Association between carotid and coronary atherosclerotic plaque morphology: a virtual histology intravascular ultrasound study.

Background and Aim: Atherosclerosis is considered to be a systemic disease; however, evidence exists on the heterogeneous nature of atherosclerotic disease. To date, continuous research seeks to determine the morphological differences between carotid and coronary artery disease. This study aimed to evaluate the relationship of morphological characteristics assessed by virtual histology intravascular ultrasound (VH-IVUS) between carotid and coronary plaque composition among patients with and without a history of cerebrovascular events. Methods: This study was a single-center prospective study (n = 100; age 69.6 ± 8.4). All patients were scheduled for carotid or coronary artery stenting and underwent VH-IVUS examination of the carotid and coronary arteries before intervention. Results: There was a modest, but statistically significant correlation between the carotid and coronary necrotic core ([NC] r = 0.46, P < 0.01), fibrofatty ([FF] r = 0.38, P < 0.01), dense calcium (r = 0.56, P < 0.01), and fibrous (r = 0.42, P < 0.01) plaque composition. The high amount of NC was detected in both arteries of the carotid artery stenting (CAS) group with higher proportion in the coronary artery (20.2% ± 9.4 % vs. 22.7% ± 6.8%, P = 0.02). More fibrolipid content was observed in carotid plaque compared to coronary (19.6% ± 9.9% vs. 12.2% ± 8.1%, P < 0.01). Patients with a history of cerebrovascular events had a numerically greater proportion of necrotic tissue in the carotid artery compared to asymptomatic and symptomatic CAS group patients (23.5% ± 10.7% vs. 18.9% ± 8.2% and 18.7% ± 9.5%, P = 0.11). Conclusion: The percentage of all analyzed plaque components was moderately correlated between coronary and carotid artery plaques. Nevertheless, the proportion of NC plaque tissue was greater in the coronary arteries, while the carotid arteries showed more %FF atherosclerotic lesions. CAS group patients with a history of cerebrovascular events had a tendency of greater proportion of necrotic tissue in analyzed carotid plaques compared to others in the CAS group. Relevance for Patients: In this study, we found that patients with a history of cerebrovascular event had a tendency of increased NC content in culprit lesion of carotid artery. Complementary use of non-invasive and invasive imaging modalities allows to detect high-risk atherosclerotic plaques and adjust treatment strategy.

Two-year clinical outcomes after implantation of an everolimus-eluting bioresorbable scaffold (Absorb) in stable angina and acute coronary syndrome patients. Single-centre real-life registry data.

AIM: The aim of this long-term registry data was to evaluate 2-year clinical and angiographic outcomes after implantation of everolimus-eluting bioresorbable scaffolds (Absorb) from the Latvian Centre of Cardiology Real-life Registry. MATERIAL AND METHODS: Between November 2012 and December 2014 in the Centre of Cardiology Real-life Bioresorbable Vascular Scaffold Registry, 187 patients with stable angina or acute coronary syndrome and available 2-year follow-up were selected. All patients had percutaneous coronary intervention (PCI) following bioresorbable scaffold (Absorb) implantation. At 2 years, clinical parameters were analysed in stable angina and acute coronary syndrome subgroups: all-cause death, cardiac death, non-cardiac death, myocardial infarction (MI), target lesion revascularization (TLR), target vessel revascularization (TVR), scaffold thrombosis (ST), cerebral infarction, in-scaffold restenosis and bleeding. RESULTS: The clinical follow-up rate at 2 years was 96.2%. In-hospital death occurred in 2 (1.1%) patients, and 1 (0.5%) patient had in-hospital MI. At 2 years, the rate of all-cause death was 3.9% (n = 7), MI 1.6% (n = 3), TLR 3.9% (n = 7), and TVR 8.4% (n = 15). Between hospital discharge and 2-year follow-up scaffold thrombosis occurred in 2 (1.1%) patients. In-hospital scaffold thrombosis occurred in 1 (0.5%) patient due to clopidogrel resistance, and 1 additional case of scaffold thrombosis occurred at 5 days after implantation (0.5%). CONCLUSIONS: Bioresorbable scaffolds showed acceptable efficacy (target lesion revascularization) and safety (cardiac death, myocardial infarction, and scaffold thrombosis) results at mid-term follow-up in stable angina and acute coronary syndrome patients.

In-vivo iMap IVUS comparison of in-stent neointima and native coronary atherosclerosis.

PURPOSE: The purpose of this study was to compare plaque characteristics of native coronary atherosclerosis and in-stent neointima ten months after ST elevation myocardial infarction (STEMI) using iMap intravascular ultrasound (IVUS). METHODS: In 49 patients in-stent neointima and the coronary segment proximal to the stent were analyzed with iMap intravascular ultrasound (IVUS) ten months after primary PCI for STEMI. RESULTS: A higher percentage of necrotic tissue was observed in the proximal coronary segment compared to the in-stent neointima by iMap IVUS (25.5% ± 12.8% vs 12.3% ± 3.3%, p < 0.0001) ten months after STEMI. The proportion of fibrotic tissue in the proximal segment was lower (63.6% ± 14.8% vs 72.0% ± 5.7%, p = 0.002) and the proportion of the lipidic tissue was higher (8.8% ± 3.0% vs 5.9% ± 2.0%, p < 0.0001) than in-stent neointima. CONCLUSIONS: In patients ten months after STEMI, in-stent neointima contained a higher proportion of fibrotic tissue and lower proportion of necrotic and lipidic tissue compared the native atherosclerotic lesion.

Plaque and blood vulnerability in ST segment elevation myocardial infarction patients: association between lesion morphology using intravascular ultrasound radiofrequency analysis and circulating biomarkers.

AIM: The purpose of the study was to evaluate associations between iMap intravascular ultrasound tissue characterization of culprit and nonculprit lesions in infarct-related artery and plasma biomarkers during ST segment elevation myocardial infarction (STEMI) and at 10-month follow-up. METHODS AND RESULTS: Sixty-three STEMI patients at the time of index hospitalization and 10-month follow-up underwent coronary angiography and intravascular ultrasound with iMap tissue characterization of the culprit artery. Proximal and culprit segments were analyzed. A higher percentage of necrotic tissue in the nonculprit segment was found in patients in the top soluble intercellular adhesion molecule 1 (sICAM-1) quartile compared with the other three quartiles (34.3±10.9 vs. 26.3±11.6%, P=0.041) in the acute setting. At 10-month follow-up the top quartile of sICAM-1 in both the acute and stable setting was associated with a lower percentage of fibrotic tissue, but a higher percentage of lipidic and necrotic tissue in the nonculprit segment. In the top quartile of plasminogen activator inhibitor 1 during STEMI, a lower percentage of fibrotic tissue (53.0±13.9 vs. 63.0±13.3%, P=0.014), higher percentage of lipidic tissue (11.7±3.1 vs. 9.4±2.4%, P=0.004), and higher percentage of necrotic tissue (33.4±11.6 vs. 25.7±11.3%, P=0.025) were found in the nonculprit segment. CONCLUSION: Nonculprit plaque vulnerability characteristics were associated with elevated plasma biomarkers for sICAM-1 and plasminogen activator inhibitor 1.

iMap intravascular ultrasound evaluation of culprit and non-culprit lesions in patients with ST-elevation myocardial infarction.

OBJECTIVE: The purpose of this study was to evaluate plaque characteristics of culprit and non-culprit lesions in ST-elevation myocardial infarction (STEMI) patients at the index procedure and 10 months later using iMap intravascular ultrasound (IVUS). BACKGROUND: The exact site of the plaque rupture or erosion in coronary arteries with subsequent thrombosis cannot be precisely defined. Our hypothesis is that in STEMI patients angiographically guided stenting could fail to identify necrotic tissue and thus may leave an uncovered significant amount of vulnerable plaque. METHODS: In 63 consecutive STEMI patients the culprit artery was analyzed with iMap IVUS at the time of the index procedure and 10 months later. The most stenotic culprit segment was compared to the segment proximal to the culprit lesion. RESULTS: A high percentage of necrotic tissue was observed in the culprit lesion and a comparatively lower percentage of necrotic tissue was observed in the non-culprit lesions proximal to the culprit at the index procedure by iMap IVUS (31.9%±10.0% vs 27.8%±11.8%, p=0.012). The proportion of necrotic tissue in the segment proximal to the culprit lesion was unchanged at 10-month follow-up (27.1%±11.9% vs 25.5%±12.8%, p=0.147). The percentage of lipidic tissue in the proximal segment decreased at 10-month follow-up (9.8%±2.9% vs 8.8±3.0%, p=0.009). CONCLUSIONS: In STEMI patients, culprit lesion segments and non-culprit segments contain high proportions of necrotic tissue. However, a comparatively higher proportion of necrotic tissue was found in the culprit lesions according to iMap IVUS. The percentage of necrotic tissue remained high at 10-month follow-up in both culprit and non-culprit segments.