Abstract
Introduction
Coronary angiography is commonly performed following non-ST segment elevation myocardial infarction (NSTEMI) to assess the need for revascularization. Some of these patients have myocardial infarction (MI) with no obstructive coronary atherosclerosis (MINOCA). Patients without severe obstructive lesions are usually treated conservatively. However, coronary angiography has known limitations in the assessment of lesion severity. We report our experience of using coronary Optical Coherence Tomography (OCT) in a series of patients without severe obstructive coronary lesions.
Methods
165 patients underwent coronary OCT at Vancouver General Hospital. NSTEMI was the clinical presentation in 70 patients and 26 had angiographically intermediate lesions with 40%–69% diameter stenosis. Prior to OCT image acquisition, intracoronary nitroglycerin 100–200 μg was administered. Blood in the vessel was displaced using contrast media by manual injections.
Results
OCT of the angiographically intermediate lesions showed larger minimal luminal area (MLA) than the angiographically severe lesions (MLA 3.3 mm 2 ± 1.8 mm 2 vs. 1.6 mm 2 ± 0.6 mm 2 , p < 0.001) and less severe % lumen area stenosis (54.2% ± 11.4% vs. 70.9% ± 6.8%, p = 0.001). Plaque rupture or intracoronary thrombus was detected in 8/26 (31%) patients. PCI with stent deployment was performed in 16 patients (62%).
Conclusion
In stabilized patients with NSTEMI and angiographically intermediate disease, OCT examination confirmed the lack of severe anatomical stenosis in most patients. However, OCT also identified coronary lesions with unstable features. Further research is needed to help guide management of this subgroup of patients.
1
Introduction
Pathological examination of patients with acute coronary syndrome (ACS) typically showed intracoronary thrombus with plaque rupture, erosion or calcium nodules . Optical coherence tomography (OCT) has high spatial resolution, and previous studies have documented its ability in characterizing such complicated plaque features. Consensus documents on image acquisition, measurement and reporting as well as detailed image description have been published .
Patients with recent non-ST elevation myocardial elevation (NSTEMI) have elevated cardiac biomarkers, and in general, have higher short-term cardiac risk . Most of these patients have severe angiographic lesions (≥ 70% diameter stenosis), and they are typically treated with revascularization . A minority of patients present with less severe angiographic lesions, and are more likely treated with medical therapy alone. A recent clinical review by Nicoli et al. used the term “myocardial infarctions (MI) with no obstructive coronary atherosclerosis (MINOCA)” to describe this smaller, but important subgroup of patients. The authors also proposed treatment algorithm including the use of intracoronary imaging . Coronary angiography has known limitations in the assessment of lesion severity . OCT maybe particularly useful in this setting to better evaluate lesion severity and characteristics. We report our experience with OCT in patients with intermediate lesions who are clinically stable.
2
Methods
We retrospectively evaluated all consecutive OCTs that were performed in 165 patients at Vancouver General Hospital from November 2010 to March 2013. Seventy (42%) were performed in patients presenting with NSTEMI. We excluded OCTs that were performed in lesions with prior stenting in the same vessel (n = 22), bypass vein grafts (n = 2), inadequate imaging (n = 4) and imaging for other indications (spasm, spontaneous coronary artery dissection and intramural hematoma) (n = 6). The current report focuses on the remaining 36 cases. Based on the angiographic visual estimates, 26 cases were classified as intermediate (40% to 69% diameter stenosis) and 10 cases were classified as severe (≥ 70% diameter stenosis) ( Fig. 1 ). We did not perform OCT examination in any patient with < 40% diameter stenosis.
All imaging was acquired using the second generation Fourier domain (FD) OCT (C7-XR/ILUMIEN™ system from St. Jude Medical/LightLab Imaging, Westford MA, USA). Prior to image acquisition, 100–200 μg of nitroglycerin was administered. Scanning of the region of interest was performed by automated pullback at a speed of 20 mm/s. We typically inject 9–14 ml of contrast media manually via the guiding catheter to clear blood from the imaging field. Images were acquired digitally and stored locally for evaluation and analysis on a dedicated work-station.
Longitudinal image runs were scanned to examine the areas of interests. Minimal luminal area (MLA) was measured after proper Z-offset calibration. Proximal and distal reference areas were measured and the average was registered as average reference vessel luminal area.
2
Methods
We retrospectively evaluated all consecutive OCTs that were performed in 165 patients at Vancouver General Hospital from November 2010 to March 2013. Seventy (42%) were performed in patients presenting with NSTEMI. We excluded OCTs that were performed in lesions with prior stenting in the same vessel (n = 22), bypass vein grafts (n = 2), inadequate imaging (n = 4) and imaging for other indications (spasm, spontaneous coronary artery dissection and intramural hematoma) (n = 6). The current report focuses on the remaining 36 cases. Based on the angiographic visual estimates, 26 cases were classified as intermediate (40% to 69% diameter stenosis) and 10 cases were classified as severe (≥ 70% diameter stenosis) ( Fig. 1 ). We did not perform OCT examination in any patient with < 40% diameter stenosis.
All imaging was acquired using the second generation Fourier domain (FD) OCT (C7-XR/ILUMIEN™ system from St. Jude Medical/LightLab Imaging, Westford MA, USA). Prior to image acquisition, 100–200 μg of nitroglycerin was administered. Scanning of the region of interest was performed by automated pullback at a speed of 20 mm/s. We typically inject 9–14 ml of contrast media manually via the guiding catheter to clear blood from the imaging field. Images were acquired digitally and stored locally for evaluation and analysis on a dedicated work-station.
Longitudinal image runs were scanned to examine the areas of interests. Minimal luminal area (MLA) was measured after proper Z-offset calibration. Proximal and distal reference areas were measured and the average was registered as average reference vessel luminal area.
4
Results
Angiography was performed at a median of 2 days (range 1–7 days) following admission with NSTEMI. Twenty-six cases were classified as intermediate (40%–69% diameter stenosis) and 10 cases as angiographically severe (≥ 70% diameter stenosis) ( Fig. 1 ). Distributions of ECG findings, LV function and studied coronary vessel were similar in both groups ( Table 1 ). Culprit lesion was identified based on ECG, wall motion abnormality on ventriculogram and angiographic findings.
| Severity of Angiographic Stenosis | Intermediate (n = 26) | Severe (n = 10) | p-value |
|---|---|---|---|
| Age (mean ± SD) | 64 ± 14 | 57 ± 10 | 0.16 |
| Male (n, %) | 16 (62%) | 7 (70%) | 0.64 |
| Days: admission to procedure (median, range) | 2 [1–7] | 2(1–3) | 0.35 |
| ECG (n, %) | 0.17 | ||
| New ST elevation | 0 | 0 | |
| New ST depression | 1 (4%) | 0 | |
| New T wave inversion | 8 (31%) | 6 (60%) | |
| Non-specific ST changes | 6 (23%) | 2 (20%) | |
| Normal | 11 (42%) | 2 (20%) | |
| LV function (n, %) | 0.47 | ||
| Regional wall motion abnormality | 8 (31%) | 2 (20%) | |
| LV EF < 50% | 8 (30%) | 0 | |
| Location of culprit lesion (n, %) | 0.97 | ||
| LM | 1 (4%) | 0 | |
| LAD | 19 (73%) | 8 (80%) | |
| LCx | 0 | 1 (10%) | |
| RCA | 6 (23%) | 1 (10%) | |
| Peak Troponin-I level (median and range) | 1.7 (0.07–22) | 0.7 (0.06–8.5) | 0.35 |
Based on OCT measurements, both the minimal luminal area (MLA) and % area stenosis were significantly less severe in the angiographically intermediate group (p < 0.001, Table 2 and Figs. 2 and 3 ). Using the criteria established by Gonzalo et al. , OCT showed small MLA ≤ 1.9 mm 2 in 3 patients (12%) in the angiographically intermediate group. Qualitatively, lipid arc was observed in 18 patients (69%), thin cap fibroatheroma in 10 patients (38%) and neovascularization in 4 patients (15%). Plaque rupture was seen in 7 patients (27%) and intraluminal thrombus in 6 (23%) patients. Both plaque rupture and thrombus were observed in 5 patients, while 3 patients had either of the two features. A total of 8 patients (31%) had both or either of the two features. FFR was performed in 6 patients (23%) and PCI with stent deployment was done in 16 patients (62%) with angiographically intermediate lesions. All patients except one received drug eluting stent. The decision to perform PCI was done at the discretion of the treating physicians mostly based on the small size of the MLA (ranging from 1.9 to 2.2 mm 2 ), or the desire to “seal” a ruptured plaque. (See Tables 3 and 4 .)
| Severity of Angiographic Stenosis | Intermediate (n = 26) | Severe (n = 10) | p-value |
|---|---|---|---|
| OCT MLA (mm 2 , mean ± SD) | 3.3 ± 1.8 | 1.6 ± 0.6 | < 0.001 |
| OCT average reference lumen area (mm 2 , mean ± SD) | 7.4 ± 3.1 | 5.5 ± 1.9 | 0.033 |
| OCT % area stenosis (mean ± SD) | 54.2 ± 11.4 | 70.9 ± 6.8 | 0.001 |
| OCT morphology (n, %) | 0.41 | ||
| Thrombus | 7 (27%) | 3 (30%) | |
| Plaque rupture | 6 (23%) | 1 (10%) | |
| Calcific nodule | 1 (4%) | 0 | |
| Thrombus and rupture | 5 (19%) | 0 | |
| Thrombus, rupture and calcific nodule | 1 (4%) | 0 | |
| Lipid plaque | 18 (69) | 7 (70) | |
| TCFA a | 10 (38) | 2 (20) | |
| Neovascularization | 4 (15) | 0 | |
| Patients with MLA ≤ 1.9 mm 2 (n, %) | 3 (12) | 8 (80) | < 0.001 |
| Case # | Age | Gender | ECG | Troponin | LV fun. | Angiography | OCT | FFR | Days after admission | PCI done | ||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| vessel | % steno. | MLA | Ave ref. | % area ste. | thrombus | rupture | Calc.nod. | |||||||||
| 1 | 64 | M | T inver. | 0.08 | normal | LAD | 50 | 2.9 | 7.62 | 62 | none | none | none | not sig | 1 | no |
| 2 | 67 | F | normal | 0.16 | normal | LAD | 50 | 2.3 | 7.08 | 60 | none | none | none | not sig | 2 | no |
| 3 | 44 | M | normal | 6.90 | normal | RCA | 60 | 2.7 | 6.26 | 57 | yes | yes | none | no FFR | 3 | yes (D) |
| 4 | 70 | M | normal | 0.07 | normal | LAD | 60 | 2.1 | 6.65 | 68 | none | none | none | no FFR | 2 | yes (D) |
| 5 | 51 | M | normal | 1.80 | normal | LAD | 60 | 2.7 | 6.80 | 77 | Yes | yes | none | no FFR | 1 | yes (D) |
| 6 | 48 | F | ST depr. | 3.40 | WMA | LAD | 50 | 2.4 | 5.56 | 58 | none | none | none | no FFR | 1 | no |
| 7 | 82 | F | normal | 0.20 | normal | LAD | 50 | 4.8 | 9.96 | 51 | none | none | none | no FFR | 2 | no |
| 8 | 65 | F | T inver. | 0.40 | WMA | LAD | 60 | 2.1 | 6.00 | 65 | none | none | none | no FFR | 1 | yes (D) |
| 9 | 76 | F | normal | 0.70 | normal | LAD | 30 | 1.6 | 3.32 | 48 | none | none | none | no FFR | 7 | no a |
| 10 | 85 | F | normal | 3.98 | normal | RCA | 50 | 2.1 | 3.32 | 55 | none | none | none | no FFR | 4 | yes (D) |
| 11 | 67 | M | normal | 0.34 | normal | LAD | 50 | 4.2 | 6.71 | 38 | none | none | none | no FFR | 1 | no |
| 12 | 75 | M | T inver. | 1.50 | WMA | LAD | 40 | 2.1 | 7.75 | 68 | none | none | none | no FFR | 3 | yes (D) |
| 13 | 73 | M | non spec. | 22 | WMA | LAD | 50 | 1.9 | 5.59 | 65 | none | none | none | no FFR | 4 | yes (D) |
| 14 | 75 | M | normal | 2.30 | normal | LM | 50 | 5.0 | 12.8 | 53 | yes | none | none | no FFR | 5 | yes (D) |
| 15 | 43 | M | non spec. | 3.80 | normal | LAD | 60 | 7.2 | 15.1 | 48 | yes | yes | yes | no FFR | 2 | yes (D) |
| 16 | 67 | F | T inver. | 5.85 | WMA | LAD | 60 | 2.1 | 5.80 | 64 | none | none | none | no FFR | 1 | yes (D) |
| 17 | 67 | F | non spes | 4.0 | normal | LAD | 50 | 2.7 | 4.35 | 39 | none | none | none | not sig | 3 | no |
| 18 | 73 | F | T inver. | 2.8 | WMA | LAD | 50 | 2.7 | 5.19 | 48 | none | none | none | not sig | 3 | no |
| 19 | 50 | M | non spec. | 0.4 | WMA | RCA | 50 | 2.2 | 3.54 | 61 | yes | yes | none | no FFR | 2 | no b |
| 20 | 51 | M | non spec. | 0.12 | normal | LAD | 30 | 9.7 | 14.0 | 31 | none | no | none | no FFR | 1 | no |
| 21 | 77 | M | non spec. | 2.7 | WMA | LAD | 50 | 4.5 | 11.5 | 57 | yes | yes | none | no FFR | 1 | yes (D) |
| 22 | 45 | F | T inver. | 0.95 | normal | LAD | 60 | 2.6 | 5.99 | 57 | none | none | none | no FFR | 3 | yes (D) |
| 23 | 55 | M | normal | 1.25 | WMA | LAD | 60 | 1.8 | 4.95 | 64 | none | none | none | signifi. | 1 | yes (D) |
| 24 | 68 | M | normal | – c | normal | RCA | 50 | 3.6 | 9.50 | 38 | none | yes | none | not sig | 7 | yes (D) |
| 25 | 37 | M | T inver. | 19.4 | normal | RCA | 60 | 4.0 | 9.5 | 42 | yes | none | none | no FFR | 2 | yes (D) |
| 26 | 77 | M | T inver. | 4.6 | WMA | RCA | 60 | 3.1 | 7.5 | 41 | none | none | none | no FFR | 7 | yes (B) |
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
