| 1. |
- Erlinge, David, et al.
(författare)
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Identification of vulnerable plaques and patients by intracoronary near-infrared spectroscopy and ultrasound (PROSPECT II) : a prospective natural history study
- 2021
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Ingår i: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 397:10278, s. 985-995
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Tidskriftsartikel (refereegranskat)abstract
- Background: Near-infrared spectroscopy (NIRS) and intravascular ultrasound are promising imaging modalities to identify non-obstructive plaques likely to cause coronary-related events. We aimed to assess whether combined NIRS and intravascular ultrasound can identify high-risk plaques and patients that are at risk for future major adverse cardiac events (MACEs).Methods: PROSPECT II is an investigator-sponsored, multicentre, prospective natural history study done at 14 university hospitals and two community hospitals in Denmark, Norway, and Sweden. We recruited patients of any age with recent (within past 4 weeks) myocardial infarction. After treatment of all flow-limiting coronary lesions, three-vessel imaging was done with a combined NIRS and intravascular ultrasound catheter. Untreated lesions (also known as non-culprit lesions) were identified by intravascular ultrasound and their lipid content was assessed by NIRS. The primary outcome was the covariate-adjusted rate of MACEs (the composite of cardiac death, myocardial infarction, unstable angina, or progressive angina) arising from untreated non-culprit lesions during follow-up. The relations between plaques with high lipid content, large plaque burden, and small lumen areas and patient-level and lesion-level events were determined. This trial is registered with ClinicalTrials.gov, NCT02171065.Findings: Between June 10, 2014, and Dec 20, 2017, 3629 non-culprit lesions were characterised in 898 patients (153 [17%] women, 745 [83%] men; median age 63 [IQR 55-70] years). Median follow-up was 3.7 (IQR 3.0-4.4) years. Adverse events within 4 years occurred in 112 (13.2%, 95% CI 11.0-15.6) of 898 patients, with 66 (8.0%, 95% CI 6.2-10.0) arising from 78 untreated non-culprit lesions (mean baseline angiographic diameter stenosis 46.9% [SD 15.9]). Highly lipidic lesions (851 [24%] of 3500 lesions, present in 520 [59%] of 884 patients) were an independent predictor of patient-level non-culprit lesion-related MACEs (adjusted odds ratio 2.27, 95% CI 1.25-4.13) and nonculprit lesion-specific MACEs (7.83, 4.12-14.89). Large plaque burden (787 [22%] of 3629 lesions, present in 530 [59%] of 898 patients) was also an independent predictor of non-culprit lesion-related MACEs. Lesions with both large plaque burden by intravascular ultrasound and large lipid-rich cores by NIRS had a 4-year non-culprit lesion-related MACE rate of 7.0% (95% CI 4.0-10.0). Patients in whom one or more such lesions were identified had a 4-year non-culprit lesion-related MACE rate of 13.2% (95% CI 9.4-17.6).Interpretation: Combined NIRS and intravascular ultrasound detects angiographically non-obstructive lesions with a high lipid content and large plaque burden that are at increased risk for future adverse cardiac outcomes.
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| 2. |
- Gyldenkerne, Christine, et al.
(författare)
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Coronary Artery Lesion Lipid Content and Plaque Burden in Diabetic and Nondiabetic Patients : PROSPECT II
- 2023
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Ingår i: Circulation. - : Lippincott Williams & Wilkins. - 0009-7322 .- 1524-4539. ; 147:6, s. 469-481
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Patients with diabetes have increased rates of major adverse cardiac events (MACEs). We hypothesized that this is explained by diabetes-associated differences in coronary plaque morphology and lipid content.METHODS: In PROSPECT II (Providing Regional Observations to Study Predictors of Events in the Coronary Tree), 898 patients with acute myocardial infarction with or without ST-segment elevation underwent 3-vessel quantitative coronary angiography and coregistered near-infrared spectroscopy and intravascular ultrasound imaging after successful percutaneous coronary intervention. Subsequent MACEs were adjudicated to either treated culprit lesions or untreated nonculprit lesions. This substudy stratified patients by diabetes status and assessed baseline culprit and nonculprit prevalence of high-risk plaque characteristics defined as maximum plaque burden ≥70% and maximum lipid core burden index ≥324.7. Separate covariate-adjusted multivariable models were performed to identify whether diabetes was associated with nonculprit lesion-related MACEs and high-risk plaque characteristics.RESULTS: Diabetes was present in 109 of 898 patients (12.1%). During a median 3.7-year follow-up, MACEs occurred more frequently in patients with versus without diabetes (20.1% versus 13.5% [odds ratio (OR), 1.94 (95% CI, 1.14-3.30)]), primarily attributable to increased risk of myocardial infarction related to culprit lesion restenosis (4.3% versus 1.1% [OR, 3.78 (95% CI, 1.12-12.77)]) and nonculprit lesion-related spontaneous myocardial infarction (9.3% versus 3.8% [OR, 2.74 (95% CI, 1.25-6.04)]). However, baseline prevalence of high-risk plaque characteristics was similar for patients with versus without diabetes concerning culprit (maximum plaque burden ≥70%: 90% versus 93%, P=0.34; maximum lipid core burden index ≥324.7: 66% versus 70%, P=0.49) and nonculprit lesions (maximum plaque burden ≥70%: 23% versus 22%, P=0.37; maximum lipid core burden index ≥324.7: 26% versus 24%, P=0.47). In multivariable models, diabetes was associated with MACEs in nonculprit lesions (adjusted OR, 2.47 [95% CI, 1.21-5.04]) but not with prevalence of high-risk plaque characteristics (adjusted OR, 1.21 [95% CI, 0.86-1.69]).CONCLUSIONS: Among patients with recent myocardial infarction, both treated and untreated lesions contributed to the diabetes-associated ≈2-fold increased MACE rate during the 3.7-year follow-up. Diabetes-related plaque characteristics that might underlie this increased risk were not identified by multimodality imaging.
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| 3. |
- Matsumura, Mitsuaki, et al.
(författare)
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Serial NIRS-IVUS Assessment of Changes in Coronary Lumen Area During 2-Year Follow-Up : Insights From the PROSPECT ABSORB Trial
- 2021
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Ingår i: Journal of the American College of Cardiology. - : Elsevier. - 0735-1097 .- 1558-3597. ; 78:19 Suppl., s. B35-B36
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Background: In PROSPECT II, 182 patients with plaque burden (PB) ≥ 65% were randomized to bioresorbable vascular scaffold (BVS) + guideline-directed medical therapy (GDMT) versus GDMT alone. Protocol-directed 3-vessel near-infrared spectroscopy (NIRS)-IVUS was repeated at 25 months.Methods: Excluding lesions treated by BVS, paired (baseline and follow-up) NIRS-IVUS was available in 626 nonculprit lesions in 165 patients. Follow-up minimum lumen area (MLA) and the corresponding baseline sites were measured: rapid lesion progression (RLP) was a ≥ 0.5 mm2 decrease of MLA, and rapid lesion regression (RLR) was a ≥ 0.5 mm2 increase of MLA.Results: RLP occurred in 34.5%, RLR occurred in 15.5%, and 49.8% had “no change.” The % change in vessel area correlated with the % change of plaque area (r = 0.81, P < 0.001), demonstrating vessel remodeling (Figure 1). At baseline, the RLP lesions had larger plaque areas, longer lesions, and higher prevalence of lipid-rich plaque (maxLCBI4mm ≥ 324.7). During follow-up, 80.2% of RLP lesions had negative remodeling irrespective of the change in plaque area, whereas 76.3% of RLR lesions had a decrease in plaque area irrespective of negative or positive remodeling. In lesions without change in lumen area, there were compensatory changes in plaque and vessel areas.Conclusion: In stabilized patients post-MI treated with GDMT, half of untreated non–flow- limiting lesions had significant lumen changes at 25 months, with RLP twice as frequent as RLR. The predominant mechanism of RLP was negative vessel remodeling whereas the predominant mechanism of RLR was reduction in plaque area.
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| 4. |
- Sharma, T., et al.
(författare)
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Biomarkers associated with vulnerable plaques
- 2022
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Ingår i: European Heart Journal. - : Oxford University Press. - 0195-668X .- 1522-9645. ; 43:Suppl. 2, s. 1292-1292
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Background: Cardiovascular heart disease is the leading cause of mortality worldwide, with the rupture or thrombosis of an atherosclerotic plaque being the main reason behind an acute coronary syndrome. It has already been established that the morphology of atherosclerotic plaques determine their stability. A lipid rich lesion with a thin fibrous cap is more prone to rupture compared to solid fibrous lesions. In the PROSPECTII study we used Near infrared spectroscopy (NIRS) and Intravascular ultrasound (IVUS) to identify atherosclerotic plaques in the coronary arteries; NIRS-derived lipid core burden index (LCBI) and IVUS-derived plaque burden (PB) identified plaques that caused adverse cardiovascular events.Purpose: Our aim is to find biomarkers associated with LCBI or PB, to understand the development of vulnerable plaques.Methods: 902 patients were enrolled in this study after successful percutaneous coronary intervention (PCI). A combined NIRS-IVUS catheter was then used to analyze approximately 200m of coronary arteries. Blood samples for biomarker analysis were taken before the PCI procedure and plasma levels of 182 proteins associated with cardiovascular disease were assessed using a novel method for measuring proximity extension assay. Adjusted linear regression models were calculated between the biomarkers and the outcomes of interest, followed by a false discovery rate (FDR) correction.Results: We found 24 proteins associated with plaque burden and 28 proteins associated with LCBI after using a cut off of two tailed P value <0.05. An overlap of 8 biomarkers could be seen between the two groups. After adjusting the P values with FDR, Angiopoeitin like 3 (ANGPTL3) retain edits association to LCBI, and Interleukin 18 receptor 1 (IL18R1) and colony stimulating factor 1 (CSF-1) to plaque burden.Conclusion: We were able to identify different biomarker patterns associated with plaque burden compared to lipid rich vulnerable plaques. ANGPTL3 was shown to only have an association with lipid rich plaques and not with solid fibrous lesions which further supports its role in vulnerable plaques.
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