Postprocedural myocardial infarction is an ominous complication of percutaneous coronary intervention (PCI). Despite several patient, lesion, and procedural factors that may affect its occurrence and severity, it is unclear if implanting a stent edge on a coronary lipid pool, as appraised by optical coherence tomography (OCT), adversely affects outcomes. The aim of this study was to assess the association between postprocedural myocardial infarction and the implantation of a stent edge on a lipid pool, as assessed by OCT. A database was screened for patients without ongoing myocardial infarctions; who underwent PCI with stenting for single, native, de novo lesions; without periprocedural side-branch occlusion or compromise; who underwent post-PCI OCT; and had postprocedural myocardial infarctions. These subjects were matched 1:1 with patients with similar features but without postprocedural myocardial infarctions. Plaque characterization with OCT was performed using established criteria. Specifically, lipid pools within stent edges were quantified by computing the number of involved quadrants and the degree of lipid arc on cross-sectional images. A total of 30 patients were included (15 with postprocedural myocardial infarctions and 15 controls without infarctions). Whereas no patient or control subject had lipid pools in correspondence to distal stent edges, landing of proximal stent edges on lipid pools was significantly more frequent in patients than in controls (10 [66%] vs 2 [13%], p = 0.009), Moreover, patients with postprocedural myocardial infarctions had more extensive lipid pools at proximal stent edges than those without postprocedural myocardial infarctions. Accordingly, lipid pool arc at proximal stent edge was significantly associated with peak post-PCI creatine kinase-MB/upper limit of normal ratio (Spearman’s ρ = 0.49, p = 0.006). In conclusion, incomplete stent coverage of coronary lipid pools appears to be associated with an increased risk for postprocedural myocardial infarction in patients who undergo PCI.
The association between percutaneous coronary intervention (PCI) and subsequent myonecrosis has been intensely researched. Previous studies suggest that post-PCI biomarker elevations could be due to distal embolization or side-branch occlusion. However, available studies are limited by reliance on imaging modalities with suboptimal resolution. Accumulating data suggest that stenting lesions containing lipid plaques can result in adverse angiographic and clinical outcomes, including no-reflow, distal embolization, and myocardial infarction. However, there is uncertainty regarding the impact of implanting the edge of a stent within a lipid pool. Time-domain optical coherence tomography (OCT) has suggested that the pre-PCI presence of thin-cap fibroatheroma can be associated with post-PCI myocardial infarction. We hypothesized that the implantation of stent edges in lipid pools, as appraised by frequency-domain OCT after PCI, may be associated with postprocedural myocardial infarction, irrespective of angiographic findings or clinical success.
Methods
This was a retrospective case-control study. All patients gave written informed consent. Given the observational design, the requirement for ethical approval was waived. From our comprehensive OCT database, we selected patients without ongoing myocardial infarction, who underwent PCI with stenting for single, native, de novo lesions, without angiographic evidence of periprocedural side-branch occlusion or compromise, but having postprocedural myocardial infarctions ( Table 1 ). Notably, patients with significant left main coronary artery disease were excluded, as well as those with long (>30 mm) lesions, those with congestive heart failure or renal failure (serum creatinine >1.8 mg/dl), those who underwent atheroablative procedures, and those receiving embolic protection devices. These subjects were matched 1:1 with patients with similar features but without postprocedural myocardial infarctions.
| Patient | Age (yrs) | Gender | DM | Admission Diagnosis | Target Vessel | Stent Length (mm) | Stent Diameter (mm) | Stent Type | Baseline RVD (mm) | Baseline MLD (mm) | Stent MLA (mm 2 ) | Lipid Pool Arc (°) | Cap Thickness (μm) |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 1 | 39 | M | No | CSA | RCA | 13 | 3.5 | DES | 3.08 | 1.53 | 9.1 | 154 | 0.07 |
| 2 | 42 | M | No | NSTEACS | LAD | 30 | 2.75 | DES | 2.42 | 0.58 | 5.4 | 235 | 0.14 |
| 3 | 49 | M | No | CSA | RCA | 28 | 2.5 | DES | 2.34 | 0.66 | 4.8 | 186 | 0.07 |
| 4 | 50 | M | Yes | CSA | LAD | 15 | 3.00 | DES | 1.74 | 0.36 | 5.6 | 0 | NA |
| 5 | 52 | M | Yes | NSTEACS | LAD | 28 | 3.0 | DES | 2.56 | 1.07 | 6.6 | 178 | NA |
| 6 | 59 | M | Yes | NSTEACS | LAD | 18 | 2.75 | DES | 2.42 | 0.53 | 5.6 | 195 | 0.08 |
| 7 | 64 | M | Yes | CSA | LCX | 18 | 3.00 | BMS | 2.81 | 0.26 | 5.4 | 170 | 0.06 |
| 8 | 74 | M | No | NSTEACS | LCX | 16 | 3.0 | DES | 3.23 | 0.85 | 12.0 | 0 | NA |
| 9 | 76 | M | No | CSA | RCA | 35 | 3.5 | BMS | 2.91 | 0.97 | 7.1 | 0 | NA |
| 10 | 78 | M | No | NSTEACS | LAD | 16 | 3.0 | BMS | 2.47 | 0.73 | 10.0 | 0 | NA |
| 11 | 79 | F | No | NSTEACS | LAD | 14 | 2.5 | BMS | 2.50 | 1.32 | 5.1 | 170 | 0.06 |
| 12 | 82 | M | No | NSTEACS | LAD | 24 | 3.50 | BMS | 3.03 | 1.04 | 10.7 | 166 | 0.06 |
| 13 | 82 | M | Yes | CSA | LAD | 12 | 3.0 | BMS | 2.13 | 0.57 | 7.5 | 167 | 0.07 |
| 14 | 85 | M | No | NSTEACS | RCA | 20 | 3.00 | DES | 2.65 | 0 | 7.5 | 0 | NA |
| 15 | 85 | M | No | CSA | LAD | 20 | 2.75 | BMS | 1.77 | 0.69 | 4.0 | 166 | 0.06 |
In patients with stable angina or normal baseline creatine kinase-MB (CK-MB) levels, postprocedural myocardial infarction was defined as an increase of CK-MB >3 times the upper limit of normal (ULN) (25 U/L) after PCI. In patients with non–ST-segment elevation acute coronary syndromes and elevated baseline values of CK-MB, postprocedural myocardial infarction was defined as a pre-PCI CK-MB decrease pattern, followed by a post-PCI increase of >20% in ≥1 of 2 post-PCI determinations. CK-MB activity was determined using an immunoinhibition assay and confirmed by mass spectrometry. Elevated CK-MB levels were defined as a level higher than the URL. CK-MB measurements were performed before and immediately after the procedure and again at 6 to 12 and 18 to 24 hours. The maximum CK-MB value was used to define the presence or absence of postprocedural myocardial infarction.
Patients with postprocedural myocardial infarctions were matched 1:1 with controls without postprocedural myocardial infarctions, according to established methods ( Table 2 ). Our post-PCI OCT database was reviewed sequentially and patients were selected and matched according to all the following parameters: (1) diabetes mellitus (yes or no), (2) clinical presentation (stable angina, non–ST-segment elevation acute coronary syndromes), (3) target vessel (left anterior descending, left circumflex, or right coronary artery), (4) lesion type (A, B1, B2, or C), (5) stent length (±5 mm), and (6) stent diameter (±0.5 mm). Notably, in none of the included patients or controls was post-PCI OCT followed by additional interventions.
| Patient | Age (yrs) | Gender | DM | Admission Diagnosis | Target Vessel | Stent Length (mm) | Stent Diameter (mm) | Stent Type | Baseline RVD (mm) | Baseline MLD (mm) | Stent MLA (mm 2 ) | Lipid Pool Arc (°) | Cap Thickness (μm) |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 1 | 48 | F | No | NSTEACS | LCX | 15 | 3.5 | BMS | 3.13 | 1.28 | 9.8 | 0 | NA |
| 2 | 49 | M | No | NSTEACS | LAD | 28 | 3.0 | DES | 2.93 | 0.80 | 6.0 | 0 | NA |
| 3 | 52 | M | No | NSTEACS | LAD | 16 | 3.0 | DES | 2.58 | 1.41 | 6.2 | 0 | NA |
| 4 | 52 | M | Yes | NSTEACS | LCX | 14 | 3.0 | DES | 2.33 | 0.79 | 7.5 | 0 | NA |
| 5 | 54 | M | No | CSA | LAD | 15 | 3.5 | DES | 1.90 | 0.60 | 4.5 | 0 | NA |
| 6 | 55 | M | Yes | CSA | RCA | 8 | 2.75 | DES | 3.08 | 0.73 | 11.8 | 159 | 0.12 |
| 7 | 56 | M | Yes | CSA | LAD | 18 | 3.0 | DES | 2.87 | 0.76 | 9.3 | 0 | NA |
| 8 | 62 | M | No | CSA | LAD | 33 | 2.75 | DES | 2.14 | 0.97 | 6.1 | 0 | NA |
| 9 | 65 | M | No | CSA | RCA | 16 | 3.0 | DES | 2.66 | 0.86 | 7.2 | 0 | NA |
| 10 | 69 | M | No | NSTEACS | LAD | 24 | 2.75 | DES | 2.54 | 1.40 | 7.9 | 0 | NA |
| 11 | 75 | M | No | NSTEACS | LAD | 18 | 2.75 | DES | 2.17 | 0.77 | 5.4 | 180 | 0.15 |
| 12 | 78 | M | No | CSA | LCX | 20 | 3.0 | DES | 2.45 | 1.09 | 7.8 | 0 | NA |
| 13 | 80 | M | Yes | CSA | LAD | 15 | 2.75 | BMS | 2.63 | 0.98 | 4.5 | 0 | NA |
| 14 | 81 | F | Yes | NSTEACS | LAD | 12 | 2.5 | BMS | 2.07 | 0.61 | 5.0 | 0 | NA |
| 15 | 81 | M | No | NSTEACS | LAD | 18 | 2.5 | BMS | 2.47 | 0.94 | 4.9 | 0 | NA |
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