A 70-year-old male patient was admitted to our hospital for exertional chest discomfort. Diagnostic coronary angiography revealed multiple giant coronary arterial aneurysms (CAAs). The 1.8- and 2.3-cm-sized saccular aneurysms were tandemly located at proximal left circumflex artery (Panels A and B; Supplemental Video 1) and another 3.5-cm-sized saccular aneurysm was located at mid right coronary artery (Panel C; Supplemental Video 2). Serological tests were taken to investigate the potential aetiology of CAAs; however, the results were inconclusive. 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT) molecular imaging explored the inflammatory activity of coronary aneurysmal walls. We constructed a three-dimensional (3D) rendering of the coronary vasculature from the co-registered CT images, and PET signals were superimposed on the coronary trees after suppressing the 18F-FDG uptake of myocardium (Panel D). Intriguingly, newly constructed 3D-rendered image demonstrated a markedly enhanced PET signal uptake on the arterial walls of giant...
Abstract Background: High-intensity statin is typically used in patients with acute myocardial infarction (AMI) for secondary prevention; however, concern regarding its association with diabetes mellitus has been consistent. We investigated and compared the impact of high-intensity atorvastatin on new-onset diabetes mellitus (NODM) and cardiovascular outcomes with that of high-intensity rosuvastatin for a 3-year follow-up period. Methods: Data from the Korea Acute Myocardial Infarction Registry were collected from November 2011 to October 2015, and 13,104 AMI patients were enrolled from major cardiovascular centers. Among them, 2,221 patients without diabetes who had been administered with high-intensity atorvastatin (40–80 mg) and rosuvastatin (20 mg) were investigated. The atorvastatin and rosuvastatin groups were compared and evaluated for the incidence of NODM and major adverse cardiac event (MACE) including total death, myocardial infarction, and revascularization cases in the following 3 years. Results: Baseline characteristics were comparable between two groups. Event-free survival rate of NODM and MACE was not significantly different between the atorvastatin and rosuvastatin groups (92.5% vs. 90.8%, respectively; Log-rank P-value = 0.550). The event-free survival rate of MACE was also not significantly different between atorvastatin and rosuvastatin groups (89.0% vs. 89.6%, respectively; Log rank p-value = 0.662). Multivariable Cox analysis revealed that the statin type was not a prognostic factor in the development of NODM and MACE. Conclusions: Administering high-intensity atorvastatin and rosuvastatin in AMI patients produced comparable effects on NODM and clinical outcome, suggesting their clinical equivalence in secondary prevention.
Backgrounds: Atherosclerosis is a chronic inflammatory disease causing a fatal plaque rupture and its key aspect is a failure to resolve inflammation. We hypothesized that macrophage targeted near-infrared fluorescence (NIRF) emitting photoactivation could simultaneously in vivo assess the inflamed high-risk plaques and facilitate the inflammation resolution. Method and results: We newly synthesized a Dectin-1 targeted photoactivatable theranostic agent by the chemical conjugation of photosensitizer chlorin e6 (Ce6) and Dectin-1 ligand laminarin (LAM-Ce6). Intravascular photoactivation through a customized fiber-based diffuser effectively reduced inflammation in the targeted plaques 4 weeks after LAM-Ce6 administration as serially assessed by dual-modal optical coherence tomography (OCT)-NIRF catheter imaging. The number of TUNEL-positive apoptotic macrophages peaked at 1 day after laser irradiation, and then resolved until 4 weeks. One hour after the light therapy, autophagy was strongly augmented with the formation of autophagolysosomes revealed by co-localization of enhanced microtubule-associated protein light-chain 3 (LC3) and lysosome-associated membrane protein 2 (LAMP2) expressions in the plaques (Figure). LAM-Ce6 photoactivation increased the TUNEL/RAM11- and MerTK-positive cells in the plaques, suggestive of enhanced efferocytosis. In line with inflammation resolution, photoactivation reduced the plaque burden with collagen-rich fibrotic replacement via TGF-β pathway confirmed by corroborative immunostainings ( p <0.01). Conclusions: OCT-NIRF imaging-guided macrophage Dectin-1 targetable photoactivation could stabilize the inflamed high-risk plaques by autophagy-mediated inflammation resolution and TGF-β dependent fibrotic replacement. This novel targeted photoactivation will offer new opportunity for the catheter based theranostic strategy.
Introduction and Hypothesis: Endothelial shear stress (ESS) is the tangential force produced by luminal blood flow on arterial endothelium. Both high ESS and low ESS are known to have atherogenic effects, however, it remains poorly understood how these different forces influence coronary atherosclerosis. We evaluated the impact of ESS changes on biochemical and phenotypic difference of coronary atheroma, as assessed by a novel dual-modal optical coherence tomography-fluorescence lifetime imaging (OCT-FLIm) in vivo in beating human coronary arteries. Methods and Results: We constructed a fully-integrated OCT and multispectral FLIm system based on a low-profile dual-modal imaging catheter. High-speed OCT-FLIm could be performed safely in patients undergoing coronary revascularization (Pullback speed: 10-20mm/sec). 3D artery model for computational fluid dynamics was reconstructed by fusion of OCT and angiography. We analyzed spatial associations between ESS and multispectral FLIm information: ch.3(542nm) = fibroatheroma with inflammation; ch.1 (390nm) = loose fibrous tissue (healed plaque). OCT-FLIm visualized coronary microstructure clearly and offered correctly-coregistered biochemical readouts of coronary atherosclerotic plaque in vivo in a label-free manner. Fibroatheromas with increased inflammation activity, as assessed by ch.3 FLIm, were found in low ESS area. On the other hands, high ESS area colocalized with regions with increased ch.1 lifetime, a FLIm signature of loose fibrous tissue (healed plaque). Based on a coregistered ESS-FLIm data, we found a statistically significant negative correlation between ESS and ch.3 lifetime (p>0.001) and a positive correlation between ESS and ch.1 lifetime (p>0.001). Conclusions: Low ESS was associated with lipid and macrophage infiltration whereas high ESS was associated with presence of loose fibrous tissue, a histologic marker of recent plaque disruption leading to rapid plaque progression. Our novel imaging strategy enabling comprehensive evaluation of complex interaction between ESS and biochemical phenotype of plaques is expected to enhance understanding of coronary atherosclerosis biology.
Background/Objectives: Spotty calcification linked with macrophage activity is a major target for high-risk plaque but the biological interconncetion remains questionable. To address this issue, we newly developed intravascular multimodal imaging strategy by fully integration of OCT with dual-targeted near-infrared fluorescence (NIRF) molecular imaging using customized osteogenic activity and macrophage targetable probes. Methods/Results: We newly integrated intravascular OCT structural imaging with dual-targeted NIRF imaging. Scale-up novel NIRF emitting probe targeting osteogenic activity was fabricated by chemically coupling alendronate ligand and Cy5.5 to the ends of azide-PEG-NHS ester (Al-Cy5.5). Based on biodistribution, OCT/dual-NIRF in vivo imaging of rabbit aortoiliac atheroma was acquired 72 hrs after intravenous injection of Al-Cy5.5 (5.0 mg/kg) and macrophage mannose receptor targeted Cy7-emitting probe (7.5 mg/kg). NIRF signals of Cy5.5 and Cy7 were highly enhanced in spotty calcification and inflammatory sites of the plaque, respectively (Figure) (p<0.01). Fluorescence microscopy and immunostainings from the corresponding sections well corroborated the in vivo findings. Intriguingly, an interconnection of osteogenic activity (TRAP stain) with macrophages was more prominent in superficial spotty calcification rather than outer dense calcification (Figure) (p<0.01). Conclusions: Our intravascular OCT/dual-NIRF imaging was feasible to simultaneously image osteogenic activity and macrophages in the coronary-sized atheroma. This novel imaging strategy is expected to expand the understanding for the biological behavior of calcifying inflamed activity in the high-risk plaques existing on cap microcalcification.
Sleep apnea and hypertension are known to be closely related to the development of the cardiovascular disease, so these diseases must be treated properly. Moreover, it has been continuously reported that sleep apnea syndrome and hypertension are highly correlated, and they share not only many risk factors such as obesity, but also some pathophysiological mechanisms. The ultimate aim of treatment for hypertension is not simply to lower blood pressure but to prevent cardiovascular diseases such as angina, myocardial infarction, stroke, heart failure, and death. Sleep apnea treatment is similarly aimed at preventing related complications and lowering mortality by controlling many risk factors including the occurrence of hypertension. It is important to understand the pathophysiology of the relationship between sleep apnea and hypertension. Thereby we can understand why physicians should pay more attention and why they should treat sleep apnea. Key Words: Key WordsSleep apnea; Hypertension; Pathophysiology
Abstract Background Acute decompensated heart failure (ADHF) is a systemic congestion state requiring timely management. Admission for ADHF is closely related to the readmission and post-discharge mortality in patients, which makes it imperative to detect ADHF in its early stage. Methods Patients with ADHF needed admission were eligible for enrollment, and those with respiratory infection, sepsis, lung/vocal cord disease, acute coronary syndrome, or serum creatinine>3mg/dL were excluded. A total of 112 patients were enrolled between July, 2020 and December, 2022. Voice was recorded two times: at admission for ADHF, and at discharge. Patients were asked to phonate five Korean vowels (‘a/e/i/o/u’) for 3 seconds each, and then to repeat the sentence ‘daehan minkook manse’ five times. Low-level audio features were extracted for classification. Then, Mel-Spectrogram was extracted from waveform and used as input features of the deep learning-based classification models. Two kinds of the deep learning-based classification models, convolutional neural networks and Transformer, were adapted for the further analysis. Results For 100 patients in the final analysis, we randomized patients into two mutually exclusive groups: a training group (n=88) and a test group (n=12). In the analysis with low-level audio features, harmonics-to-noise ratio and Shimmer showed classification potential. Then, deep learning models were trained to classify whether certain voice belongs to ADHF state or recovered state. We treated it as a binary classification task, and the best performing model achieved a classification accuracy of 85.11% with DenseNet201. The classification accuracy was improved as 92.76% with ViT-16-large after inputting additional classic features of heart failure. With adding the low-level audio features in a training process, classification task accuracy was improved in DenseNet201 for about 2%. Conclusions Our results proposed the clinical possibility of voice as a useful and noninvasive biomarker to detect ADHF in its early stage.
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