H-type Hypertension Status and Influencing Factors of the Elderly People Over 80 Years Old Based on Random Forest Model.

Hypertension is a common chronic disease in elderly people over 80 years old. Clinically, H-type hypertension occurs when hypertension coexists with hyperhomocysteinemia level of ≥ 10 umol/L. Effective identification of risk factors for H-type hypertension in the elderly can greatly improve patient prognosis.Consecutively, 494 patients with hypertension admitted to the Fourth Affiliated Hospital of Harbin Medical University from January 2019 to December 2021 were selected as the study population. They were divided into H-type hypertension (n = 197) and non-H-type hypertension groups (n = 297). Patient data were collected, including basic information, history, and clinical data. The random forest model and LASSO analysis were used to screen the influencing factors for H-type hypertension. Multiple stepwise regression analysis was used to analyze the selected variables.A total of 197 elderly people over 80 years old suffered from H-type hypertension, with an incidence rate of 39.88%. The random forest model and LASSO analysis results showed that the top 8 independent variables in importance ranking were ejection fraction (EF), fibrinogen, glycated hemoglobin (HbA1c), B-type natriuretic peptide, creatinine, fasting blood glucose, uric acid, and serum triiodothyronine levels. The results of multivariate analysis showed that EF was the protective factor, while fibrinogen, HbA1c, and creatinine were the risk factors for H-type hypertension in elderly people over 80 years old (P < 0.05).Healthcare professionals can indirectly assess the prevalence of H-type hypertension by focusing on EF, fibrinogen, creatinine, and HbA1c in elderly hypertensive patients. This provided proactive intervention and medical services to improve prognosis outcomes.

Revisiting an old relationship: the causal associations of the ApoB/ApoA1 ratio with cardiometabolic diseases and relative risk factors-a mendelian randomization analysis.

BACKGROUND: It has been confirmed that the ApoB/ApoA1 ratio is closely associated with the incidence of cardiometabolic diseases (CMD). However, due to uncontrolled confounding factors in observational studies, the causal relationship of this association remains unclear. METHODS: In this study, we extracted the ApoB/ApoA1 ratio and data on CMD and its associated risk factors from the largest European Genome-Wide Association Study. The purpose was to conduct Mendelian Randomization (MR) analysis. The causal relationship between the ApoB/ApoA1 ratio and CMD was evaluated using both univariable and multivariable MR analyses. Furthermore, bidirectional MR analysis was performed to estimate the causal relationship between the ApoB/ApoA1 ratio and risk factors for CMD. The final verification confirmed whether the ApoB/ApoA1 ratio exhibits a mediating effect in CMD and related risk factors. RESULTS: In terms of CMD, a noteworthy correlation was observed between the increase in the ApoB/ApoA1 ratio and various CMD, including ischemic heart disease, major adverse cardiovascular events, aortic aneurysm, cerebral ischemic disease and so on (all PFDR<0.05). Meanwhile, the ApoB/ApoA1 ratio was significantly associated with CMD risk factors, such as hemoglobin A1c, fasting insulin levels, waist-to-hip ratio, sedentary behavior, and various others, demonstrating a notable causal relationship (all PFDR<0.05). Additionally, the ApoB/ApoA1 ratio played a mediating role in CMD and relative risk factors. CONCLUSIONS: This MR study provides evidence supporting the significant causal relationship between the ApoB/ApoA1 ratio and CMD and its risk factors. Moreover, it demonstrates the mediating effect of the ApoB/ApoA1 ratio in CMD and its risk factors. These findings suggest that the ApoB/ApoA1 ratio may serve as a potential indicator for identifying the risk of developing CMD in participants.

Pancoronary plaque characteristics in STEMI patients with rapid plaque progression: An optical coherence tomography study.

BACKGROUND: Non-culprit plaque progression is associated with recurrent cardiac ischemic events and worse clinical outcomes. Given that atherosclerosis is a systemic disease, the pancoronary characteristics of patients with rapid plaque progression are unknown. This study aims to identify pancoronary plaque features in patients with ST-segment elevation myocardial infarction (STEMI) with and without rapid plaque progression, focused on the patient level. METHODS AND RESULTS: From January 2017 to July 2019, 291 patients underwent 3-vessel optical coherence tomography imaging at the time of the primary procedure and a follow-up angiography interval of 12 months. The final analysis included 237 patients. Overall, 308 non-culprit lesions were found in 78 STEMI patients with rapid plaque progression, and 465 non-culprit plaques were found in 159 STEMI patients without rapid plaque progression. These patients had a higher pancoronary vulnerability (CLIMA-defined high-risk plaque: 47.4% vs. 33.3%; non-culprit plaque rupture: 25.6% vs. 14.5%) and a significantly higher prevalence of other vulnerable plaque characteristics (i.e., lipid-rich plaque, cholesterol crystal, microchannels, calcification, spotty calcification, and thrombus) at baseline versus those without rapid plaque progression. Lesions with rapid progression were highly distributed at the LAD, tending to be near the bifurcation. In multivariate analysis, age ≥ 65 years was an independent predictor of subsequent rapid lesion progression at the patient level, whereas microchannel, spotty calcification, and cholesterol crystal were independent predictors for STEMI patients ≥65 years old. CONCLUSIONS: STEMI patients with subsequent rapid plaque progression had higher pancoronary vulnerability and commonly presented vulnerable plaque morphology. Aging was the only predictor of subsequent rapid plaque progression.

CTRP13 Mitigates Endothelial Cell Ferroptosis via the AMPK/KLF4 Pathway: Implications for Atherosclerosis Protection.

BACKGROUND C1q/tumor necrosis factor-related protein 13 (CTRP13) preserves endothelial function and possesses anti-oxidation activity. However, its effects on ferroptosis of human umbilical vein endothelial cells (HUVECs) remain unclear. We investigated the effects of CTRP13 on HUVEC ferroptosis induced by oxidized low-density lipoprotein (ox-LDL) and explored the underlying mechanisms of CTRP13 against ferroptosis via the AMPK/KLF4 pathway. MATERIAL AND METHODS Cell Counting Kit-8 assay was used to evaluate cell viability. Lactate dehydrogenase activity and malondialdehyde content analysis were performed to evaluate the cell membrane integrity and lipid peroxidation. Mito-Tracker, JC-1, and 2',7'-dichlorofluorescein di-acetate were used to evaluate the biological activity of mitochondria, mitochondrial membrane potential, and reactive oxygen species (ROS) in endothelial cells. The ferroptosis indicator expressions, recombinant solute carrier family 7, member 11, glutathione peroxidase 4 (GPX4), and acyl-CoA synthetase long-chain family member 4 were examined using real-time reverse transcription-polymerase chain reaction and Western blot. Immunofluorescence staining detected GPX4 location in endothelial cells. RESULTS The results demonstrate that CTRP13 (450 ng/mL) prevented HUVEC ferroptosis by inhibiting ROS overproduction and mitochondrial dysfunction, and CTRP13 accelerated antioxidant enzyme expression levels, such as heme oxygenase 1, superoxide dismutase 1, and superoxide dismutase 2, compared with the ox-LDL (100 µg/mL) group for 48 h. Additionally, CTRP13 treatment increased p-AMPK/AMPK expression by 47.65% (P<0.05) while decreasing Krüppel-like factor 4 expression by 37.43% (P<0.05) in ox-LDL-induced HUVECs and elucidated the protective effect on endothelial dysfunction from ferroptosis. CONCLUSIONS These findings provide new insights for understanding the effects and mechanism of CTRP13 on preventing endothelial cell ferroptosis.

Achieved low-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio predicts the pathophysiological evolution of lipid-rich plaques in acute coronary syndromes: an optical coherence tomography study.

Background: As a novel lipoprotein ratio, baseline low-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (LHR) is closely related to the clinical outcomes of acute coronary syndromes (ACS) after percutaneous coronary intervention. However, the pathophysiological impact of achieved LHR (aLHR) on the evolution of non-culprit lipid-rich plaques has not been systematically explored. Methods: Between September 2013 and December 2018, ACS patients with both baseline and 1-year follow-up optical coherence tomography (OCT) examinations were included in current study. They were divided into two groups according to the median value of aLHR at 1 year. Results: Overall, 132 patients with 215 lipid-rich plaques were enrolled, with a median aLHR: 1.62. There were thinner fibrous cap thickness (FCT) (133.3 [70.0-180.0] µm vs. 160.0 [100.0-208.3] µm, p = 0.025) and higher prevalence of thin-cap fibroatheroma (TCFA) (24 [22.4%] vs. 13 [12.0%], p = 0.044) and CLIMA-defined high-risk plaques (12 [11.2%] vs. 3[2.8%], p = 0.015) in the high aLHR group at 1 year. Compared with other serum lipid indexes, aLHR showed the best robust correlation with the evolution of plaque vulnerability in both unadjusted and adjusted analyses. Cut-off value of aLHR to predict the progression of maximal lipid arc and FCT was 1.51. In the adjusted model, aLHR ≥1.51 was an independent predictor of TCFA [odds ratio (OR): 3.008, 95% CI: 1.370 to 6.605, p = 0.006] at 1 year. Conclusions: aLHR correlates well with the evolution of lipid-rich plaques and vulnerable phenotypes at 1-year follow-up, which might be an important and convenient serum indicator in the secondary prevention of ACS.

A novel protective role of lipoxin in inhibiting diabetic vascular calcification via YAP signalling: Health prevention and regulation.

Vascular calcification is highly prevalent in diabetes patients, with detrimental consequences and no effective prevention and treatment strategies are currently available. Though the protective effect of lipoxin (LX) against vascular diseases has been demonstrated, its effect on diabetic vascular calcification remains unknown. AGEs dose-dependently induced calcification and the expression of osteogenesis-related markers, coupled with the activation of yes-associated protein (YAP). Mechanistically, YAP activation enhanced the AGE-induced osteogenic phenotype and calcification, but inhibition of YAP signalling alleviated this response. Further, an in vivo diabetic mouse model was established using a combination of a high-fat diet and multiple formulations of low-dose streptozotocin. Consistent with the in vitro results, diabetes promoted YAP expression and its subcellular localization in the nucleus in the arterial tunica media. The results demonstrate that LX attenuates the trans-differentiation and calcification of VSMCs in diabetes mellitus via YAP signalling, suggesting LX to be a potent therapeutic for preventing diabetic vascular calcification.

Peripheral atherosclerosis in acute coronary syndrome patients with plaque rupture vs plaque erosion: A prospective coronary optical coherence tomography and peripheral ultrasound study.

BACKGROUND: Plaque rupture (PR) and plaque erosion (PE) are 2 distinct, different, and most common culprit lesion morphologies responsible for acute coronary syndrome (ACS). However, the prevalence, distribution, and characteristics of peripheral atherosclerosis in ACS patients with PR vs PE has never been studied. The aim of this study was to assess peripheral atherosclerosis burden and vulnerability evaluated by vascular ultrasound in ACS patients with coronary PR vs PE identified by optical coherence tomography (OCT). METHODS: Between October 2018 and December 2019, 297 ACS patients who underwent preintervention OCT examination of the culprit coronary artery were enrolled. Peripheral ultrasound examinations of carotid, femoral, and popliteal arteries were performed before discharge. RESULTS: Overall, 265 of 297 (89.2%) patients had at least one atherosclerotic plaque in a peripheral arterial bed. Compared with coronary PE, patients with coronary PR had a higher prevalence of peripheral atherosclerotic plaques (93.4% vs 79.1%, P < .001), regardless of location: carotid, femoral, or popliteal arteries. The number of peripheral plaques per patient was significantly larger in the coronary PR group than coronary PE (4 [2-7] vs 2 [1-5], P < .001). Additionally, there was a greater prevalence of peripheral vulnerable characteristics including plaque surface irregularity, heterogeneous plaque, and calcification in patients with coronary PR vs PE. CONCLUSIONS: Peripheral atherosclerosis exists commonly in patients presenting with ACS. Patients with coronary PR had greater peripheral atherosclerosis burden and more peripheral vulnerability compared to those with coronary PE, suggesting that comprehensive evaluation of peripheral atherosclerosis and multidisciplinary cooperative management maybe necessary, especially in patients with PR. TRIAL REGISTRATION: clinicaltrials.gov (NCT03971864).

Identification of High-Risk Coronary Lesions by 3-Vessel Optical Coherence Tomography.

BACKGROUND: Optical coherence tomography (OCT) may provide a method for detecting histologically defined high-risk plaques in vivo. OBJECTIVES: The authors aimed to investigate the prognostic value of OCT for identifying patients and lesions that are at risk for adverse cardiac events. METHODS: Between January 2017 and May 2019, OCT of all the 3 main epicardial arteries was performed in 883 patients with acute myocardial infarction (MI) who were referred for primary percutaneous coronary intervention. The primary endpoint was the composite of cardiac death, nonculprit lesion-related nonfatal MI, and unplanned coronary revascularization. Patients were followed for up to 4 years (median 3.3 years). RESULTS: The 4-year cumulative rate of the primary endpoint was 7.2%. In patient-level analysis, thin-cap fibroatheroma (TCFA) (adjusted HR: 3.05; 95% CI: 1.67-5.57) and minimal lumen area (MLA) <3.5 mm2 (adjusted HR: 3.71; 95% CI: 1.22-11.34) were independent predictors of the primary endpoint. In lesion-level analysis, nonculprit lesions responsible for subsequent events were not angiographically severe at baseline (mean diameter stenosis 43.8% ± 13.4%). TCFA (adjusted HR: 8.15; 95% CI: 3.67-18.07) and MLA <3.5 mm2 (adjusted HR: 4.33; 95% CI: 1.81-10.38) were predictive of events arising from each specific lesion. TCFAs with an MLA <3.5 mm2 carried a higher risk and were sufficient for identifying patients at risk for the composite of cardiac death and nonculprit lesion-related nonfatal MI. CONCLUSIONS: OCT imaging of angiographically nonobstructive territories in patients with acute MI can aid in identifying patients and lesions at increased risk for adverse cardiac events.

A landscape of Long non-coding RNAs reveals the leading transcriptome alterations in murine aorta during aging.

Considerable studies have given convincing evidence of a forefront position for vascular aging in preventing cardiovascular disease. Various functions of Long non-coding RNAs (lncRNAs) are becoming increasingly distinct in aging-related diseases. This study aims at a better insight into the expression profile and mechanisms of lncRNAs in vascular senescence. High-throughput sequencing was used to detect the differential expression (DE) of lncRNAs and mRNAs in the aorta of 96 W and 8 W-old mice, while 1423 lncRNAs and 80 mRNAs were differentially expressed. By performing GO and KEGG enrichment analysis, we found that DE lncRNAs were mainly involved in purine metabolism and cGMP-PKG signaling pathways. In addition, a co-expression functional network of DE lncRNAs and DE mRNAs was constructed, and ENSMUST00000218874 could interact with 41 DE mRNAs, suggesting that it may play an essential role in vascular senescence. This study reveals DE lncRNAs in naturally aging vascular, which may provide new ideas and targets for aging-related cardiovascular diseases.

Vaspin alleviates the lncRNA LEF1-AS1-induced osteogenic differentiation of vascular smooth muscle cells via the Hippo/YAP signaling pathway.

Vascular calcification (VC) is closely related to higher cardiovascular mortality and morbidity, and vascular smooth muscle cell (VSMC) switching to osteogenic-like cells is crucial for VC. LncRNA LEF1-AS1 promotes atherosclerosis and dental pulp stem cells calcification, while its role in VC remains unknown. Visceral adipose tissue-derived serine protease inhibitor (vaspin) is an adipokine regulating bone metabolism. However, the relationship between vaspin and VC is still unclear. We aimed to explore the role of LEF1-AS1 on VSMC osteogenic transition, whether vaspin inhibited LEF1-AS1-mediated osteogenic differentiation of VSMCs, and the responsible mechanism. In this study, quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting analysis indicated that LEF1-AS1 overexpression significantly upregulated osteogenic marker Runt-related transcription factor-2 (RUNX2) level and downregulated VSMC contractile marker α-smooth muscle actin (α-SMA) level. Alizarin red staining, alkaline phosphatase (ALP) staining, ALP activity assay, and calcium content assay also suggested that LEF1-AS1 overexpression promoted calcium deposition in VSMCs. However, vaspin treatment abolished this phenomenon. Mechanistically, LEF1-AS1 markedly decreased phosphorylated YAP level, while vaspin reversed LEF1-AS1-induced phosphorylated YAP decline. Our results revealed that LEF1-AS1 accelerated the osteogenic differentiation of VSMCs by regulating the Hippo/YAP pathway, while vaspin eliminated the LEF1-AS1-meditated VSMCs osteogenic phenotype switch.

Irisin inhibits PCSK9 expression through activating AMPK-SREBP2 pathway.

AIMS: Previous studies found that irisin attenuated the vascular wall inflammation caused by Oxidized low-density lipoprotein (ox-LDL), and recent experiments have shown that proprotein convertase subtilisin/kexin type 9 (PCSK9) can act on various cells in the vascular wall to induce inflammatory responses. But, the relationship between irisin and PCSK9 has not been reported. The aim of this study was to investigate the effect of irisin on PSCK9 in endothelial cells and hepatocytes under the induction of ox-LDL. METHODS: Experiments were performed using human umbilical vein endothelial cells and Hep G2, and cells were treated with irisin and (or) ox-LDL for evaluating expression of PCSK9 and downstream inflammatory proteins, while the expression levels of AMP-dependent protein kinase (AMPK) and sterol-regulatory element binding protein 2 (SREBP2) were also examined. Then Compound C was used to inhibit AMPK activation and SiAMPK for silencing of AMPK mRNA, and the above assays were also performed to deeply validate the role of the AMPK-SREBP2 pathway. RESULTS: Irisin treatment significantly downregulated the expression of PCSK9 and inflammation-related proteins induced by ox-LDL, also restored the content of p-AMPK and reduced the SREBP2 content. After the use of Compound C or SiAMPK, the content of p-AMPK was obviously decreased, and the positive effect of irisin was greatly weakened. CONCLUSIONS: This study demonstrates that irisin suppresses PCSK9 expression through the AMPK-SREBP2 pathway and ameliorates ox-LDL-induced endothelial cells inflammation.

Comparison of protective effects of alprostadil with Salvia miltiorrhiza against myocardial ischemia-reperfusion injury in rats.

OBJECTIVES: Our study aimed to investigate the effects of alprostadil and Salvia miltiorrhiza extract on myocardial ischemia-reperfusion injury (IRI) and related underlying molecular mechanisms. METHODS: A myocardial IRI model was established in Wistar rats via surgical ligation of the left anterior descending coronary artery followed by loosening of the occlusion. The rats were divided into four groups: saline, sham, alprostadil, and S. miltiorrhiza. Rats in the saline and sham groups were injected with normal saline by tail vein once daily for 10 consecutive days. Rats in the S. miltiorrhiza and alprostadil groups were injected with S. miltiorrhiza extract (20 µg/kg) or alprostadil. Histological differences in myocardial tissues between rats in the sham group and in the myocardial IRI model were observed by hematoxylin and eosin staining. India ink perfusion was used to quantify the number of capillary microvessels. Real-time quantitative reverse transcription polymerase chain reaction was used to determine serum expression levels of soluble intercellular adhesion molecule (sICAM), soluble vascular adhesion molecule (sVCAM), CD11b and CD18. RESULTS: The alprostadil and S. miltiorrhiza groups had significantly higher numbers of microvessels than the saline group. Serum sICAM and sVCAM expression was significantly reduced in the alprostadil and S. miltiorrhiza groups. Meanwhile, sICAM and sVCAM in the alprostadil group were markedly lower than in the S. miltiorrhiza group. Moreover, the alprostadil group had markedly lower mRNA expression of CD11b and CD18, which were clearly lower than in the S. miltiorrhiza group. CONCLUSION: Alprostadil may have cardioprotective effects for myocardial IRI, with down-regulated expression of sICAM, sVCAM, CD11b, and CD18.

Long Noncoding RNA SBF2-AS1 Promotes Abdominal Aortic Aneurysm Formation through the miRNA-520f-3p/SMARCD1 Axis.

Abdominal aortic aneurysm (AAA) is a chronic vascular inflammatory disease. The regulatory mechanisms during AAA formation remain unclear. Bone marrow stem cells (BMSCs) are pluripotent cells capable of regulating the progression of various diseases by delivering exosomes and exosomal lncRNAs. In this study, we investigated its function in AAA by isolating BMSC exosome-derived lncRNA SBF2-AS1. The results showed that BF2-AS1 could be transferred to vascular smooth muscle cells (VSMCs) and human aortic VSMCs (HASMCs) via BMSC-derived exosomes. Depletion of SBF2-AS1 enhanced the cell viability and proliferation of VSMCs. Conversely, SBF2-AS1 knockdown inhibited VSMC apoptosis. Caspase-3 activity was inhibited by depletion of SBF2-AS1, whereas overexpression of SBF2-AS1 in VSMC promoted Caspase-3 activity. SBF2-AS1 enhances SMARCD1 expression by forming miR-520f-3p in VSMC and HASMC. Overexpression of SMARCD1 or miR-520f-3p inhibitor reversed cell viability and caspase-3 activity mediated by SBF2-AS1 depletion in VSMC and HASMC. Therefore, BMSC exosome-derived SBF2-AS1 promotes AAA formation through the miRNA-520f-3p/SMARCD1 axis. Targeting SBF2-AS1 could serve as a promising therapeutic strategy for AAA.

A Novel Risk Score to Predict In-Hospital Mortality in Patients With Acute Myocardial Infarction: Results From a Prospective Observational Cohort.

Objectives: The aim of this study was to develop and validate a novel risk score to predict in-hospital mortality in patients with acute myocardial infarction (AMI) using the Heart Failure after Acute Myocardial Infarction with Optimal Treatment (HAMIOT) cohort in China. Methods: The HAMIOT cohort was a multicenter, prospective, observational cohort of consecutive patients with AMI in China. All participants were enrolled between December 2017 and December 2019. The cohort was randomly assigned (at a proportion of 7:3) to the training and validation cohorts. Logistic regression model was used to develop and validate a predictive model of in-hospital mortality. The performance of discrimination and calibration was evaluated using the Harrell's c-statistic and the Hosmer-Lemeshow goodness-of-fit test, respectively. The new simplified risk score was validated in an external cohort that included independent patients with AMI between October 2019 and March 2021. Results: A total of 12,179 patients with AMI participated in the HAMIOT cohort, and 136 patients were excluded. In-hospital mortality was 166 (1.38%). Ten predictors were found to be independently associated with in-hospital mortality: age, sex, history of percutaneous coronary intervention (PCI), history of stroke, presentation with ST-segment elevation, heart rate, systolic blood pressure, initial serum creatinine level, initial N-terminal pro-B-type natriuretic peptide level, and PCI treatment. The c-statistic of the novel simplified HAMIOT risk score was 0.88, with good calibration (Hosmer-Lemeshow test: P = 0.35). Compared with the Global Registry of Acute Coronary Events risk score, the HAMIOT score had better discrimination ability in the training (0.88 vs. 0.81) and validation (0.82 vs. 0.72) cohorts. The total simplified HAMIOT risk score ranged from 0 to 121. The observed mortality in the HAMIOT cohort increased across different risk groups, with 0.35% in the low risk group (score ≤ 50), 3.09% in the intermediate risk group (50 < score ≤ 74), and 14.29% in the high risk group (score > 74). Conclusion: The novel HAMIOT risk score could predict in-hospital mortality and be a valid tool for prospective risk stratification of patients with AMI. Clinical Trial Registration: [https://clinicaltrials.gov], Identifier: [NCT03297164].

EROSION III: A Multicenter RCT of OCT-Guided Reperfusion in STEMI With Early Infarct Artery Patency.

OBJECTIVES: The aim of this study was to test whether optical coherence tomographic (OCT) guidance would provide additional useful information beyond that obtained by angiography and lead to a shift in reperfusion strategy and improved clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI) with early infarct artery patency. BACKGROUND: Angiography is limited in assessing the underlying pathophysiological mechanisms of the culprit lesion. METHODS: EROSION III (Optical Coherence Tomography-Guided Reperfusion in ST-Segment Elevation Myocardial Infarction With Early Infarct Artery Patency) is an open-label, prospective, multicenter, randomized, controlled study approved by the ethics committees of participating centers. Patients with STEMI who had angiographic diameter stenosis ≤ 70% and TIMI (Thrombolysis In Myocardial Infarction) flow grade 3 at presentation or after antegrade blood flow restoration were recruited and randomized to either OCT guidance or angiographic guidance. The primary efficacy endpoint was the rate of stent implantation. RESULTS: Among 246 randomized patients, 226 (91.9%) constituted the per protocol set (112 with OCT guidance and 114 with angiographic guidance). The median diameter stenosis was 54.0% (IQR: 48.0%-61.0%) in the OCT guidance group and 53.5% (IQR: 43.8%-64.0%) in the angiographic guidance group (P = 0.57) before randomization. Stent implantation was performed in 49 of 112 patients (43.8%) in the OCT group and 67 of 114 patients (58.8%) in the angiographic group (P = 0.024), demonstrating a 15% reduction in stent implantation with OCT guidance. In patients treated with stent implantation, OCT guidance was associated with a favorable result with lower residual angiographic diameter stenosis (8.7% ± 3.7% vs 11.8% ± 4.6% in the angiographic guidance group; P < 0.001). Two patients (1 cardiac death, 1 stable angina) met the primary safety endpoint in the OCT guidance group, as did 3 patients (3 cardiac deaths) in the angiographic guidance group (1.8% vs 2.6%; P = 0.67). Reinfarction was not observed in either group. At 1 year, the rates of predefined cardiocerebrovascular events were comparable between the groups (11.6% after OCT guidance vs 9.6% after angiographic guidance; P = 0.66). CONCLUSIONS: In patients with STEMI with early infarct artery patency, OCT guidance compared with angiographic guidance of reperfusion was associated with less stent implantation during primary percutaneous coronary intervention. These favorable results indicate the value of OCT imaging in optimizing the reperfusion strategy of patients with STEMI. (EROSION III: OCT- vs Angio-Based Reperfusion Strategy for STEMI; NCT03571269).

Feasibility and Safety of Very-Low Contrast Combined Ringer's Solution in Optical Coherence Tomography Imaging.

Background: Optical coherence tomography (OCT) is an important modality used in coronary intervention. However, OCT requires a high amount of contrast media, limiting its extensive application in clinical practice. This study compared OCT images of coronary lesions obtained using contrast media and very-low contrast combined Ringer's solution (VLCCR) in patients with acute coronary syndrome (ACS). Methods: Thirty ACS patients with a total of 36 native lesions and stenoses from 70 to 90% were included in this study. Two kinds of flushing media (a contrast medium and VLCCR) were used in succession in a random order for OCT image pullback of each lesion. VLCCR method is using low volume contrast (4-5 ml) injected into the guiding catheter previously combination with injector infused Ringer's solution instead of pure contrast medium. The safety of procedure was evaluated by recording the patients 'symptoms, changes of ECG, blood pressure and heart rate. OCT images were analyzed to determine the image clarity. Lumen area and diameter were also measured and the consistency between the two media was compared. Results: OCT procedure using either contrast or VLCCR did not show any peri-procedural adverse events. There was no difference in changes of blood pressure and heart rate in both procedures, however, VLCCR procedure showed less procedure-related symptoms and ECG changes. We found that the percentage of clear image frame was equivalent between the contrast and VLCCR media (98.0 vs. 96.9%, P = 0.90). We also observed a high degree of similarity between the different lesion phenotypes of ACS for both media. There was a linear correlation of the phenotypes obtained with these two different methods, and a significant correlation was observed between measurements obtained with contrast and VLCCR without correction for the refractive index of VLCCR (correlation coefficients ranged between 0.829 and 0.948). Conclusions: OCT imaging using VLCCR for blood clearance is feasible and safe and provides similar imaging quality compared to OCT imaging obtained using radiographic contrast media for ACS patients.

Morphological Characteristics of Eroded Plaques with Noncritical Coronary Stenosis: An Optical Coherence Tomography Study.

AIMS: Recent studies suggested plaque erosion with noncritical stenosis could be treated distinctly from that with critical stenosis, but their morphological features remained largely unknown. The present study aimed to investigate morphological features of eroded plaques with different lumen stenosis using optical coherence tomography (OCT). METHODS: A total of 348 ST-segment elevated myocardial infarction patients with culprit OCT-defined plaque erosion (OCT-erosion) were analyzed. Based on the severity of lumen area stenosis, all patients with OCT-erosions were divided into the following three groups: Group A (area stenosis ＜50%, n=50); Group B (50% ≤ area stenosis ＜75%, n=146); Group C (area stenosis ≥ 75%, n=152). RESULTS: Compared with patients in Groups A and B, patients in Group C were older (p=0.008) and had higher prevalence of hypertension (p=0.029). Angiographic analysis showed that 72.0% of the eroded plaques in Group A were located in the left anterior descending artery, followed by 67.8% in Group B, and 53.9% in Group C (p=0.039). OCT analysis showed that Group A had the highest prevalence of fibrous plaques (p＜0.001) and nearby bifurcation (p=0.036), but the lowest prevalence of lipid-rich plaques (p＜0.001), macrophage accumulation (p＜0.001), microvessels (p=0.009), cholesterol crystals (p＜0.001), and calcification (p=0.023). Multivariable regression analysis showed fibrous plaque (odds ratio [OR]: 3.014, 95% confidence interval [CI]: 1.932-4.702, p＜0.001) and nearby bifurcation (OR: 1.750, 95% CI: 1.109-2.761, p=0.016) were independently associated with OCT-erosion with an area stenosis of ＜75%. CONCLUSIONS: More than half of OCT-erosions presented with ＜75% area stenosis, having distinct morphological features from those of OCT-erosions with critical stenosis. Fibrous plaque and nearby bifurcation were independently associated with noncritically stenotic OCT-erosion, suggesting that eroded plaques might need individualized treatment.

Increased Vulnerability and Distinct Layered Phenotype at Culprit and Nonculprit Lesions in STEMI Versus NSTEMI.

OBJECTIVES: This study aimed to investigate the pancoronary plaque vulnerability (including culprit and nonculprit lesions) and layered phenotype in patients with ST-segment elevation myocardial infarction (STEMI) vs non-STEMI (NSTEMI). BACKGROUND: Pancoronary vulnerability should account for distinct clinical manifestations of acute myocardial infarction (AMI). Layered plaque is indicative of previous coronary destabilization and thrombosis. METHODS: A total of 464 patients with AMI who underwent 3-vessel optical coherence tomography imaging were consecutively studied and divided into a STEMI group (318 patients; 318 culprit and 1,187 nonculprit plaques) and a NSTEMI group (146 patients; 146 culprit and 560 nonculprit plaques). Patients were followed up for a median period of 2 years. RESULTS: Compared with NSTEMI, culprit lesions in STEMI had more plaque rupture, thrombus, thin-cap fibroatheroma (TCFA), calcification, macrophage accumulation, and microvessels. The prevalence of plaque rupture (8.2% vs 4.8%; P = 0.018), microvessels (57.5% vs 45.2%; P < 0.001), and calcification (40.7% vs 30.2%; P = 0.003) at nonculprit lesions was higher in STEMI than NSTEMI. The layer area and thickness at the culprit and nonculprit lesions were significantly larger in STEMI than in NSTEMI. Multivariate analyses showed that culprit layer area (odds ratio: 1.443; 95% CI: 1.138-1.830; P = 0.002) was predictive of STEMI (vs NSTEMI), in addition to culprit TCFA, culprit thrombus, and non-left circumflex artery location of the culprit lesion. Although the type of AMI was not related to clinical outcomes, high-sensitivity C-reactive protein, culprit calcified nodule, and nonculprit TCFA predicted the 2-year major adverse cardiovascular events in patients with AMI. CONCLUSIONS: Patients with STEMI had increased plaque vulnerability (ie, more plaque rupture and microvessels) and distinct layered phenotype at the culprit and nonculprit lesions compared with patients with NSTEMI. Culprit lesion features of large layer area, TCFA, thrombus, and non-left circumflex artery location predicted the clinical presentation of STEMI.