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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 -
Arteriosclerosis, Thrombosis, and... Jul 2024
Topics: Atherosclerosis; Interleukin-1beta; Animals; Humans; Disease Models, Animal; Signal Transduction; Anti-Inflammatory Agents; Plaque, Atherosclerotic; Mice; Interleukin 1 Receptor Antagonist Protein
PubMed: 38813698
DOI: 10.1161/ATVBAHA.124.321113 -
Journal of Medicine and Life Feb 2024Numerous studies have established a link between gene variants within the inflammasome complex and the incidence of periodontitis and cardiovascular illness across...
Numerous studies have established a link between gene variants within the inflammasome complex and the incidence of periodontitis and cardiovascular illness across various ethnic groups. This study investigated the association between gene polymorphism and susceptibility to periodontal disease and coronary heart disease (CHD) and their correlation with clinical periodontal indices. A total of 120 participants were enrolled, categorized into four groups: 30 healthy controls (C), 30 patients with generalized periodontitis (P), 30 patients with atherosclerotic CHD but clinically healthy periodontium (AS-C), and 30 patients with both atherosclerotic CHD and generalized periodontitis (AS-P). We recorded demographic data, collected blood samples, and measured periodontal indices, including plaque index, clinical attachment loss, bleeding on probing, and pocket depth. The genomic variant of the gene was analyzed using a conventional polymerase reaction. A significant prevalence of T and G allele mutations and a higher distribution of CT and TT genotypes in C/T (rs8056505) and the AG genotype in A/G (rs372507365) were observed in groups P, AS-P, and AS-C. These single nucleotide polymorphisms (SNPs) were also positively correlated with the severity of clinical periodontitis indices. Our findings suggest that the increased frequency of T and G alleles and the distribution of CT, TT, and AG genotypes in SNPs are significantly associated with an elevated risk for periodontal disease and CHD. These SNPs may participate in the pathogenesis of these conditions. The study reinforces the potential role of these genetic markers as risk factors for both diseases in the Iraqi population.
Topics: Adult; Female; Humans; Male; Middle Aged; Alleles; CARD Signaling Adaptor Proteins; Case-Control Studies; Coronary Disease; Genetic Predisposition to Disease; Genotype; Periodontal Diseases; Periodontitis; Polymorphism, Single Nucleotide
PubMed: 38813354
DOI: 10.25122/jml-2023-0263 -
Scientific Reports May 2024Atherosclerosis is the build-up of fatty plaques within blood vessel walls, which can occlude the vessels and cause strokes or heart attacks. It gives rise to both...
Atherosclerosis is the build-up of fatty plaques within blood vessel walls, which can occlude the vessels and cause strokes or heart attacks. It gives rise to both structural and biomolecular changes in the vessel walls. Current single-modality imaging techniques each measure one of these two aspects but fail to provide insight into the combined changes. To address this, our team has developed a dual-modality imaging system which combines optical coherence tomography (OCT) and fluorescence imaging that is optimized for a porphyrin lipid nanoparticle that emits fluorescence and targets atherosclerotic plaques. Atherosclerosis-prone apolipoprotein (Apo)e mice were fed a high cholesterol diet to promote plaque development in descending thoracic aortas. Following infusion of porphyrin lipid nanoparticles in atherosclerotic mice, the fiber-optic probe was inserted into the aorta for imaging, and we were able to robustly detect a porphyrin lipid-specific fluorescence signal that was not present in saline-infused control mice. We observed that the nanoparticle fluorescence colocalized in areas of CD68 macrophages. These results demonstrate that our system can detect the fluorescence from nanoparticles, providing complementary biological information to the structural information obtained from simultaneously acquired OCT.
Topics: Tomography, Optical Coherence; Animals; Plaque, Atherosclerotic; Nanoparticles; Mice; Porphyrins; Optical Imaging; Disease Models, Animal; Atherosclerosis; Macrophages; Lipoproteins, HDL
PubMed: 38811670
DOI: 10.1038/s41598-024-63132-6 -
Journal of Biomedical Research Apr 2024Atherosclerosis poses a significant and widespread problem at the population level. Consequently, there is a pressing need to develop effective methods to reduce the...
Atherosclerosis poses a significant and widespread problem at the population level. Consequently, there is a pressing need to develop effective methods to reduce the risk associated with this condition, which holds a prominent position in cardiology research. The primary manifestation of atherosclerosis involves plaque formation on the walls of coronary arteries. These plaques not only disrupt blood flow but also raise the likelihood of thrombosis and subsequent cardiovascular events. Unfortunately, atherosclerosis itself is usually asymptomatic, resulting in challenges with diagnosis and a delayed initiation of treatment. Hence, strategies focusing on the regression of existing plaques within blood vessels play a crucial role. The present review encompasses comprehensive data on the regression of coronary atherosclerotic plaques, examining both the underlying mechanisms and a range of regression strategies, encompassing lifestyle modifications to medical interventions.
PubMed: 38808553
DOI: 10.7555/JBR.37.20230223