Intraprocedural stent thrombosis (IPST) is a rare complication of percutaneous coronary intervention that leads to poor outcomes; however, the factors contributing to IPST remain largely unknown. Accordingly, we used intravascular ultrasound (IVUS) to examine the lesion characteristics in patients with IPST. We retrospectively analyzed 1,504 consecutive stent-implanted lesions in 1,324 patients (326 with ST-segment elevation myocardial infarction [STEMI], 403 patients with non–ST-segment elevation acute coronary syndrome [NSTE-ACS], and 595 patients with stable angina). Of these, IPST occurred in 5 patients during percutaneous coronary intervention (0.4% per patient; 3 with STEMI, 2 with NSTE-ACS). The IVUS characteristics of plaques that developed IPST were compared with those of controls without the evidence of IPST (non-IPST; n = 15) who were matched by age, gender, lesion location, and clinical presentation (STEMI, NSTE-ACS, or stable angina). All 5 lesions that led to IPST had ruptured plaques with positive remodeling and attenuation. Plaque rupture was also observed in 40% of the non-IPST group. Multiple plaque ruptures in the culprit lesion were more common in the IPST group (80% vs 7%; p <0.01). The maximum cavity area was larger in the IPST group than in the non-IPST group having plaque rupture (4.6 mm 2 [interquartile range, 4.3 to 6.5] vs 2.4 mm 2 [1.8 to 2.9]; p <0.01). In conclusion, we found using IVUS that multiple plaque ruptures with larger cavities more often evolved into IPST.
Stent thrombosis after percutaneous coronary intervention (PCI) is a rare but fatal complication. Over the past decade, intravascular imaging and pathologic studies have revealed the underlying mechanisms and contributing factors of stent thrombosis. Although intraprocedural stent thrombosis (IPST) is an infrequent event, it has been strongly associated with subsequent adverse cardiovascular events. Therefore, the prevention of IPST is clinically important. Previous studies have suggested possible risk factors of IPST including ST-segment elevation myocardial infarction (STEMI) presentation, baseline angiographic thrombus, longer stent length, smaller baseline minimum luminal diameter, higher white cell blood count, bifurcation lesions, the use of bare-metal stents, and lower baseline Thrombolysis In Myocardial Infarction flow grade. Moreover, recent large-scale Clinical Trial Comparing Cangrelor to Clopidogrel Standard of Care Therapy in Subjects Who Require Percutaneous Coronary Intervention (CHAMPION PHOENIX) trial proved that STEMI and non–ST-segment elevation acute coronary syndrome (NSTE-ACS) at presentation, baseline angiographic thrombus, and longer stent length are independent predictors of IPST. However, they have not been studied using intravascular ultrasound (IVUS). Accordingly, we sought to use IVUS to determine the plaque features that predicted the development of IPST.
Methods
We retrospectively analyzed 1,504 consecutive stent-implanted lesions in 1,324 patients who underwent PCI from August 2011 to March 2015 at either Kitaishikai Hospital or Uwajima City Hospital. The institutional review boards of both hospitals approved the retrospective use of patient data.
The sample comprised 326 patients with STEMI, 403 with NSTE-ACS, and 595 with stable angina. All patients received dual antiplatelet therapy with aspirin and clopidogrel before PCI and a 70 IU/kg bolus of unfractionated heparin at the beginning of the procedure to achieve an activated clotting time (ACT) of ≥250 seconds. IPST was defined as any angiographically new or worsening thrombus within or adjacent to a deployed stent occurring during the PCI procedure, whether occlusive or nonocclusive, according to previous reports.
To investigate the factors contributing to IPST, the characteristics of plaques associated with IPST (IPST group) were compared with those of matched controls without evidence of IPST (non-IPST group). The non-IPST group was selected from among the 1,319 patients without IPST and we made it 3 times the size of the IPST group. The following matching criteria were applied: (1) age, (2) gender, (3) lesion location, and (4) clinical presentation (STEMI, NSTE-ACS, or stable angina). We included lesion location because it could influence vulnerable plaque morphologies (i.e., plaque rupture and thin-cap fibroatheroma), particularly in the left anterior descending artery ; and the clinical presentation of ACS was included because it is a known predictive factor of IPST.
Qualitative angiographic analysis was performed by one interventional cardiologist (TM) who was blinded to the clinical and IVUS data. The Thrombolysis In Myocardial Infarction flow grades were determined using standard definitions.
IVUS imaging was performed after intracoronary administration of 0.1 to 0.2 mg nitroglycerin, using commercially available IVUS systems (iLab with 40-MHz Atlantis SR Pro catheters; Boston Scientific, Fremont, California; VISIWAVE with 40-MHz ViewIT catheters; Terumo, Tokyo, Japan; or s5 with 45-MHz Revolution catheters; Volcano Therapeutics, Rancho Cordova, California) with automatic pullback at 0.5 or 1.0 mm/s. If necessary, at the operator’s discretion, we used the aspiration catheter or a small balloon to open either the occluded artery or an area of severe stenosis before IVUS examination.
IVUS analyses were performed by agreement of 2 independent cardiologists (TM and SI) who were blinded to the clinical data, stent type, and time of occurrence of the stent thrombosis. Plaque rupture was defined as the presence of a cavity that communicated with the lumen, with an overlying residual fibrous cap fragment. In the ruptured plaque, we also measured the cavity area inside the plaque, using previously described methods. A thrombus was defined as an intraluminal mass with a layered or lobulated appearance, evidence of blood flow (microchannels) within the mass, and speckling or scintillation. Positive remodeling was defined as a lesion greater than the mean cross-sectional area of the reference external elastic membrane (EEM). Attenuated plaque was defined as the absence of the ultrasound signal behind a plaque that was either hypoechoic or isoechoic to the reference adventitia. A mean attenuation score was calculated according to previously reported method. Spotty calcification was defined as a lesion containing only small calcium deposits within a 90° arc.
Quantitative IVUS analysis was performed using computerized planimetry (echoPlaque; INDEC Medical Systems, Mountain View, California or VISIATLAS, version 2.0; TERUMO, Tokyo, Japan). IVUS measurements included the cross-sectional area of the EEM, the lumen, and the plaque and media (P + M; calculated as EEM − lumen) and plaque burden (calculated as [P + M]/EEM). The methods of subdata are presented in Supplementary Methods .
Statistical analysis was performed using StatView 5.0 (SAS Institute, Cary, North Carolina). Categorical variables were summarized as frequencies and comparisons were made using Fisher’s exact test. Continuous variables were displayed as median values with the interquartile range (IQR; first and third), and compared between groups using the Mann–Whitney U test. Values of p <0.05 were considered statistically significant.
Results
The baseline clinical presentations and lesion locations are listed in the Supplementary Table 1 . Of the 1,504 consecutive stent-implanted lesions in 1,324 patients, IPST was identified in 5 stent-treated lesions (0.3% per lesion) in 5 patients (0.4% per patient; 3 with STEMI, 2 with NSTE-ACS). A representative case of IPST is shown in Figure 1 , with supplemental movies available online. Table 1 summarizes main clinical and lesional characteristics in each of 5 patients with IPST and 15 patients with non-IPST. Other subdata are shown in the Supplementary Tables 2 to 4 .
| Patient Number | Age, years | Sex | Clinical presentation | Lesion location | MLA site | Plaque rupture | Number of plaque rupture | Maximum cavity area, mm 2 | Positive remodeling | Attenuated plaque | Thrombus | ||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| EEM CSA, mm 2 | Lumen CSA, mm 2 | Plaque burden, % | |||||||||||
| IPST (n = 5) | |||||||||||||
| 1 | 40 | M | STEMI | LAD proximal | 24.8 | 1.1 | 95.8 | Present | 2 | 6.5 | Present | Present | Present |
| 2 | 53 | M | NSTE-ACS | LAD proximal | 18.3 | 1.3 | 93.0 | Present | 3 | 4.0 | Present | Present | Present |
| 3 | 69 | M | STEMI | RCA proximal | 30.8 | 1.7 | 94.4 | Present | 2 | 4.6 | Present | Present | Present |
| 4 | 83 | M | STEMI | LAD proximal | 16.4 | 1.3 | 91.9 | Present | 1 | 6.5 | Present | Present | Present |
| 5 | 86 | M | NSTE-ACS | LM | 25.6 | 2.4 | 90.5 | Present | 2 | 4.3 | Present | Present | Present |
| Non-IPST (n = 15) | |||||||||||||
| 6 | 41 | M | STEMI | LAD proximal | 16.6 | 2.0 | 87.9 | 0 | 0 | 0 | Present | 0 | Present |
| 7 | 43 | M | STEMI | LAD proximal | 11.8 | 3.3 | 71.9 | 0 | 0 | 0 | Present | Present | 0 |
| 8 | 44 | M | STEMI | LAD proximal | 11.3 | 1.7 | 84.7 | 0 | 0 | 0 | Present | Present | 0 |
| 9 | 50 | M | NSTE-ACS | LAD proximal | 13.3 | 1.3 | 90.1 | 0 | 0 | 0 | 0 | Present | Present |
| 10 | 52 | M | NSTE-ACS | LAD proximal | 18.3 | 2.4 | 86.8 | 0 | 0 | 0 | 0 | Present | Present |
| 11 | 55 | M | NSTE-ACS | LAD proximal | 19.0 | 2.6 | 86.6 | Present | 1 | 1.6 | 0 | Present | 0 |
| 12 | 64 | M | STEMI | RCA proximal | 25.1 | 2.0 | 92.1 | Present | 1 | 2.7 | Present | Present | 0 |
| 13 | 66 | M | STEMI | RCA proximal | 14.5 | 1.4 | 90.3 | 0 | 0 | 0 | 0 | 0 | 0 |
| 14 | 69 | M | STEMI | RCA proximal | 15.8 | 1.5 | 90.8 | Present | 2 | 3.7 | 0 | Present | 0 |
| 15 | 78 | M | STEMI | LAD proximal | 20.0 | 2.4 | 88.2 | Present | 1 | 3.0 | Present | 0 | 0 |
| 16 | 78 | M | NSTE-ACS | LM | 15.2 | 2.4 | 84.0 | 0 | 0 | 0 | 0 | Present | 0 |
| 17 | 81 | M | STEMI | LAD proximal | 19.6 | 2.4 | 87.6 | 0 | 0 | 0 | Present | Present | Present |
| 18 | 85 | M | STEMI | LAD proximal | 14.9 | 1.3 | 91.6 | Present | 1 | 2.2 | 0 | Present | Present |
| 19 | 86 | M | NSTE-ACS | LM | 21.3 | 2.2 | 89.6 | 0 | 0 | 0 | Present | Present | 0 |
| 20 | 89 | M | NSTE-ACS | LM | 19.4 | 4.7 | 76.0 | Present | 1 | 1.6 | 0 | Present | Present |
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