR
Longitudinal follow-up with CMR was conducted. The initial exam was performed on day 6 after admission [IQR: 4; 9] and repeated at 98 days [IQR: 94; 106]. CMR machines of 1.5 or 3 Tesla power (Avanto and Skyra, Siemens Medical Solutions, Forchheim, Germany) were used. Long-axis and short-axis views were used to assess segmental and global kinetics (30-phase count). Contiguous short-axis slices (8 mm thickness) covered the entire left ventricle. Late enhancement sequences were acquired 8 to 10 minutes after the injection of 0.2 mmol/kg gadoterate meglumine (Dotarem, Guerbet Laboratories, Roissy-Charles de Gaulle, France). Inversion time was adjusted to suppress the signal from presumed healthy myocardium. Standard parameters included: repetition time = 4.9 ms, excitation time = 1.9 ms, flip angle = 15°, slice thickness = 8 mm, spatial resolution = 1.35 × 1.35 × 8 mm³. T2-weighted inversion recovery prepared fast-spin echo sequence was performed on a stack of contiguous short-axis views covering the entire LV in mid-diastole; slice thickness/gap 7/0.8 mm; TR (4,000 ms); TE 60 to 70 ms; FOV 264 × 385; matrix 176 × 320; flip angle 180°.
Analysis of CMR
CMR images were transferred to a dedicated workstation for blinded analysis (Medis Suite, Leiden, The Netherlands). Endocardial and epicardial contours were manually traced on all short-axis views, excluding trabeculations and papillary muscles. End-diastolic and end-systolic volumes, and left ventricular mass were indexed to body surface area. Infarct size was calculated using the “full width at half maximum” method on late enhancement images. Late enhancement zones were summed to determine the percentage of left ventricular mass affected.
MVO was defined as a hypointense area within the hyperintense infarct zone on late enhancement sequences. MVO extent was manually measured and expressed in grams. Reproducibility of this measurement has been published.
IMH was identified on T2-weighted images as a region of hypointense signal within the hyperintense area of myocardial edema.
Statistical analysis
Variables will be described as a mean ± a standard deviation if the variable follows a normal distribution and a median [interquartile range] otherwise. Normality has been validated graphically through appropriate plots. For qualitative variables, they will be presented as numbers (proportions). Groups will be compared according to standard tests: Student’s test ( t test) or Wilcoxon’s nonparametric test for quantitative variables based on the distribution of variables and chi-square test ( χ ²) or Fischer’s test ( F -test) for qualitative variables. These tests comparing the two groups were performed descriptively.
To estimate the effect of thrombus aspiration (TA) on coronary microcirculation in STEMI patients, we used a propensity score-based inverse probability weighting approach with the average treatment effect (ATE) estimand. This allowed us to balance baseline covariates between patients who received TA and those managed with other reperfusion strategies, thereby emulating a randomized treatment assignment ( Figure 1 and Supplementary Figure 3 ). The ATE estimand aims to quantify the average effect of TA in the overall study population, independent of actual treatment allocation. In other words, it addresses the counterfactual question: “How would outcomes, on average, have differed if all patients had received TA versus none?”
Impact of thromboaspiration (TA) on microvascular obstruction (MVO) assessed by cardiac magnetic resonance (CMR): in 460 patients with ST elevation myocardial infarction (STEMI). Using an average treatment effect (ATE) propensity score, TA emerged as an independent predictor of MVO occurrence (OR 1.52; 95% CI: 1.16 to 1.98; p = 0.0024) and its extent (standardized mean difference [SMD] 0.42; 95% CI: 0.02 to 0.72; p = 0.041). Subgroup analyses showed that TA significantly increased MVO risk when performed more than 6 hours after symptom onset (OR 3.46; 95% CI: 1.92 to 6.23; p < 0.0001) and in patients with nonocclusive thrombus (TTS “1 to 4”) (OR 2.23; 95% CI: 1.29 to 3.85; p = 0.004). In sex-based analysis, TA was associated with a higher MVO risk (OR 1.52; 95% CI: 1.14 to 2.05; p = 0.005) and extent (SMD 0.44; 95% CI: 0.006 to 0.747; p = 0.049) in men, but not in women (OR 0.74; 95% CI: 0.38 to 1.46; p = 0.386; SMD 0.93; 95% CI:–0.166 to 2.019; p = 0.12).
Once covariate balance was achieved, weighted logistic regression models were used for binary outcomes, yielding odds ratios (OR) and 95% confidence intervals (CI), while weighted linear regression models were used for continuous outcomes, yielding standardized mean differences and 95% CI. Stratified analyses were also performed according to sex, symptom-to-treatment time (TTS), and treatment delay to explore potential effect modifications. All results were summarized using forest plots for visual comparison of treatment effects across outcomes. Statistical analyses were performed using R software (version 4.4.1; R Foundation for Statistical Computing, Vienna, Austria).
Results
Among 460 STEMI patients, 193 (42.3%) underwent TA (TA+). The mean age was 58.4 ± 11.2 years, and 82.3% were male. Anterior infarction was present in 267 patients (58.0%), and the mean LVEF was 46.4 ± 9.7%. The thrombus burden, assessed by the TTS, was higher in TA+ versus TA– (median 5 [IQR 5 to 5] vs 5 [3 to 5]; p < 0.0001). Overall, IMH was identified in 68 patients. The prevalence was similar between the TA and non-TA groups ( n = 36, 15.7% vs n = 32, 20.1%; p = 0.278). Baseline characteristics are summarized in Tables 1 and 2 .
Table 1
Baselines characteristics patients
| Total | TA– | TA+ | p | |
|---|---|---|---|---|
| n = 460 | n = 261 | n = 199 | ||
| Age, years | 58.4 ± 11.2 | 58.0 ± 11 | 58.8 ± 11.4 | 0.45 |
| Men, N (%) | 379 (82.3%) | 212 (81.2%) | 167 (83.9%) | 0.45 |
| BMI, kg/m² | 26.9 ± 4.1 | 26.6 ± 4 | 27.3 ± 4.1 | 0.06 |
| Hypertension, N (%) | 154 (33.4%) | 84 (32.1%) | 70 (35.1%) | 0.50 |
| Diabetes, N (%) | 55 (11.9%) | 30 (11.4%) | 25 (12.5%) | 0.72 |
| Hypercholesterolemia, N (%) | 246 (53.4%) | 135 (51.7%) | 111 (55.7%) | 0.38 |
| Active smocking, N (%) | 217 (47.1%) | 124 (47.5%) | 93 (46.7%) | 0.86 |
| Angina, N (%) | 177 (38.4%) | 107 (40.9%) | 70 (35.1%) | 0.20 |
| AT admission in the Cath lab | ||||
| Pain-to-PCI time, minutes | 302.4 ± 333.1 | 310.2 ± 330.8 | 292.1 ± 336.7 | 0.56 |
| Systolic blood pressure, mm Hg | 141.4 ± 27 | 143.9 ± 27.7 | 138.2 ± 25.6 | 0.024 |
| Diastolic blood pressure, mm Hg | 88.5 ± 18.7 | 89.5 ± 18.5 | 87.0 ± 19 | 0.16 |
| Heart rate, bpm | 75.2 ± 18.4 | 75.9 ± 19.4 | 74.4 ± 16.9 | 0.39 |
| Thrombolysis, N (%) | 39 (8.4%) | 25 (9.5%) | 14 (7%) | 0.33 |
| Primary angioplasty, N (%) | 409 (88.9%) | 227 (86.9%) | 182 (91.4%) | 0.12 |
| Anterior infarction, N (%) | 267 (58%) | 150 (57.4%) | 117 (58.7%) | 0.77 |
| Single-vessel disease, N (%) | 279 (60.6%) | 150 (57.4%) | 129 (64.8%) | 0.11 |
| Complete revascularization, N (%) | 312 (67.8%) | 169 (64.7%) | 143 (71.8%) | 0.10 |
| GP IIb/IIIa inhibitor use, N (%) | 158 (34.4%) | 75 (28.8%) | 83 (41.9%) | 0.004 |
| Median TIMI thrombus score | 5 [4; 5] | 5 [3; 5] | 5 [5; 5] | <0.0001 |
| Heart failure during hospitalization, N (%) | 76 (16.5%) | 39 (14.9%) | 37 (18.5%) | 0.29 |
| Creatinine, μmol/L | 80.7 ± 22.6 | 79.5 ± 24.9 | 82.2 ± 19.2 | 0.20 |
| Blood glucose, mmol/L | 8.0 ± 3 | 7.8 ± 2.6 | 8.4 ± 3.4 | 0.046 |
| Peak of CK, UI/L | 2,959.5 ± 2,359 | 2,724.6 ± 2,383.5 | 3,267.7 ± 2,296.2 | 0.014 |
| Peak CRP, mg/L | 16.7 ± 34.2 | 14.7 ± 25.6 | 19.3 ± 43.1 | 0.16 |
| Total cholesterol, g/L | 2.1 ± 0.5 | 2.1 ± 0.5 | 2.1 ± 0.5 | 0.95 |
| LDL, g/L | 1.3 ± 0.4 | 1.3 ± 0.4 | 1.3 ± 0.3 | 0.53 |
| HDL, g/L | 0.4 ± 0.1 | 0.4 ± 0.1 | 0.4 ± 0.1 | 0.21 |
| Triglycerides, g/L | 1.5 ± 1 | 1.5 ± 1 | 1.6 ± 1 | 0.22 |
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