Inter-Domain Repulsion of Dumbbell-Shaped Calmodulin during Electrospray Ionization Revealed by Molecular Dynamics Simulations.

The mechanisms whereby protein ions are released from nanodroplets at the liquid-gas interface have continued to be controversial since electrospray ionization (ESI) mass spectrometry was widely applied in biomolecular structure analysis in solution. Several viable pathways have been proposed and verified for single-domain proteins. However, the ESI mechanism of multi-domain proteins with more complicated and flexible structures remains unclear. Herein, dumbbell-shaped calmodulin was chosen as a multi-domain protein model to perform molecular dynamics simulations to investigate the structural evolution during the ESI process. For [Ca4CAM], the protein followed the classical charge residue model. As the inter-domain electrostatic repulsion increased, the droplet was found to split into two sub-droplets, while stronger-repulsive apo-calmodulin unfolded during the early evaporation stage. We designated this novel ESI mechanism as the domain repulsion model, which provides new mechanistic insights into further exploration of proteins containing more domains. Our results suggest that greater attention should be paid to the effect of domain-domain interactions on structure retention during liquid-gas interface transfer when mass spectrometry is used as the developing technique in gas phase structural biology.

Impact of Bivalirudin on Patients with Acute Coronary Syndrome Undergoing Rotational Atherectomy in Real-Life Setting: A Retrospective Cohort Study.

BACKGROUND: No evidence exists on the impact of bivalirudin in patients with the acute coronary syndrome undergoing rotational atherectomy. This study aimed to evaluate the impact of bivalirudin on patients with acute coronary syndrome undergoing rotational atherectomy. METHODS: This was a retrospective cohort study conducted in our hospital between January 2017 and December 2019. The study included patients with acute coronary syndrome undergoing rotational atherectomy. Furthermore, 2 cohorts were included in this study (bivalirudin cohort and control cohort unfractionated heparin). The primary end-point was in-hospital net adverse clinical events. The secondary endpoint was all-cause mortality at 23 months. RESULTS: The study included 157 patients with 33 (21.0%) in the bivalirudin cohort and 124 (79.0%) in the control cohort. Net adverse clinical events during hospitalization in the bivalirudin cohort were higher than that in the control cohort [9 (27.3%) vs. 14 (11.3%), P = .021]. However, there was no significant difference in all-cause mortality at 23 months between the 2 cohorts [25 (20.2%) vs. 10 (30.3%), P =.214]. After adjusting for potential confounders, the usage of bivalirudin was not associated with net adverse clinical event (odds ratio = 0.90; 95% CI: 0.18-4.45; P =.890), and the hazard ratio for all-cause mortality at 23 months was 1.01 (95% CI: 0.33-3.15; P =.983). CONCLUSION: Bivalirudin appears to exhibit a similar impact as unfractionated heparin on patients with acute coronary syndrome undergoing rotational atherectomy in real-life setting.

Quantitative flow ratio derived pullback pressure gradient and CZT-SPECT measured longitudinal flow gradient for hemodynamically significant coronary artery disease.

BACKGROUND: Whether physiological coronary diffuseness assessed by quantitative flow reserve (QFR) pullback pressure gradient (PPG) correlates with longitudinal myocardial blood flow (MBF) gradient and improves diagnostic performances for myocardial ischemia remains unknown. METHODS AND RESULTS: MBF was measured in mL g-1 min-1 with 99mTc-MIBI CZT-SPECT at rest and stress, corresponding myocardial flow reserve (MFR = MBF stress/MBF rest) and relative flow reserve (RFR = MBF stenotic area/MBF reference) were calculated. Longitudinal MBF gradient was defined as apical and basal left ventricle MBF gradient. △longitudinal MBF gradient was calculated by longitudinal MBF gradient at stress and rest. QFR-PPG was acquired from virtual QFR pullback curve. QFR-PPG significantly correlated with hyperemic longitudinal MBF gradient (r = 0.45, P = 0.007) and △longitudinal MBF gradient (stress-rest) (r = 0.41, P = 0.016). Vessels with lower RFR had lower QFR-PPG (0.72 vs. 0.82, P = 0.002), hyperemic longitudinal MBF gradient (1.14 vs. 2.22, P = 0.003) and △longitudinal MBF gradient (0.50 vs. 1.02, P = 0.003). QFR-PPG, hyperemic longitudinal MBF gradient and △longitudinal MBF gradient showed comparable diagnostic performances for predicting decreased RFR (area under curve [AUC]: 0.82 vs. 0.81 vs. 0.75, P = NS) or QFR (AUC: 0.83 vs. 0.72 vs. 0.80, P = NS). In addition, QFR-PPG and QFR in combination showed incremental value compared with QFR for predicting RFR (AUC = 0.83 vs. 0.73, P = 0.046, net reclassification index = 0.508, P = 0.001). CONCLUSION: QFR-PPG significantly correlated with longitudinal MBF gradient and △longitudinal MBF gradient when used for physiological coronary diffuseness assessment. All three parameters had high accuracy in predicting RFR or QFR. Adding physiological diffuseness assessment increased accuracy for predicting myocardial ischemia.

Comparison of 2D-QCA, 3D-QCA and coronary angiography derived FFR in predicting myocardial ischemia assessed by CZT-SPECT MPI.

BACKGROUND: Angiography derived fractional flow reserve (angio-FFR) has been proposed. This study aimed to assess its diagnostic performance with cadmium-zinc-telluride single emission computed tomography (CZT-SPECT) as reference. METHODS AND RESULTS: Patients underwent CZT-SPECT within 3 months of coronary angiography were included. Angio-FFR computation was performed using computational fluid dynamics. Percent diameter (%DS) and area stenosis (%AS) were measured by quantitative coronary angiography. Myocardial ischemia was defined as a summed difference score ≥ 2 in a vascular territory. Angio-FFR ≤ 0.80 was considered abnormal. 282 coronary arteries in 131 patients were analyzed. Overall accuracy of angio-FFR to detect ischemia on CZT-SPECT was 90.43%, with a sensitivity of 62.50% and a specificity of 98.62%. The diagnostic performance (= area under ROC = AUC) of angio-FFR [AUC = 0.91, 95% confidence intervals (CI) 0.86-0.95] was similar as those of %DS (AUC = 0.88, 95% CI 0.84-0.93, p = 0.326) and %AS (AUC = 0.88, 95% CI 0.84-0.93 p = 0.241) by 3D-QCA, but significantly higher than those of %DS (AUC = 0.59, 95% CI 0.51-0.67, p < 0.001) and %AS (AUC = 0.59, 95% CI 0.51-0.67, p < 0.001) by 2D-QCA. However, in vessels with 50-70% stenoses, AUC of angio-FFR was significantly higher than those of %DS (0.80 vs. 0.47, p < 0.001) and %AS (0.80 vs. 0.46, p < 0.001) by 3D-QCA and %DS (0.80 vs. 0.66, p = 0.036) and %AS (0.80 vs. 0.66, p = 0.034) by 2D-QCA. CONCLUSION: Angio-FFR had a high accuracy in predicting myocardial ischemia assessed by CZT-SPECT, which is similar as 3D-QCA but significantly higher than 2D-QCA. While in intermediate lesions, angio-FFR is better than 3D-QCA and 2D-QCA in assessing myocardial ischemia.

Transcription factor 21 accelerates vascular calcification in mice by activating the IL-6/STAT3 signaling pathway and the interplay between VSMCs and ECs.

Vascular calcification is caused by the deposition of calcium salts in the intimal or tunica media layer of the aorta, which increases the risk of cardiovascular events and all-cause mortality. However, the mechanisms underlying vascular calcification are not fully clarified. Recently it has been shown that transcription factor 21 (TCF21) is highly expressed in human and mouse atherosclerotic plaques. In this study we investigated the role of TCF21 in vascular calcification and the underlying mechanisms. In carotid artery atherosclerotic plaques collected from 6 patients, we found that TCF21 expression was upregulated in calcific areas. We further demonstrated TCF21 expression was increased in an in vitro vascular smooth muscle cell (VSMC) osteogenesis model. TCF21 overexpression promoted osteogenic differentiation of VSMC, whereas TCF21 knockdown in VSMC attenuated the calcification. Similar results were observed in ex vivo mouse thoracic aorta rings. Previous reports showed that TCF21 bound to myocardin (MYOCD) to inhibit the transcriptional activity of serum response factor (SRF)-MYOCD complex. We found that SRF overexpression significantly attenuated TCF21-induced VSMC and aortic ring calcification. Overexpression of SRF, but not MYOCD, reversed TCF21-inhibited expression of contractile genes SMA and SM22. More importantly, under high inorganic phosphate (3 mM) condition, SRF overexpression reduced TCF21-induced expression of calcification-related genes (BMP2 and RUNX2) as well as vascular calcification. Moreover, TCF21 overexpression enhanced IL-6 expression and downstream STAT3 activation to facilitate vascular calcification. Both LPS and STAT3 could induce TCF21 expression, suggesting that the inflammation and TCF21 might form a positive feedback loop to amplify the activation of IL-6/STAT3 signaling pathway. On the other hand, TCF21 induced production of inflammatory cytokines IL-1ß and IL-6 in endothelial cells (ECs) to promote VSMC osteogenesis. In EC-specific TCF21 knockout (TCF21ECKO) mice, VD3 and nicotine-induced vascular calcification was significantly reduced. Our results suggest that TCF21 aggravates vascular calcification by activating IL-6/STAT3 signaling and interplay between VSMC and EC, which provides new insights into the pathogenesis of vascular calcification. TCF21 enhances vascular calcification by activating the IL-6-STAT3 signaling pathway. TCF21 inhibition may be a new potential therapeutic strategy for the prevention and treatment of vascular calcification.

Metabolite profiling and identification in living cells by coupling stable isotope tracing and induced electrospray mass spectrometry.

Direct observation of metabolites in living cells by mass spectrometry offers a bright future for biological studies but also suffers a severe challenge to untargeted peak assignment to tentative metabolite candidates. In this study, we developed a method combining stable isotope tracing and induced electrospray mass spectrometry for living-cells metabolite measurement and identification. By using 13C6-glucose and ammonium chloride-15N as the sole carbon and nitrogen sources for cell culture, Escherichia coli synthesized metabolites with 15N and 13C elements. Tracing the number of carbon and nitrogen atoms could offer a complementary dimension for candidate peak searching. As a result, the identification confidence of metabolites achieved a universal improvement based on carbon/nitrogen labelling and filtration.

Combination of Colchicine and Ticagrelor Inhibits Carrageenan-Induced Thrombi in Mice.

The formation of a thrombus is closely related to oxidative stress and inflammation. Colchicine is one of the most commonly prescribed medication for gout treatment, with anti-inflammation and antioxidative stress properties. Therefore, we speculated that it is possible for colchicine to treat thrombosis. In this study, we used carrageenan to induce thrombosis in BALB/c mice and fed mice with colchicine, ticagrelor, and their combination, respectively. We found colchicine inhibited carrageenan-induced thrombi in mouse tail, and the inhibition was enhanced by ticagrelor. In vitro, colchicine inhibited thrombin-induced retraction of human platelet clots. Mechanically, colchicine inhibited platelet activation by reducing the expression of platelet receptors, protease-activated receptor 4 (PAR4) and CD36, and inactivating of AKT and ERK1/2 pathways. Furthermore, in human umbilical vein endothelial cells (HUVECs), colchicine showed antioxidative stress effects through increasing protein expression of glutathione peroxidase-1 (GPx-1), and mRNA levels of forkhead box O3 (FOXO3a) and superoxide dismutase 2 (SOD2). In RAW264.7 cells, colchicine reduced LPS-enhanced inflammatory response through attenuating toll-like receptor 4 (TLR4) activation. In addition, colchicine reduced LPS or ox-LDL-induced monocyte adhesion to HUVECs by inhibiting intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) levels. Taken together, our study demonstrates that colchicine exerts antithrombotic function by attenuating platelet activation and inhibiting oxidative stress and inflammation. We also provide a potential new strategy for clinical treatment.

Increased serum bile acid level is associated with high-risk coronary artery plaques in an asymptomatic population detected by coronary computed tomography angiography.

BACKGROUND: There are limited data on the association between serum total bile acid level and coronary plaque characteristics. This study investigated the relationship between serum total bile acid level and the severity of coronary stenosis and coronary plaque features in an asymptomatic population using coronary computed tomography angiography (CTA). METHODS: A total of 1,137 consecutive participants with no known coronary artery disease (CAD) undergoing CTA as part of a general routine health evaluation were recruited. Serum total bile acid level and clinical parameters were assayed. Coronary stenosis and high-risk plaques features (napkin-ring sign, low-attenuation plaque, spotty calcification, positive remodelling) were evaluated. Associations between serum total bile acid concentration and high-risk coronary plaques was tested through univariate and multivariate analyses. RESULTS: A total of 101 high-risk coronary plaques subjects and 93 controls were eligible for study inclusion. The severity of coronary artery stenosis and high-risk coronary plaques increased with serum total bile acid level quartiles (all P<0.001). The independent predictor of high-risk coronary plaques in multivariate analysis was serum total bile acid level (P<0.001). Receiver operating characteristic (ROC) confirmed that serum total bile acid concentration significantly differentiated high-risk coronary plaques [the area under the curve (AUC) =0.876; P<0.001, with a sensitivity of 87.13% and a specificity of 86.02%]. CONCLUSIONS: Higher serum total bile acid level was associated with the severity of coronary artery stenosis and high-risk coronary artery plaques detected by CTA in asymptomatic populations.

Efficacy Evaluation of High-Dose Atorvastatin Pretreatment in Patients with Acute Coronary Syndrome: A Meta-Analysis of Randomized Controlled Trials.

BACKGROUND It is unclear whether high-dose atorvastatin pretreatment benefits acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI). To clarify this issue, we performed a meta-analysis of the published literature. MATERIAL AND METHODS Randomized controlled trials (RCTs) assessing high-dose atorvastatin pretreatment in ACS patients undergoing PCI were enrolled. Short-term major adverse cardiac events (MACEs), changes in serum high-sensitivity C-reactive protein (hs-CRP), peak creatine kinase-myocardial band (CK-MB) level, and thrombolysis in myocardial infarction (TIMI) grade 3 flow after PCI were studied as clinical outcomes. RESULTS Seventeen RCTs including 10 072 patients were retrieved. High-dose atorvastatin showed greater benefits in reducing the incidence of short-term MACEs (OR 0.72; 95% CI: 0.56 to 0.94; P=0.01) and hs-CRP level (SMD -1.59; 95% CI: -2.38 to -0.80; P<0.0001) among ACS patients after PCI. No significant difference was found between the 2 groups in terms of peak CK-MB (SMD -0.34; 95% CI: -0.79 to 0.10; P=0.13) or final TIMI flow grade 3 (OR 1.31; 95% CI: 0.73 to 2.36; P=0.36) after PCI. High-dose atorvastatin therapy also was not associated with alanine aminotransferase (ALT) elevation (OR 1.95; 95% CI: 0.95 to 4.03; P=0.07). CONCLUSIONS The results of this meta-analysis suggest that high-dose atorvastatin pretreatment reduces the incidence of short-term MACEs and hs-CRP level without increasing drug-induced hepatotoxicity in ACS patients after PCI.

Luteolin alleviates NLRP3 inflammasome activation and directs macrophage polarization in lipopolysaccharide-stimulated RAW264.7 cells.

Pure plant extract luteolin has been demonstrated to possess numerous biological effects. However, the specific effect of luteolin on macrophage polarization and NOD-like receptor protein 3 (NLRP3) inflammasome activation has not been documented. In this study, Cultured RAW264.7 cells were treated with or without luteolin in the presence or absence of LPS. Subsequently, cell viability was tested by CCK-8 assay. Total reactive oxygen species (ROS) were measured by flow cytometry. NLRP3, apoptosis-associated speck-like protein containing CARD (ASC), caspase-1, inducible nitric oxide synthase (iNOS) and Arginase (Arg-1) protein expression was detected using western blotting. Enzyme-linked immunosorbent assay (ELISA) kits were used to detect the level of TNF-α, IL-18, and Interleukin-1ß (IL-1ß). Increased production of ROS and expression of NLRP3, ASC, caspase-1, IL-18 and IL-1ß proteins were observed in RAW264.7 cells incubated with LPS and were effectively inhibited by 2 µM luteolin. Furthermore, 2 µM luteolin pretreatment enhanced the expression of M2 macrophage markers (Arg-1 and IL-10), and decreased the expression of markers associated with M1 macrophage polarization (TNF-α, IL-6 and iNOS). These results indicated that low-dose luteolin inhibits NLRP3 inflammasomes activation and promotes macrophage polarization toward an M2 phenotype, which provides new evidence for the anti-inflammation activity of luteolin.

SIRT2 decreases atherosclerotic plaque formation in low-density lipoprotein receptor-deficient mice by modulating macrophage polarization.

Compelling evidence has demonstrated that the M1 macrophage phenotype is central to atherosclerotic lesion development. SIRT2, an NAD+-dependent sirtuin deacetylase, is involved in modulating macrophage polarization. However, the role of SIRT2 in atherosclerotic progression remains unknown. Female LDL receptor knockout (LDLr-/-) mice were randomly divided into four groups for treatment with saline, empty lentivirus, lentivirus-SIRT2, or shRNA-SIRT2 for 4 weeks. Thereafter, the mice were fed an atherogenic high-fat diet (HFD) for another 8 weeks. Atherosclerotic plaques were assessed in the aortic sinus by morphometry, immunohistochemistry and immunofluorescence analyses. Aortic levels of macrophage polarization markers were analysed by Western blot and immunofluorescence analyses. We found that lentivirus-SIRT2-treated LDLr-/- mice had decreased plaque areas in the aortic sinus and developed a more stable plaque phenotype, as shown by decreased macrophage infiltration and apoptosis. In addition, treatment with lentivirus-SIRT2 significantly reduced the expression of iNOS (inducible nitric oxide synthase) and increased the levels of ARG-1 (arginase-1) in atheromas. These findings suggest that SIRT2 inhibited atherosclerotic plaque progression and enhanced plaque stability in LDLr-/- mice by inhibiting macrophage polarization towards the M1 phenotype.

Qualitative and quantitative evaluation of dynamic changes in non-culprit coronary atherosclerotic lesion morphology: a longitudinal OCT study.

AIMS: There is limited in vivo evidence regarding the temporal evolution of non-culprit coronary plaque morphology. We aimed to evaluate changes in non-culprit plaque morphology over time by optical coherence tomography (OCT). METHODS AND RESULTS: Seventy-two (72) patients with 257 non-culprit segments with serial OCT studies were analysed. Non-culprit 5 mm-long coronary segments from the same imaged region were matched between baseline and follow-up. OCT plaque characterisation including automated attenuation analysis was performed, and changes over a median follow-up of 6.2 months were evaluated. On segment level, lumen area decreased from baseline to follow-up, whereas fibrous cap thickness increased. Similarly, plaque attenuation indices at follow-up were significantly decreased. Minimal cap thickness per patient did not change. In 68.5% of segments, plaque morphology did not change. Favourable change was observed in 18.4% of segments and unfavourable in 12.9%. There were no robust clinical predictors of change in plaque morphology. Attenuation analysis supported the qualitative characterisation, showing significantly different attenuation between different plaque types. CONCLUSIONS: In non-culprit coronary segments of patients with coronary artery disease under standard medical therapy, segment-level but not patient-level minimum fibrous cap thickness increases over time, with observations of both favourable and unfavourable changes in individual segments.

Luteolin improves cardiac dysfunction in heart failure rats by regulating sarcoplasmic reticulum Ca2+-ATPase 2a.

We previously found that luteolin (Lut) appeared to improve the contractility of cardiomyocytes during ischemia/reperfusion in rats. The enhancement was associated with the alteration in sarcoplasmic reticulum Ca2+-ATPase 2a (SERCA2a). This finding prompted us to consider if the mechanism worked in heart failure (HF). We studied the regulation of SERCA2a by Lut in failing cardiomyocytes and intact heart of rats. Improvement of contractility and the mechanisms centered on SERCA2a were studied in isolated cardiomyocytes and intact heart. We found that Lut significantly improved contractility and Ca2+ transients, ameliorated expression, activity and stability of SERCA2a and upregulated expression of small ubiquitin-related modifier (SUMO) 1, which is a newfound SERCA2a regulator. Lut also increased phosphorylation of protein kinase B (Akt), phospholaban (PLB) and sumoylation of SERCA2a, specificity protein 1 (Sp1). Transcriptions of SUMO1 and SERCA2a were concurrently increased. Inhibition of posphatidylinositol 3 kinase/Akt (PI3K/Akt) pathway and SERCA2a activity both markedly abolished Lut-induced benefits in vitro and in vivo. Lut upregulated the expression ratio of Bcl-2/Bax, caspase-3/cleaved-Caspase3. Meanwhile, Lut ameliorated the myocardium fibrosis of HF. These discoveries provide an important potential therapeutic strategy that Lut targeted SERCA2a SUMOylation related to PI3K/Akt-mediated regulations on rescuing the dysfunction of HF.

Safety of optical coherence tomography in daily practice: a comparison with intravascular ultrasound.

AIMS: Previous studies have reported the safety and feasibility of both time-domain optical coherence tomography (TD-OCT) and Fourier-domain OCT (FD-OCT) in highly selected patients and clinical settings. However, the generalizability of these data is limited, and data in unselected patient populations reflecting a routine cathlab practice are lacking. We compared safety of intracoronary FD-OCT imaging to intravascular ultrasound (IVUS) imaging in a large real-world series of consecutive patients who underwent invasive imaging during coronary catheterization in our centre. METHODS AND RESULTS: This is a prospective, single-centre registry of patients scheduled for coronary angiography or intervention undergoing intracoronary imaging with FD-OCT or IVUS between April 2008 and December 2013. Intra-procedural and major in-hospital adverse events that could be possibly related to invasive imaging were registered routinely by the operator as part of our clinical report and prospectively recorded in our database. These events were retrospectively individually adjudicated by an independent safety committee. Between April 2008 and December 2013, 13 418 diagnostic or interventional coronary catheterization procedures were performed. Of these, 1142 procedures used OCT and 2476 procedures used IVUS. Invasive imaging-related complications were rare, did not differ between the two imaging methods (OCT: n = 7, 0.6%; IVUS: n = 12, 0.5%; P = 0.6), and were self-limiting after retrieval of the imaging catheter or easily treatable in the catheterization laboratory. No major adverse events, prolongation of hospital stay, or permanent patient harm was observed. CONCLUSION: FD-OCT is safe in an unselected and heterogeneous group of patients with varying clinical settings.

Luteolin Attenuates Foam Cell Formation and Apoptosis in Ox-LDL-Stimulated Macrophages by Enhancing Autophagy.

BACKGROUND: Our previous studies demonstrated that luteolin, which is rich in flavones, has various biological properties and can exert anti-oxidant, anti-inflammatory and anti-apoptotic activities. However, its effect on ox-LDL-induced macrophage lipid accumulation and apoptosis has not been revealed. AIMS: This study aimed to explore the role of luteolin in ox-LDL-induced macrophage-derived foam cell formation and apoptosis and to delineate the underlying mechanism. METHODS: Murine RAW264.7 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) (50 µg/ml) for 24 h and then pretreated with 25 µM luteolin for another 24 h. The effects of luteolin on lipid accumulation in RAW264.7 cells induced by ox-LDL were assayed using Oil red O staining and high performance liquid chromatography (HPLC). Apoptosis was confirmed by acridine orange/ethidium bromide (AO/EB) staining, flow cytometric analysis and the TUNEL assay. Immunofluorescence, Western blot and monodansylcadaverine (MDC) staining analyses were then used to further investigate the molecular mechanisms by which luteolin protects macrophages from ox-LDL-induced foam cell formation and apoptosis. 3-Methyladenine (3-MA), an autophagy inhibitor, was used as a positive control. RESULTS: Treatment with 25 µM luteolin not only significantly attenuated ox-LDL-induced macrophage lipid accumulation but also decreased the apoptotic rate of RAW264.7 cells, the number of TUNEL-positive macrophages and the expression of Bax, Bak, cleaved caspase-9 and cleaved caspase-3. In addition, luteolin pretreatment significantly increased autophagosome formation and Beclin-1 activity, thus increasing the ratio of LC3-II/LC3-I. Moreover, these effects were abolished by 3-MA. CONCLUSIONS: Taken together, these results highlight that luteolin treatment attenuates foam cell formation and macrophage apoptosis by promoting autophagy and provide new insights into the molecular mechanism of luteolin and its therapeutic potential in the treatment of atherosclerosis.

Coronary Plaque Characteristics Affect No-Reflow During Primary Percutaneous Coronary Intervention: A Pooled Analysis of 14 Observational Studies Using Intravascular Ultrasound.

The association between coronary plaque composition and no-reflow during percutaneous coronary intervention (PCI) is still debated. We performed a systematic literature search using MEDLINE, Embase, Cochrane, and Ovid databases for intravascular ultrasound (IVUS) studies evaluating the relationship between coronary plaque characteristics and no-reflow after PCI. Fourteen observational trials were included in the meta-analysis, including 1457 patients (237 in the no-reflow group, 1220 in the normal reflow group). Pooled analysis indicated that the no-reflow group had a significantly higher absolute volume of fibrofatty plaque (weighted mean differences [WMD], 4.94 mm(3); 95% confidence interval [CI], 1.83-l8.06; P = .002), external elastic membrane cross-sectional area (EEM-CSA) (WMD, 3.40 mm2; 95% CI, 2.22-4.58; P = .00001), plaque area (WMD, 4.06 mm(2); 95% CI, 2.24-5.89; P = .0001), and artery remodeling index (WMD, 0.09; 95% CI, 0.06-0.13; P = .00001), and a smaller percentage of fibrous plaque (WMD, -5.89 %; 95% CI, -0.66 to -11.12; P = .03) than in the normal reflow group. There were no significant differences in the other plaque components between the two groups. This meta-analysis confirmed that high absolute volume of fibrofatty plaque, EEM-CSA, plaque area, and coronary artery remodeling index, and a decreased percentage of fibrous plaque as detected by IVUS in culprit lesions, are linked with the development of the no-reflow phenomenon after PCI.

Critical analysis of the correlation between optical coherence tomography versus intravascular ultrasound and fractional flow reserve in the management of intermediate coronary artery lesion.

The appropriate assessment of intermediate coronary artery stenosis continues to be a challenge for cardiologists. Several studies have shown that anatomic parameters obtained by intravascular ultrasound (IVUS) and optical coherence tomography (OCT) showed a correlation with fractional flow reserve (FFR) values in identifying hemodynamically severe coronary stenoses. However, the efficacy of IVUS/OCT versus FFR integration in intermediate coronary lesions is still debated. This review will allow for an independent analysis of research data and outlines the diagnostic efficiency of IVUS and OCT derived-anatomical parameters in identifying the hemodynamic significance of an angiographically intermediate stenosis as determined by FFR.