PET evaluation of myocardial perfusion function after percutaneous coronary intervention in patients with chronic total occlusion: a systematic review and meta-analysis.

Objective. The benefit of percutaneous coronary intervention (PCI) in chronic complete coronary artery occlusion (CTO) remains controversial. PCI is currently indicated only for symptom and myocardial ischemia abolition, but large chronically occluded vessels with extensive afferent myocardial territories may benefit most from this procedure. The noninvasive evaluation of myocardial perfusion is critical before and after revascularization, and positron emission tomography (PET) can determine absolute myocardial perfusion. Here, we aimed to explore and compare myocardial perfusion in CTO territories and their remote associated areas before and after PCI. Design. We searched for relevant articles published before November 28, 2022, in the Cochrane Library and PubMed. We calculated 95% confidence intervals (CIs) and standardized mean differences (SMDs) for parameters related to myocardial perfusion in CTO territories and remote areas in CTO patients before and after PCI. Results. We included five studies published between 2017 and 2022, with a total of 592 patients. Stress myocardial blood flow (MBF) was increased in CTO territories after PCI when compared to pre-PCI (mean difference [MD]: 1.70, 95% confidence interval [CI] 1.33-2.08, p < 0.001). Coronary flow reserve (CFR) in CTO regions was also higher after PCI (MD 1.37,95% [CI]1.13-1.61, p < 0.001). Stress MBF in remote regions was also increased after PCI (MD 0.27,95% [CI]0.99 ∼ 0.45, p = 0.004), as was CFR in remote regions (MD 0.32,95% [CI] 0.14-0.5, p = 0.001). Conclusions. According to our pooled analysis of current literature, there was an increase in stress MBF and CFR in both CTOs and remote regions after PCI, suggesting that patients with CTO have widespread recovery of blood perfusion after the procedure. These results provide evidence that patients with CTO arteries and high ischemic burdens would indeed benefit from CTO-PCI. Future research on the correlation of ischemia burden reduction with hard clinical endpoints would contribute to a clearer demarcation of the role of CTO PCI with prognostic potential.

The Chains of Ferroptosis Interact in the Whole Progression of Atherosclerosis.

Atherosclerosis (AS), a category of cardiovascular disease (CVD) that can cause other more severe disabilities, increasingly jeopardizes human health. Owing to its imperceptible and chronic symptoms, it is hard to determine the pathogenesis and precise therapeutics for AS. A novel type of programmed cell death called ferroptosis was discovered in recent years that is distinctively different from other traditional cell death pathways in morphological and biochemical aspects. Characterized by iron overload, redox disequilibrium, and accumulation of lipid hydroperoxides (L-OOH), ferroptosis influences endothelial cells, vascular smooth muscle cells (VSMCs), and macrophages, as well as inflammation, partaking in the pathology of many cardiovascular diseases such as atherosclerosis, stroke, ischemia-reperfusion injury, and heart failure. The mechanisms behind ferroptosis are so sophisticated and interwoven that many molecules involved in this procedure are unknown. This review systematically depicts the initiation and modulation of ferroptosis and summarizes the contribution of ferroptosis to AS, which may open a feasible approach for target treatment in the alleviation of AS progression.

Evaluation of left ventricular diastolic function in patients with coronary microvascular dysfunction via cardiovascular magnetic resonance feature tracking.

Background: Coronary microvascular dysfunction (CMD) has been suggested to be one of the pathologic mechanisms contributing to heart failure with preserved left ventricular ejection fraction (LVEF) and left ventricular (LV) diastolic dysfunction. We therefore aimed to evaluate LV diastolic function in patients with CMD using cardiovascular magnetic resonance feature tracking (CMR-FT). Methods: We prospectively enrolled 115 patients referred to cardiology clinics for chest pain assessment who subsequently underwent coronary computed tomography angiogram and stress perfusion CMR. CMD was defined as the presence of subendocardial inducible ischemia detected through visual assessment. LV diastolic function was evaluated using CMR-derived volume-time curves and CMR-FT parameters. The former included early peak filling rate (PFR) and time to PFR; the latter included LV global/regional peak longitudinal diastolic strain rate (LDSR), circumferential diastolic strain rate (CDSR), and radial diastolic strain rate (RDSR). Results: A total of 92 patients with 1,312 segments were eventually included. Of these, 19 patients were classified as non-CMD (48.8±11.2 years; 63.2% male) and 73 as with CMD (52.3±11.9 years; 54.8% male). The LVEFs were similar and preserved in both groups (P=0.266). At the per-patient level, no differences were observed in PFR, time to PFR, or LV global diastolic strain rates between the two groups. At the per-segment level, 51% (665/1,312) of the myocardial segments were classified as CMD, whereas 49% (647/1,312) were classified as non-CMD. CMD segments showed significantly lower regional CDSR (P=0.019) and RDSR (P=0.006) compared with non-CMD segments. Conclusions: Despite normal LV ejection fraction in CMD patients, decreased LV diastolic function in CMD myocardial segments indicates early diastolic impairment.

The therapeutic efficacy and clinical translation of mesenchymal stem cell-derived exosomes in cardiovascular diseases.

Exosomes, mainly derived from mesenchymal stem cells, provide a good reference for cardiac function repair and clinical application in cardiac and vascular diseases by regulating cardiomyocyte viability, inflammatory levels, angiogenesis, and ventricular remodeling after a heart injury. This review presents the cardioprotective efficacy of mesenchymal stem cell-originated exosomes and explores the underlying molecular mechanisms. Furthermore, we expound on several efficient approaches to transporting exosomes into the heart in clinical application and comment on the advantages and disadvantages of each method.

Bone Marrow Mesenchymal Stem Cell-Derived Exosomes Alleviate Diabetic Kidney Disease in Rats by Inhibiting Apoptosis and Inflammation.

BACKGROUND AND AIMS: Previous studies have confirmed the anti-inflammation effect of bone marrow mesenchymal stem cell-derived exosomes (BMSC-Exo). We aimed to investigate the therapeutic effect of BMSC-Exo on diabetic kidney disease (DKD), as well as the underlying mechanisms. METHODS: SD rats were induced by streptozotocin combined with a high-fat diet to establish a diabetes disease model. BMSCs-Exo were injected via tail veins at a weekly dose of 100 µg for 12 weeks. Pathological changes in the rat kidneys were evaluated using HE, Masson, and Periodic Acid-Schiff and immunohistochemical staining. TUNEL staining and western blot were used to evaluate the expression levels of apoptosis-related proteins in the rat kidney cells. The TNF-α level was detected by PCR and NF-κB (p65) by western blotting to examine the inflammatory responses in the renal tissue. RESULTS: BMSCs-Exo significantly alleviated the renal structural damage and the distribution of apoptotic cells in diabetic rats. Furthermore, BMSCs-Exo increased the expression of pro-apoptosis protein Bax and decreased the expression of apoptosis-executing protein Cleaved Caspase 9 and Cleaved caspase 3. In addition, the transcription level of TNF-α in kidney tissue and NF-κB (p65) expression was also decreased through BMSCs-Exo treatment. Besides, the levels of glucose (GLU), creatinine (Cr), and burea nitrogen (BUN) in diabetic rats were decreased by the BMSC-Exo treatment. CONCLUSIONS: BMSCs-Exo may alleviate diabetic kidney damage by inhibiting apoptosis and inflammation.

Drug-Coated Balloon-Only Strategy for De Novo Coronary Artery Disease: A Meta-analysis of Randomized Clinical Trials.

Backgrounds: Many clinical trials have demonstrated the value of drug-coated balloons (DCB) for in-stent restenosis. However, their role in de novo lesions is not well documented. The aim of this study is to evaluate the safety and efficacy of the DCB-only strategy compared to other percutaneous coronary intervention strategies for de novo coronary lesions. Methods: The PubMed, Embase, Web of Science, and Cochrane Library Central Register of Controlled Trials (CENTRAL) electronic databases were searched for randomized controlled trials published up to May 6, 2023. The primary outcomes were major adverse cardiac events and late lumen loss. Results: A total of eighteen trials with 3336 participants were included. Compared with drug-eluting stents, the DCB-only strategy was associated with a similar risk of major adverse cardiac events (risk ratio (RR) = 0.90; 95% confidence interval (CI): 0.59 to 1.37, P = 0.631) and a significant decrease in late lumen loss (standardized mean difference (SMD) = -0.29, 95% CI: -0.53 to -0.04, P = 0.021). This effect was consistent in subgroup analysis regardless of indication, follow-up time, drug-eluting stent type, and dual antiplatelet therapy duration. However, DCBs were inferior to DESs for minimum lumen diameter and percentage diameter stenosis. The DCB-only strategy showed significantly better outcomes for most endpoints compared to plain-old balloon angioplasty or bare metal stents. Conclusions: Interventions with a DCB-only strategy are comparable to those of drug-eluting stents and superior to plain-old balloon angioplasty or bare metal stents for the treatment of selected de novo coronary lesions. Additional evidence is still warranted to confirm the value of DCB before widespread clinical utilization can be recommended.

The cGAS-STING Pathway: A Ubiquitous Checkpoint Perturbing Myocardial Attributes.

As an innate immune route of defense against microbial infringement, cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) synthase (cGAS)- stimulator of interferon genes (STING) signaling does not simply participate in amplifying inflammatory responses via releasing type-I interferon (IFN) or enhance the expression of pro-inflammatory genes, but also interplays with multifarious pathophysiological activities, such as autophagy, apoptosis, pyroptosis, ferroptosis, and senescence in a broad repertoire of cells like endothelial cells, macrophages and cardiomyocyte. Thus, the cGAS-STING pathway is closely linked with aberrant heart morphologically and functionally via these mechanisms. The past few decades have witnessed an increased interest in the exact relationship between the activation of the cGAS-STING pathway and the initiation or development of certain cardiovascular diseases (CVD). A group of scholars has gradually investigated the perturbation of myocardium affected by the overactivation or suppression of the cGAS-STING. This review focuses on how the cGAS-STING pathway interweaves with other pathways and creates a pattern of dysfunction associated with cardiac muscle. This sets treatments targeting the cGAS-STING pathway apart from traditional therapeutics for cardiomyopathy and achieves better clinical value.

Regulation of cardiovascular and cardiac functions by caveolins.

Caveolae are intracellular vesicles with diameters ranging from 50 to 100 nm. The role of caveolins in mediating oxidative stress, autophagy, apoptosis, fibrosis, and vascular remodeling has attracted increasing attention in cardiovascular therapy. Several studies have suggested that caveolin could be a therapeutic target for the treatment of cardiac and/or vascular injury via several pathophysiological mechanisms. Despite substantial advances in our understanding of the basic biology of vesicles over the past decade, the relevance and specific role of these mechanisms in cardiovascular homeostasis remains ambiguous. Here, we review the macroscopic role of caveolins in protecting cardiac function and, at the microscopic level, examine possible cardioprotective caveolar mechanisms, including their antioxidative stress, antiapoptosis, autophagy-regulatory, antifibrosis, and angiogenesis-promoting properties. We believe that the role of caveolins in cardiac functioning has not been fully elucidated and is an important line of future research with several cardioprotective implications.

HbA1c is related to microcirculation blood perfusion in patients with coronary microvascular disease using stress perfusion cardiac magnetic resonance: An observational study.

BACKGROUND: In coronary microvascular disease (CMD) patients, the incidence of major adverse cardiovascular events (MACEs) in patients with myocardial perfusion reserve index (MPRI) ≤ 1.47 is three times higher than that in MPRI > 1.47. We investigated whether the increase of glycated hemoglobin A1c (HbA1c) could increase the risk of MPRI ≤1.47 in diabetic and non-diabetic patients. METHODS: From November 2019, patients with ischemic symptoms but without obstructive coronary disease were screened. Use MPRI measured by stress perfusion cardiac magnetic resonance (CMR) to reflect microcirculation blood perfusion, and MPRI <2.5 were included. The patients were divided into two groups based on MPRI was greater or <1.47. The risk factors for CMD were explored using logistic regression analysis. RESULTS: A total of 80 patients with an MPRI of 1.69 ± 0.79 were included. CMD patients with an MPRI of ≤1.47(n = 33) were higher than MPRI of >1.47(n = 47) in age, presence of diabetes mellitus, fasting blood glucose levels and HbA1c levels (P < 0.05). In non-diabetic patients, increased HbA1c was associated with the risk of MPRI≤1.47 (OR = 0.017, 95%CI: 0.050-1.107, P = 0.045). Compared with non-diabetic patients with HbA1c < 6.0, non-diabetic patients with HbA1c ≥ 6.0 increased the risk of MPRI of ≤1.47 (OR = 0.219, 95%CI: 0.069-0.697, P = 0.010). In diabetic patients, HbA1c was not associated with the risk of MPRI of ≤1.47 (OR = 1.043, 95%CI: 0.269, 4.044, P = 0.952). And compared with non-diabetic patients with HbA1c <6.0, diabetic patients with HbA1c <6.0 (OR = 0.917, 95%CI: 0.233-3.610, P = 0.901) or ≥6.0 (OR = 0.326, 95%CI: 0.073-1.446, P = 0.140), the risk of MPRI ≤ 1.47 was not further increased. CONCLUSIONS: In non-diabetic patients, elevated HbA1c is related to MPRI≤1.47(a value increased incidence of MACEs). Therefore, in patients with undiagnosed diabetes, early management of glycosylated hemoglobin is very important. TRIAL REGISTRATION: This clinical trial has been registered in the Chinese clinical Trial Registry with an identifier: ChiCTR1900025810.

Ginkgo biloba extract protects against diabetic cardiomyopathy by restoring autophagy via adenosine monophosphate-activated protein kinase/mammalian target of the rapamycin pathway modulation.

Studies demonstrated that Ginkgo biloba extract (GBE) played a cardioprotective role in diabetic conditions. Impaired autophagy is one of the mechanisms underlying diabetic cardiomyopathy (DCM). The effect of GBE on autophagy has been observed in several diseases; however, whether GBE can ameliorate DCM by regulating autophagy remains unclear. Here, we investigated the effect of GBE on DCM and the potential mechanisms regarding autophagy using a streptozotocin (STZ)-induced diabetic rat model and a high-glucose (HG)-stimulated H9C2 cell model. We demonstrated that GBE attenuated metabolic disturbances, improved cardiac function, and reduced myocardial pathological changes in diabetic rats. Impaired autophagy as well as dysregulation of the adenosine monophosphate-activated protein kinase/ mammalian target of the rapamycin (AMPK/mTOR) signaling pathway were observed in diabetic hearts, as evidenced by the reduced conversion of LC3B-I to LC3B-II along with excessive p62 accumulation, decreased AMPK phosphorylation, and increased mTOR phosphorylation, which could be reversed by GBE treatment. In vitro, GBE reduced the apoptosis induced by HG in H9C2 cells by activating AMPK and inhibiting mTOR to restore autophagy. However, this effect was inhibited by the AMPK inhibitor Compound C. In conclusion, the ameliorative effect of GBE on DCM might be dependent on the restoration of autophagy through modulation of the AMPK/mTOR pathway.

Exosomes as a Cell-free Therapy for Myocardial Injury Following Acute Myocardial Infarction or Ischemic Reperfusion.

Exosomes, which contain miRNA, have been receiving growing attention in cardiovascular therapy because of their role in mediating cell-cell communication, autophagy, apoptosis, inflammation, and angiogenesis. Several studies have suggested that miRNA derived from exosomes can be used to detect myocardial infarctions (MI) in patients. Basic research also suggests that exosomes could serve as a potential therapeutic target for treating acute myocardial infarction. Ischemia/reperfusion (IR) injury is associated with adverse cardiac events after acute MI. We aim to review the potential benefits and mechanisms of exosomes in treating MI and IR injury.

cGAS-STING Pathway Performance in the Vulnerable Atherosclerotic Plaque.

The important role of Ca2+ in pathogenic store-operated calcium entry (SOCE) is well-established. Among the proteins involved in the calcium signaling pathway, Stromal interacting molecule 1 (STIM1) is a critical endoplasmic reticulum transmembrane protein. STIM1 is activated by the depletion of calcium stores and then binds to another calcium protein, Orai1, to form a channel through which the extracellular Ca2+ can enter the cytoplasm to replenish the calcium store. Multiple studies have shown that increased STIM1 facilitates the aberrant proliferation and apoptosis of vascular smooth cells (VSMC) and macrophages which can promote the formation of rupture-prone plaque. Together with regulating the cytosolic Ca2+ concentration, STIM1 also activates STING through altered intracellular Ca2+ concentration, a critical pro-inflammatory molecule. The cGAS-STING pathway is linked with cellular proliferation and phenotypic conversion of VSMC and enhances the progression of atherosclerosis plaque. In summary, we conclude that STIM1/cGAS-STING is involved in the progression of AS and plaque vulnerability.

Quantitative coronary computed tomography angiography assessment of chronic total occlusion percutaneous coronary intervention.

Background: Morphological and clinical characteristics are widely used to predict the success of percutaneous coronary intervention (PCI) in patients with chronic total occlusion (CTO). However, the impact of quantitative characteristics derived from coronary computed tomography angiography (CCTA) on guidewire crossing and PCI success is still unclear. This study aimed to explore the association between these quantitative characteristics and the difficulty of PCI for CTO. Methods: A total of 207 CTO lesions from 201 patients (84.6% male; mean age 58.9 years) with pre-procedural CCTA scans who had undergone PCI for CTO were retrospectively enrolled in this case-control study. A semi-automated CCTA plaque-analysis software was adopted to obtain the total plaque volume and volume of each component according to the Hounsfield Unit (HU) value, including dense calcium (>351 HU), fibrous (131-350 HU), fibrofatty (76-130 HU), and necrotic core (-30-75 HU) tissue. Differences in the quantitative characteristics of the CTO lesions were compared between: (I) the group of lesions with successful guidewire crossing (≤30 min) and the group with failed guidewire crossing (≤30 min); (II) the group of lesions with procedural success [defined as achieving residual stenosis of <30% and a grade 3 thrombolysis in myocardial infarction (TIMI) flow] and the group with procedural failure. Logistic regression was used to explore the association of quantitative characteristics with successful guidewire crossing in ≤30 min and procedural success. Results: A total of 131 (63.3%) lesions of 126 patients achieved successful guidewire crossing in ≤30 min and 157 (75.8%) lesions of 152 (75.6%) patients achieved procedural success. Quantitative characteristics such as occlusion length, plaque volume, volume of dense calcium, and fibrous and fibrofatty tissue showed significant differences between the groups of lesions with successful guidewire crossing in ≤30 min and with failed guidewire crossing in ≤30 min, as well as the groups of lesions with procedural success and with procedural failure. According to the results of logistic regression analysis, lower percentages of dense calcium [odds ratio (OR) =0.970, 95% confidence interval (CI): 0.950 to 0.991; P=0.004] and fibrous (OR =0.970, 95% CI: 0.949 to 0.992; P=0.007) tissue and higher percentage of necrotic core tissue (OR =1.018, 95% CI: 1.005 to 1.030; P=0.005) were significantly associated with successful guidewire crossing in ≤30 min. Decreased percentages of dense calcium (OR =0.969; 95% CI: 0.949 to 0.989; P=0.002) and fibrous tissue (OR =0.966, 95% CI: 0.944 to 0.990; P=0.005) and higher percentage of necrotic core tissue (OR =1.022, 95% CI: 1.008 to 1.036; P=0.002) were associated with procedural success. After adjusting for cardiovascular risk factors, the percentages of dense calcium, fibrous, and necrotic core tissue were still associated with successful guidewire crossing in ≤30 min, and the quantitative parameters showed consistent association with procedural success. Conclusions: Quantitative characteristics derived from CCTA for CTO are associated with successful guidewire crossing and procedural success of PCI.

Efficacy of Colchicine in the Treatment of Patients With Coronary Artery Disease: A Mini-Review.

PURPOSE: This review of colchicine, an effective anti-inflammatory agent, examines whether the reduction in ischemic events produced by colchicine translates to a reduction in mortality, the optimal duration of treatment, and the patient populations that benefits the most from colchicine treatment. METHODS: We performed a comprehensive PubMed database search using the key words colchicine and coronary heart disease on August 23, 2021. We also screened the included reference list of manuscripts. FINDINGS: Colchicine's role in the secondary prevention of coronary artery disease has been the focus of recent large-scale randomized controlled trials in chronic coronary syndrome (ie, the Low-Dose Colchicine and Low-Dose Colchicine 2 trials), acute myocardial infarction (the Colchicine Cardiovascular Outcomes Trial and Colchicine in Patients With Acute Coronary Syndrome trial), and after percutaneous coronary intervention (the Colchicine-Percutaneous Coronary Intervention trial). IMPLICATIONS: Current evidence suggests that low-dose colchicine (0.5 mg once a day) reduces the risk of cardiovascular events among patients with acute myocardial infarction or chronic coronary syndrome. Colchicine has the potential to become a new standard therapy for the prevention of coronary artery disease-related atherothrombotic events because it is effective and cost-efficient and has a well-tolerated safety profile.

Pathophysiology and molecular mechanism of caveolin involved in myocardial protection strategies in ischemic conditioning.

Multiple pathophysiological pathways are activated during the process of myocardial injury. Various cardioprotective strategies protect the myocardium from ischemia, infarction, and ischemia/reperfusion (I/R) injury through different targets, yet the clinical translation remains limited. Caveolae and its structure protein, caveolins, have been suggested as a bridge to transmit damage-preventing signals and mediate the protection of ultrastructure in cardiomyocytes under pathological conditions. In this review, we first briefly introduce caveolae and caveolins. Then we review the cardioprotective strategies mediated by caveolins through various pathophysiological pathways. Finally, some possible research directions are proposed to provide future experiments and clinical translation perspectives targeting caveolin based on the investigative evidence.

Corrigendum: Myocardial Viability, Functional Status, and Collaterals of Patients With Chronically Occluded Coronary Arteries.

[This corrects the article DOI: 10.3389/fcvm.2021.754826.].

Comparison of successful versus failed percutaneous coronary intervention in patients with chronic total occlusion: A systematic review and meta-analysis.

BACKGROUND: The optimal treatment strategy of chronic total occlusion (CTO) is currently debated. This meta-analysis aimed to evaluate the long-term clinical outcomes of successful percutaneous coronary intervention (PCI) of CTO. METHODS: Electronic databases were searched for studies comparing long-term outcomes between successful PCI in patients with CTO using drug-eluting stents and failed procedures. Meta-analysis was conducted with major adverse cardiac events (MACE) and all-cause mortality during the longest follow-up as endpoints. The combined hazard ratios (HRs) were applied to assess the correlation between successful CTO PCI and MACE/all-cause mortality. RESULTS: Eight studies consisting of 6,211 patients published between 2012 and 2020 met our inclusion criteria, and the CTO PCI success rate was 81.2%. Patients in the failed group were much older, and more likely to have morbidities (hypertension and prior myocardial infarction), reduced left ventricular ejection fraction, and severe lesion characteristics (multivessel disease and moderate/severe calcification). Pooled results indicated that successful CTO PCI was significantly associated with prognosis. Compared to failed recanalization, patients receiving successful procedures had an improved MACE (HR: 0.50, 95% CI: 0.40-0.61, p < 0.001). Subgroup analyses further revealed the prognostic value of successful CTO PCI. However, no difference was observed regarding all-cause mortality (HR: 0.79, 95% CI: 0.61-1.02, p = 0.074). CONCLUSIONS: The present study showed that CTO recanalization was associated with improved long-term outcomes. However, randomized trials are needed to confirm the results due to the mismatch of baseline characteristics.

A Novel Classification for Predicting Chronic Total Occlusion Percutaneous Coronary Intervention.

Aims: Chronic total occlusion (CTO) percutaneous coronary intervention (PCI) is characterized by a low success rate and an increase in complications. This study aimed to explore a new and simple classification method based on plaque composition to predict guidewire (GW) crossing within 30 min of CTO lesions. Methods: This study consecutively enrolled individuals undergoing attempted PCI of CTO who underwent coronary computed tomographic angiography (CCTA) within 2 months. Lesions were divided into soft and hard CTO groups according to the necrotic core proportion. Results: In this study, 207 lesions were divided into soft (20.3%) and hard CTO (79.7%) groups according to a necrotic core percentage cutoff value of 72.7%. The rate of successful GW crossing within 30 min (57.6 vs. 85.7%, p = 0.004) and final success (73.3 vs. 95.2%, p = 0.001) were much lower in the hard CTO group. For patients with hard CTO, previous failed attempt, proximal side branch, bending > 45 degrees calcium ≥ 50% cross-sectional area (CSA), and distal reference diameter ≤ 2.5 mm were demonstrated to be associated with GW failure within 30 min. For patients with soft CTO, only blunt entry was proved to be an independent predictive factor of GW failure within 30 min. Conclusions: Grouping CTO lesions according to the proportion of necrotic core is reasonable and necessary in predicting GW crossing within 30 min. A soft CTO with a necrotic core is more likely to be recanalized compared with a hard CTO with fibrous and/or dense calcium. Different plaque types have variable predictive factors.