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Turk Kardiyoloji Dernegi Arsivi : Turk... Jun 2024Coronary computed tomography angiography (CCTA) and CT-derived fractional flow reserve (FFRCT) provide high diagnostic accuracy for coronary artery disease (CAD),...
Coronary computed tomography angiography (CCTA) and CT-derived fractional flow reserve (FFRCT) provide high diagnostic accuracy for coronary artery disease (CAD), consistent with invasive coronary angiography (ICA), the gold standard diagnostic technique. The presence of calcified components, however, complicates the interpretation of coronary stenosis severity. We present a case where there was a discrepant assessment of coronary stenosis severity between CCTA/FFRCT (indicating significant obstructive CAD) and ICA (showing no apparent obstructive CAD). CCTA/FFRCT revealed that the stenotic lesion, located in the middle segment of the left circumflex artery, was surrounded by plaque components. The proximal and distal portions of the stenotic lesion consisted of 80.9% luminal volume, 0.2% low-attenuation plaque, 13.4% intermediate-attenuation plaque, and 5.5% calcified plaque. In contrast, the stenotic lesion itself contained 50.0% luminal volume, 0.3% low-attenuation plaque, 26.7% intermediate-attenuation plaque, and 22.9% calcified plaque. Invasive coronary angiography showed no apparent obstructive CAD, implying that the lesions appearing as significant obstructive CAD on CCTA/FFRCT were likely overestimated due to the effects of extravascular calcified plaque. Advanced extravascular calcified plaque surrounding the lesion may cause several artifacts (such as blooming and/or beam hardening artifacts) and/or vasodilator dysfunction (either organic and/or functional), potentially leading to an overestimation of the severity of coronary stenosis in CCTA/FFRCT assessments.
Topics: Humans; Coronary Stenosis; Severity of Illness Index; Coronary Angiography; Male; Plaque, Atherosclerotic; Fractional Flow Reserve, Myocardial; Computed Tomography Angiography; Middle Aged
PubMed: 38829638
DOI: 10.5543/tkda.2023.35882 -
ArXiv May 2024Despite recent advances in diagnosis and treatment, atherosclerotic coronary artery diseases remain a leading cause of death worldwide. Various imaging modalities and...
Despite recent advances in diagnosis and treatment, atherosclerotic coronary artery diseases remain a leading cause of death worldwide. Various imaging modalities and metrics can detect lesions and predict patients at risk; however, identifying unstable lesions is still difficult. Current techniques cannot fully capture the complex morphology-modulated mechanical responses that affect plaque stability, leading to catastrophic failure and mute the benefit of device and drug interventions. Finite Element (FE) simulations utilizing intravascular imaging OCT (Optical Coherence Tomography) are effective in defining physiological stress distributions. However, creating 3D FE simulations of coronary arteries from OCT images is challenging to fully automate given OCT frame sparsity, limited material contrast, and restricted penetration depth. To address such limitations, we developed an algorithmic approach to automatically produce 3D FE-ready digital twins from labeled OCT images. The 3D models are anatomically faithful and recapitulate mechanically relevant tissue lesion components, automatically producing morphologies structurally similar to manually constructed models whilst including more minute details. A mesh convergence study highlighted the ability to reach stress and strain convergence with average errors of just 5.9% and 1.6% respectively in comparison to FE models with approximately twice the number of elements in areas of refinement. Such an automated procedure will enable analysis of large clinical cohorts at a previously unattainable scale and opens the possibility for in-silico methods for patient specific diagnoses and treatment planning for coronary artery disease.
PubMed: 38827462
DOI: No ID Found -
Scientific Reports Jun 2024This study aimed to investigate the relationship between complex aortic plaque (CAP) and short-term as well as long-term outcomes following cardioembolic stroke. CAP is...
This study aimed to investigate the relationship between complex aortic plaque (CAP) and short-term as well as long-term outcomes following cardioembolic stroke. CAP is a known risk factor for occurrence and recurrence of ischemic stroke. However, the association of CAP on cardioembolic stroke remains unclear. This was retrospective study using prospective cohort of consecutive patients with cardioembolic stroke who underwent transesophageal echocardiography. The functional outcome was evaluated using the modified Rankin Scale score at 3 months, and long-term outcomes were assessed by recurrence of ischemic stroke and occurrence of major adverse cardiovascular events (MACE). Among 759 patients with cardioembolic stroke, 91 (12.0%) had CAP. Early ischemic stroke recurrence within 3 months was associated with CAP (p = 0.025), whereas CAP was not associated with functional outcome at 3 months (odd ratio 1.01, 95% confidence interval [CI] 0.57-1.84, p = 0.973). During a median follow-up of 3.02 years, CAP was significantly associated with ischemic stroke recurrence (hazard ratio = 2.68, 95% CI 1.48-4.88, p = 0.001) and MACE occurrence (hazard ratio = 1.61, 95% CI 1.03-2.51, p = 0.039). In conclusion, CAP was associated with early ischemic stroke recurrence and poor long-term outcomes in patients with cardioembolic stroke. It might be helpful to consider transesophageal echocardiography for patients with cardioembolic stroke to identify CAP.
Topics: Humans; Male; Female; Aged; Ischemic Stroke; Plaque, Atherosclerotic; Prognosis; Middle Aged; Retrospective Studies; Embolic Stroke; Echocardiography, Transesophageal; Risk Factors; Recurrence; Aortic Diseases; Prospective Studies; Aged, 80 and over
PubMed: 38825610
DOI: 10.1038/s41598-024-60294-1 -
International Heart Journal 2024Cholesterol crystal (CC) embolism is a disease in which CCs from atherosclerotic lesions embolize peripheral arteries, causing organ dysfunction. In this case, a patient...
Cholesterol crystal (CC) embolism is a disease in which CCs from atherosclerotic lesions embolize peripheral arteries, causing organ dysfunction. In this case, a patient with spontaneously ruptured aortic plaques (SRAPs) identified by non-obstructive general angioscopy (NOGA) may have developed a CC embolism. This is the first report of a CC embolism in a patient with SRAPs identified using NOGA, which further supports the previously speculated pathogenesis of CC embolism due to SRAPs.
Topics: Humans; Embolism, Cholesterol; Angioscopy; Plaque, Atherosclerotic; Male; Aortic Rupture; Rupture, Spontaneous; Aged
PubMed: 38825500
DOI: 10.1536/ihj.23-559 -
Hellenic Journal of Cardiology : HJC =... May 2024Acute myocardial infarction (AMI) usually represents the clinical manifestation of atherothrombotic coronary artery disease (CAD) resulting from atherosclerotic plaque... (Review)
Review
Acute myocardial infarction (AMI) usually represents the clinical manifestation of atherothrombotic coronary artery disease (CAD) resulting from atherosclerotic plaque rupture. However, there are cases in which coronary angiography or coronary computed tomography angiography reveals patients with acute coronary syndrome with non-obstructive CAD. This clinical entity is defined as myocardial infarction with non-obstructive coronary arteries (MINOCA) and often considered as a clinical dynamic working diagnosis that needs further investigations for the establishment of a final etiologic diagnosis. The main causes of a MINOCA working diagnosis include atherosclerotic, non-atherosclerotic (vessel-related and non-vessel-related), and thromboembolic causes This literature review aimed to investigate the major thromboembolic causes in patients presenting with MINOCA regarding their etiology and pathophysiologic mechanisms, as well as diagnostic and treatment methods.
PubMed: 38825235
DOI: 10.1016/j.hjc.2024.05.001 -
BMC Cardiovascular Disorders May 2024LY86, also known as MD1, has been implicated in various pathophysiological processes including inflammation, obesity, insulin resistance, and immunoregulation. However,...
LY86, also known as MD1, has been implicated in various pathophysiological processes including inflammation, obesity, insulin resistance, and immunoregulation. However, the role of LY86 in cholesterol metabolism remains incompletely understood. Several studies have reported significant up-regulation of LY86 mRNA in atherosclerosis; nevertheless, the regulatory mechanism by which LY86 is involved in this disease remains unclear. In this study, we aimed to investigate whether LY86 affects ox-LDL-induced lipid accumulation in macrophages. Firstly, we confirmed that LY86 is indeed involved in the process of atherosclerosis and found high expression levels of LY86 in human atherosclerotic plaque tissue. Furthermore, our findings suggest that LY86 may mediate intracellular lipid accumulation induced by ox-LDL through the SREBP2/HMGCR pathway. This mechanism could be associated with increased cholesterol synthesis resulting from enhanced endoplasmic reticulum stress response.
Topics: Humans; Lipoproteins, LDL; Sterol Regulatory Element Binding Protein 2; Up-Regulation; Signal Transduction; Macrophages; Endoplasmic Reticulum Stress; Atherosclerosis; Hydroxymethylglutaryl CoA Reductases; Plaque, Atherosclerotic; THP-1 Cells; Male; Animals; Lipid Metabolism; Cholesterol
PubMed: 38822281
DOI: 10.1186/s12872-024-03957-1 -
PloS One 2024The natural outcome of coronary plaque in acute coronary syndrome (ACS) patients with chronic kidney disease (CKD) is unique, which can be analyzed quantitatively by...
Dynamic natural components and morphological changes in nonculprit subclinical atherosclerosis in patients with acute coronary syndrome and mild chronic kidney disease at the 1-year follow-up and clinical significance at the 5-year follow-up.
INTRODUCTION
The natural outcome of coronary plaque in acute coronary syndrome (ACS) patients with chronic kidney disease (CKD) is unique, which can be analyzed quantitatively by optical flow ratio (OFR) software.
METHODS
A total of 184 ACS patients with at least one nonculprit subclinical atherosclerosis (NSA) detected by optical coherence tomography (OCT) at baseline and 1-year follow-up were divided into non-CKD group (n = 106, estimated glomerular filtration rate (eGFR)> 90 mL/(min×1.73 m2)) and mild CKD group (n = 78, 60≤eGFR<90 mL/(min×1.73 m2)). Changes of normalized total atheroma volume (TAVn) of NSA was the primary endpoint at the 1-year follow-up.
RESULTS
Patients with mild CKD showed more TAVn progression of NSA than non-CKD (p = 0.019) from baseline to the 1-year follow-up, which was mainly due to an increase in calcium TAVn (p<0.001). The morphological change in the maximal calcification thickness (p = 0.026) was higher and the change in the distance from the calcified surface to the contralateral coronary media membrane (ΔC-to-M) at the maximal cross-sectional calcium area was lower (p<0.001) in mild CKD group than in non-CKD group. Mild CKD had more NSA related MACEs at the 5-year follow-up than non-CKD (30.8% vs. 5.8%, p = 0.045).
CONCLUSIONS
Mild CKD patients had more plaque progression of NSA which showed the increase of calcium component with more protrusion into the lumen morphologically at the 1-year follow-up and a higher corresponding incidence of NSA-related MACEs at the 5-year follow-up.
TRIAL REGISTRATION
Clinical Trial registration ClinicalTrials.gov. NCT02140801. https://classic.clinicaltrials.gov/ct2/show/NCT02140801.
Topics: Humans; Male; Female; Acute Coronary Syndrome; Renal Insufficiency, Chronic; Middle Aged; Follow-Up Studies; Aged; Tomography, Optical Coherence; Glomerular Filtration Rate; Plaque, Atherosclerotic; Disease Progression; Atherosclerosis; Coronary Artery Disease; Clinical Relevance
PubMed: 38820294
DOI: 10.1371/journal.pone.0302547 -
Cardiology and Cardiovascular Medicine 2024Atherosclerosis is a chronic inflammatory disease that leads to acute embolism via the formation of atherosclerotic plaques. Plaque formation is first induced by fatty...
Atherosclerosis is a chronic inflammatory disease that leads to acute embolism via the formation of atherosclerotic plaques. Plaque formation is first induced by fatty deposition along the arterial intima. Inflammation, bacterial infection, and the released endotoxins can lead to dysfunction and phenotypic changes of vascular smooth muscle cells (VSMCs), advancing the plaque from stable to unstable form and prone to rupture. Stable plaques are characterized by increased VSMCs and less inflammation while vulnerable plaques develop due to chronic inflammation and less VSMCs. Oncostatin M (OSM), an inflammatory cytokine, plays a role in endothelial cells and VSMC proliferation. This effect of OSM could be modulated by p27, a cyclin-dependent kinase (CDK) inhibitor. However, the role of OSM in plaque vulnerability has not been investigated. To better understand the role of OSM and its downstream signaling including p27 in plaque vulnerability, we characterized the previously collected carotid arteries from hyperlipidemic Yucatan microswine using hematoxylin and eosin stain, Movat Pentachrome stain, and gene and protein expression of OSM and p27 using immunostaining and real-time polymerase chain reaction. OSM and p27 expression in carotid arteries with angioplasty and treatment with either scrambled peptide or LR12, an inhibitor of triggering receptor expressed on myeloid cell (TREM)-1, were compared between the experimental groups and with contralateral carotid artery. The results of this study elucidated the presence of OSM and p27 in carotid arteries with plaque and their association with arterial plaque and vulnerability. The findings suggest that targeting OSM and p27 axis regulating VSMC proliferation may have therapeutic significance to stabilize plaque.
PubMed: 38817407
DOI: 10.26502/fccm.92920380 -
Journal of Endovascular Therapy : An... May 2024Thrombotic material in the non-aneurysmatic and non-atherosclerotic aorta is a rare entity without any recommended standard treatment so far. We present a successful...
BACKGROUND
Thrombotic material in the non-aneurysmatic and non-atherosclerotic aorta is a rare entity without any recommended standard treatment so far. We present a successful treatment strategy for patients who do not fit into any of the common approaches.
CASE REPORT
A free-floating thrombus in the descending aorta was found as source of embolism in an 82-year-old female patient with lower limb ischemia. After initial heparinization of the patient without relevant reduction of the thrombotic mass, the thrombus was removed using an interdisciplinary approach. Under echocardiographic guidance to locate the thrombus, the AngioVac device, usually licensed to remove floating thrombi from the venous system, was used off-label to remove the thrombus by a transfemoral approach. To avoid rebuilding of a new thrombus, the attachment point with an exulcerated plaque in the descending aorta was covered by a stent graft via the same femoral access. The patient did not experience any further embolic events, and the postoperative course was uncomplicated.
CONCLUSION
Patients with uncommon aortic diseases, such as the reported free-floating thrombus, should be treated by an individualized, interdisciplinary approach. Besides the recommended treatment options, there are other uncommon approaches that might offer an alternative in complex cases.
CLINICAL IMPACT
Evidence is rare for the treatment of a free-floating thrombus in the descending aorta and the treatment strategy remains discussed controversially. We present a rather uncommon approach of successful off-label treatment for patients who do not fit into any of the common approaches (operative, endovascular, or conservative treatment based on patient's comorbidities). The AngioVac System has already been successfully used off-label in the arterial system but not in the above presented way of treating a free-floating thrombus in a patient with high embolization risk and treatment-limiting comorbidities.
PubMed: 38817015
DOI: 10.1177/15266028241256817 -
Scientific Reports May 2024The effects of low doses of ionizing radiation on atherosclerosis remain uncertain, particularly as regards the generation of pro- or anti-inflammatory responses, and...
The effects of low doses of ionizing radiation on atherosclerosis remain uncertain, particularly as regards the generation of pro- or anti-inflammatory responses, and the time scale at which such effects can occur following irradiation. To explore these phenomena, we exposed atheroprone ApoE mice to a single dose of 0, 0.05, 0.5 or 1 Gy of Cs (γ) administered at a 10.35 mGy min dose rate and evaluated short-term (1-10 days) and long-term consequences (100 days). Bone marrow-derived macrophages were derived from mice 1 day after exposure. Irradiation was associated with a significant skewing of M0 and M2 polarized macrophages towards the M2 phenotype, as demonstrated by an increased mRNA expression of Retnla, Arg1, and Chil3 in cells from mice exposed to 0.5 or 1 Gy compared with non-irradiated animals. Minimal effects were noted in M1 cells or M1 marker mRNA. Concurrently, we observed a reduced secretion of IL-1β but enhanced IL-10 release from M0 and M2 macrophages. Effects of irradiation on circulating monocytes were most marked at day 10 post-exposure, when the 1 Gy dose was associated with enhanced numbers of both Ly6C and Ly6 cells. By day 100, levels of circulating monocytes in irradiated and non-irradiated mice were equivalent, but anti-inflammatory Ly6C monocytes were significantly increased in the spleen of mice exposed to 0.05 or 1 Gy. Long term exposures did not affect atherosclerotic plaque size or lipid content, as determined by Oil red O staining, whatever the dose applied. Similarly, irradiation did not affect atherosclerotic plaque collagen or smooth muscle cell content. However, we found that lesion CD68+ cell content tended to decrease with rising doses of radioactivity exposure, culminating in a significant reduction of plaque macrophage content at 1 Gy. Taken together, our results show that short- and long-term exposures to low to moderate doses of ionizing radiation drive an anti-inflammatory response, skewing bone marrow-derived macrophages towards an IL-10-secreting M2 phenotype and decreasing plaque macrophage content. These results suggest a low-grade athero-protective effect of low and moderate doses of ionizing radiation.
Topics: Animals; Macrophages; Plaque, Atherosclerotic; Mice; Cesium Radioisotopes; Apolipoproteins E; Gamma Rays; Antigens, Differentiation, Myelomonocytic; Antigens, CD; Atherosclerosis; Male; Mice, Knockout; CD68 Molecule
PubMed: 38816571
DOI: 10.1038/s41598-024-63084-x