Comparison of intravascular ultrasound-guided with angiography-guided double kissing crush stenting for patients with complex coronary bifurcation lesions: Rationale and design of a prospective, randomized, and multicenter DKCRUSH VIII trial.

BACKGROUND: Double kissing (DK) crush approach for patients with coronary bifurcation lesions, particularly localized at distal left main or lesions with increased complexity, is associated with significant reduction in clinical events when compared with provisional stenting. Recently, randomized clinical trial has demonstrated the net clinical benefits by intravascular ultrasound (IVUS)-guided implantation of drug-eluting stent in all-comers. However, the improvement in clinical outcome after DK crush treatment guided by IVUS over angiography guidance for patients with complex bifurcation lesions have never been studied in a randomized fashion. TRIAL DESIGN: DKCRUSH VIII study is a prospective, multicenter, randomized controlled trial designed to assess superiority of IVUS-guided vs angiography-guided DK crush stenting in patients with complex bifurcation lesions according to DEFINITION criteria. A total of 556 patients with complex bifurcation lesions will be randomly (1:1 of ratio) assigned to IVUS-guided or angiography-guided DK crush stenting group. The primary end point is the rate of 12-month target vessel failure, including cardiac death, target vessel myocardial infarction, or clinically driven target vessel revascularization. The secondary end points consist of the individual component of primary end point, all-cause death, myocardial infarction, and in-stent restenosis. The safety end point is the incidence of definite or probable stent thrombosis. An angiographic follow-up will be performed for all patients at 13 months and clinical follow-up will be continued annually until 3 years after the index procedure. CONCLUSIONS: DKCRUSH VIII trial is the first study designed to evaluate the differences in efficacy and safety between IVUS-guided and angiography-guided DK crush stenting in patients with complex true bifurcation lesions. This study will also provide IVUS-derived criteria to define optimal DK crush stenting for bifurcation lesions at higher complexity.

Drug-Coated Balloon-Only Angioplasty Outcomes in Diabetic and Nondiabetic Patients with De Novo Small Coronary Vessels Disease.

BACKGROUND: The revascularization of small vessels using drug-eluting stents remains challenging. The use of the drug-coated balloon is an attractive therapeutic strategy in de novo lesions in small coronary vessels, particularly in the diabetic group. This study aimed to assess the outcomes of DCB-only angioplasty in small vessel disease. METHODS: A total of 1198 patients with small vessel disease treated with DCB-only strategy were followed. Patients were divided into the diabetic and nondiabetic groups. Clinical and angiographical follow-up were organized at 12 months. The primary endpoints were target lesion failure and secondary major adverse cardiac events. RESULTS: There was a significantly higher rate of target lesion failure among diabetic patients compared to nondiabetic [17 (3.9%) vs. 11 (1.4%), P=0.006], taken separately, the rate of target lesion revascularization significantly differed between groups with a higher rate observed in the diabetic group [9 (2%) vs. 4 (0.5%), P=0.014]. Diabetes mellitus remained an independent predictor for TLF (HR: 2.712, CI: 1.254-5.864, P=0.011) and target lesion revascularization (HR: 3.698, CI: 1.112-12.298, P=0.033) after adjustment. However, no significant differences were observed between groups regarding the target vessel myocardial infarction (0.6% vs. 0.1%, P=0.110) and MACE [19 (4.4%) vs. 21 (2.7%), P=0.120]. CONCLUSION: Drug-coated balloon-only treatment achieved lower incidence rates of TLF and MACE. Diabetes is an independent predictor for target lesion failure and target lesion revascularization at one year following DCB treatment in small coronary vessels. We observed no significant differences between groups regarding MACE in one year.

Association of long-term inhalation of caffeine-sodium benzoate with coronary heart disease in men.

OBJECTIVE: A possible correlation between caffeine and coronary heart disease (CHD) is controversial. The objective of this study was to explore the effect of long-term inhalation of caffeine-sodium benzoate (CSB) on the development of CHD in men, the severity of coronary artery lesions and the possible contributing effects of smoking. MATERIALS: A retrospective analysis was performed on 2,001 consecutive men who underwent selective coronary angiography. These men were assigned to a CSB inhalation group (CSB; 1 - 6 times/d, 274 - 1,644 mg/d, > 10 years; n = 326) or a non-inhalation group (non-CSB; n = 1,675). METHODS: The two groups were compared for the prevalence, onset age, and risk factors of CHD. The men were also stratified as CSB-only, smoking-only, combined CSB+ smoking, and the control (non-CSB+non-smoking). The prevalence, onset age, risk factors of CHD, and severity of coronary artery lesions and major adverse cardiovascular events (MACE) were compared among these groups. RESULTS: The prevalence of CHD in the CSB group was higher compared with the non-CSB group (91.72 vs. 86.09%, p < 0.01). In the CSB+smoking group, the percentages of men with CHD (93.11%) or > 70% stenosis of the coronary artery lesion (64.92%) were significantly higher than that of the smoking-only group (88.19 and 54.29%, respectively) or control (83.20 and 52.90%), while the percentage with stenosis involving the anterior descending branch was lower (62.30 vs. 72.29% and 74.17%, p < 0.01). CONCLUSION: Men who inhaled CSB long-term had a higher rate of CHD compared with those who did not take CSB. The combination of CSB inhalation and smoking appears to increase synergistically the risk and severity of CHD.

LncRNA FOXC2-AS1 protects cardiomyocytes from doxorubicin-induced cardiotoxicity through activation of WNT1-inducible signaling pathway protein-1.

Doxorubicin (Dox) is an anthracycline antibiotic that has been used to treat different cancers. Dox-induced cardiotoxicity is common in clinical practice, while its mechanism is unknown. It has been proved that lncRNA FOXC2-AS1 may promote doxorubicin resistance and WNT1-inducible signaling pathway protein-1 (WISP1) blocks doxorubicin-induced cardiomyocyte death. Our study aimed to investigate the involvement of lncRNA FOXC2-AS1 and WISP1 in doxorubicin-induced cardiotoxicity and to explore their interactions. In our study we observed that FOXC2-AS1 and WISP1 mRNA were downregulated in heart tissues of mice with Dox-induced cardiotoxicity. FOXC2-AS1 and WISP1 mRNA expression were positively correlated in mice with Dox-induced cardiotoxicity but not in healthy mice. Overexpression of FOXC2-AS1 promoted to viability of mice cardiomyocytes under Dox treatment and also increased the expression level of WISP1. In contrast, WISP1 overexpression showed no significant effect on FOXC2-AS1. We therefore conclude that lncRNA FOXC2-AS1 may upregulate WISP1 to protect cardiomyocytes from doxorubicin-induced cardiotoxicity.

Free triiodothyronine and global registry of acute coronary events risk score on predicting long-term major adverse cardiac events in STEMI patients undergoing primary PCI.

BACKGROUND: The aim of this study is to investigate the combined value of fT3 and GRACE risk score for cardiovascular prognosis in ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). METHODS: Three hundred and thirty eight patients with STEMI who received successful primary PCI were enrolled in our study. All patients underwent (33.5 ± 7.1) month's follow-up. Mace was defined as cardiac death and nonfatal myocardial infarction. RESULTS: Multivariate Cox analysis showed that both fT3 (HR = 0.462, 95%CI: 0.364-0.587, P < 0.001) and GRACE score (HR = 1.011, 95%CI: 1.004-1.018, P = 0.003) were independent predictors of Mace. Similarly, fT3 (HR = 0.495, 95%CI: 0.355-0.690, P < 0.001) and GRACE score (HR = 1.022, 95%CI: 1.011-1.034, P < 0.001) were the most important independent predictors of cardiac death. Kaplan-Meier analysis revealed that those patients with low fT3 and higher GRACE score had higher rates of Mace (Log-Rank χ2 = 25.087, P < 0.001). In ROC analysis, combining fT3 and GRACE risk score had a good area under the curve (AUC) value for Mace (AUC = 0.735, 95% CI: 0.680-0.790, P < 0.001), with net reclassification index of 11.1 and 5.3%, respectively. CONCLUSION: The low fT3 level, a common phenomenon, is a strong predictor of long-term poor prognosis in STEMI patients who underwent primary PCI. The combination of GRACE score and fT3 may be a more valuable predictor of Mace as compared to each measure alone.

Autophagy inhibits high glucose induced cardiac microvascular endothelial cells apoptosis by mTOR signal pathway.

Cardiac microvascular endothelial cells (CMECs) dysfunction is an important pathophysiological event in the cardiovascular complications induced by diabetes. However, the underlying mechanism is not fully clarified. Autophagy is involved in programmed cell death. Here we investigated the potential role of autophagy on the CMECs injury induced by high glucose. CMECs were cultured in normal or high glucose medium for 6, 12 and 24 h respectively. The autophagy of CMECs was measured by green fluorescence protein (GFP)-LC3 plasmid transfection. Moreover, the apoptosis of CMEC was determined by flow cytometry. Furthermore, 3-Methyladenine (3MA), ATG7 siRNA and rapamycin were administrated to regulate the autophagy state. Moreover, Western blotting assay was performed to measure the expressions of Akt, mTOR, LC3 and p62. High glucose stress decreased the autophagy, whereas increased the apoptosis in CMECs time dependently. Meanwhile, high glucose stress activated the Akt/mTOR signal pathway. Furthermore, autophagy inhibitor, 3-MA and ATG7 siRNA impaired the autophagy and increased the apoptosis in CMECs induced by high glucose stress. Conversely, rapamycin up-regulated the autophagy and decreased the apoptosis in CMECs under high glucose condition. Our data provide evidence that high glucose directly inhibits autophagy, as a beneficial adaptive response to protect CMECs against apoptosis. Furthermore, the autophagy was mediated, at least in part, by mTOR signaling.

Underexpression of CACNA1C Caused by Overexpression of microRNA-29a Underlies the Pathogenesis of Atrial Fibrillation.

BACKGROUND The objective of this study was to investigate the molecular mechanism of atrial fibrillation (AF), as well as the negative regulatory relationship between miR-29a-3p and CACNA1C. MATERIAL AND METHODS We searched the online miRNA database (www.mirdb.org) and identified the miR-29a-3p binding sequence within the 3'-UTR of the target gene, and then conducted luciferase assay to verify it. The cells were transfected with miR-29a-3p and ICa,L was determined in those cells. RESULTS We validated CACNA1C to be the direct target gene of miR-29a-3p. We also established the negative regulatory relationship between miR-29a-3p and CACNA1C via studying the relative luciferase activity. We also conducted real-time PCR and Western blot analysis to study the mRNA and protein expression level of CACNA1C among different groups of cells treated with scramble control, 30nM miR-29a-3p mimics, and 60nM miR-29a-3p mimics, indicating a negative regulatory relationship between miR-29a-3p and CACNA1C. We next analyzed whether miR-29a-3p transfection in cardiomyocytes produced the effects on the ICa,L induced by electrical remodeling, and found a tonic inhibition of IBa by endogenous miR-29a-3p in atrial myocytes. CONCLUSIONS We validated the negative regulation between miR-29a-3p and CACNA1C, and found that miR-29a-3p might a potential therapeutic target in the treatment of AF.

Periprocedural myocardial infarction is associated with increased mortality in patients with coronary artery bifurcation lesions after implantation of a drug-eluting stent.

OBJECTIVES: The present study aimed to investigate the association between periprocedural myocardial infarction (PMI), defined by creatine kinase (CK)-MB or troponin I (TNI) level elevations >5 times the 99 th percentile of the upper reference limit (URL) within 48 hr after implantation of a drug-eluting stent (DES), and one-year mortality in patients with coronary bifurcation. BACKGROUND: PMI is reported to be associated with increased one-year mortality after DES implantation. However, the prevalence and association of PMI with mortality after stenting bifurcation lesions remains unclear. METHODS: We prospectively followed 1,971 patients with true coronary bifurcations who underwent DES implantation as part of the multicenter DEFINITION study. These patients were grouped into categories based on PMI outcome: Non-PMI, CKMB-PMI, TNI-PMI, and CKMB/TNI-PMI. The primary endpoint was the rate of all-cause mortality at one year. RESULTS: PMI occurred in 11.4% of patients by CKMB criteria and 41.3% of patients by TNI criteria. At one-year follow-up, the mortality rate was 2.3% in the entire patient population. However, mortality was significantly higher in the CKMB-PMI (6.4%) and CKMB/TNI-PMI (6.1%) groups compared to the Non-PMI (1.7%) and TNI-PMI (2.1%) groups (all P < 0.05). A 10-fold increase in TNI levels resulted in similar PMI rate (5.2%) and mortality risk (adjusted HR 2.7, 95% CI 3.0-5.2) as a fivefold increase in CKMB levels. CONCLUSIONS: PMI, as defined by CKMB elevations following coronary bifurcation lesion stenting, was associated with increased one-year mortality. Additionally, to attain an equal frequency of PMI, the elevation in TNI levels needed to be twice as high as the elevation in CKMB levels.

Efficacy of different doses of atorvastatin treatment on serum levels of 8-hydroxy-guanin (8-OHdG) and cardiac function in patients with ischemic cardiomyopathy.

OBJECTIVE: To compare the efficacy of 40 mg and l0 mg atorvastatin on serum levels of 8-Hydroxy-Guanin (8-OHdG) and the cardiac function in patients with ischemic cardiomyopathy (ICM). METHODS: One hundred twenty three hospitalized ICM patients and 120 healthy controls were included in this study. All subjects were randomly divided into two groups: 10 mg/d atorvastatin group (n=62) and 40 mg/d atorvastatin group (n=61). Serum levels of C-reactive protein (CRP), creatine kinase, glutamic-pyruvic transaminase, lipids and B-type natriuretic peptide (BNP) were tested in all subjects both at the initial phase and the terminal phase of this study. Adverse drug reaction events were recorded in this study. Echocardiographic method was applied to compare the cardiac function before and after treatment in the double blind study. Serum 8-OHdG levels were tested by enzyme-linked immunosorbent assay (ELISA) before and after treatment, and the results in atorvastatin treatment groups were compared with the healthy controls. RESULTS: Serum 8-OHdG levels in ICM patients were significantly higher than that in normal control groups (p<0.05). There was significant difference of Serum 8-OHdG levels in 40 mg/d atorvastatin group (p<0.05), but was no significant difference in 10 mg/d atorvastatin group before and after the treatment. The 8-OHdG level in 40 mg/d atorvastatin group was significantly lower than that in 10 mg/d atorvastatin group before the treatment as well as after the treatment (p<0.05). The systolic and diastolic function improved significantly in 40 mg/d atorvastatin group before and after treatment, as well as in comparison with 10 mg/d atorvastatin group (p<0.05). CONCLUSION: Serum 8-OHdG possibly plays an important role in the pathogenesis of ICM. Atorvastatin is safe and effective in ICM treatment; furthermore atorvastatin which also has independent lipid lowering effect, is significantly better in the dose of 40 mg/day.

Lysophosphatidylcholine perpetuates macrophage polarization toward classically activated phenotype in inflammation.

Pro-inflammatory macrophages are involved in vascular inflammation and serve as the major effector cells in the pathophysiology of atherosclerosis. Phosphatidylcholine (PC) is a major phospholipid moiety affixed to oxidized low-density lipoprotein (oxLDL) and thought to play important roles in the development of atherosclerosis. In this study we described that a bioactive lipid derivative, lysophosphatidylcholine (lysoPC), generated from hydrolysis of the PC moiety of oxidized LDL, promoted and stabilized a strong M1 phenotype in macrophage polarization. Another derivative, 9-hydroxyoctadecadienoic acid (9-HODE), did not show the similar biological function. Blockade of G protein coupled receptor, G2A, which mediates the signal transduction of lysoPC, diminished the effects of lysoPC on the macrophage polarization toward M1 phenotype. The results provide insights into the new mechanism on how oxidized LDL participates in tissue inflammation in atherosclerosis.

Maslinic acid protects vascular smooth muscle cells from oxidative stress through Akt/Nrf2/HO-1 pathway.

Maslinic acid (MA) is a natural triterpenoid widely distributed in edible and medicinal plants and has been demonstrated to possess bioactivity. However, its effect on vascular smooth muscle cells (VSMC) has not been explored yet. In this study, we found that heme oxygenase-1 (HO-1) expression was increased in VSMCs treated with MA. Furthermore, MA was found to induce Akt activation in a dose- and time-dependent manner. Wortmannin suppression of Akt was able to abolish HO-1 upregulation in VSMCs, suggesting the requirement of Akt activation for MA effect on HO-1. Further investigation indicated that Akt activation resulted in the elevated expression of Nrf2, a HO-1 promoter, in MA-treated VMSCs. Finally, we found that MA was able to protect VSMCs from oxidative stress induced by H2O2. Blocking the activation of Akt/Nrf2/HO-1 was able to compromise the protective effect of MA on VSMCs. Collectively, we provided evidence that MA protected VMSCs from oxidative stress through Akt/Nrf2/HO-1 pathway.

Research on antioxidant activity of EOB-F and its function in the diagnosis of heart and cerebral vessels.

This paper introduces the research progress related to the antioxidant activity of bamboo leaf flavonoid (EOB-f) and its pharmacological activity of heart and cerebral vessels. The paper studied what role EOB-f played in the diagnosis of heart and cerebral vessels, based on the in vitro, in vivo and animal model as well as the pharmacological research experiment. 1) The in vitro and in vivo experiments indicated that EOB-f has the function of anti-reactive-oxide species, anti-aging and anti-fatigue; 2) The research of animal model indicated that EOB-f can significantly decrease the triglyceride (TG) content in serum, significantly increase high density lipoprotein cholesterol (HDL-C) content in serum, regulate blood lipids and reduce the risk of atherosclerosis; 3) The pharmacological study showed that EOB-f has the effect to resist the whole animal anoxia, can effectively dilate coronary vessels, increase coronary flow, increase myocardial contractility, obviously improve myocardial ischemia and diminish the myocardial infarction scope, inhibit the coagulation process and reduce platelet aggregation, and has certain protective effect on cerebral ischemia. EOB-f has the potential to develop as the natural drug and functional foods for prevention of cardiovascular and cerebrovascular diseases.

E3 Ubiquitin Ligase ASB14 Inhibits Cardiomyocyte Proliferation by Regulating MAPRE2 Ubiquitination.

The ubiquitin proteasome system is a highly specific and selective protein regulatory system that plays an essential role in the regulation of the cell cycle. Despite its significance, the role of ubiquitination in cardiomyocyte proliferation remains largely unclear. This study aimed to investigate the potential impact of E3 ubiquitin ligase ASB14 (Ankyrin Repeat And SOCS Box Containing 14) on cardiac regeneration. We conducted a microarray analysis of apical resection ventricle tissues, and our findings revealed that ASB14 was down-regulated during the cardiac regenerative response. Subsequently, we examined the effect of ASB14 silencing on cardiomyocyte nuclear proliferation both in vitro and in vivo. Our results indicated that ASB14 silencing promoted cardiomyocyte nuclear proliferation, suggesting that ASB14 may play a role in regulating cardiac regeneration. To further investigate the potential therapeutic implications of ASB14 deficiency, we examined the cardiac function of mice with ASB14 deficiency in response to ischemic injury. Our findings showed that mice with ASB14 deficiency exhibited preserved cardiac function and a therapeutic effect in response to ischemic injury, which was attributed to the enhancement of cardiomyocyte nuclear proliferation. To elucidate the underlying mechanisms, we investigated the effect of ASB14 on microtubule-associated protein RP/EB family member 2 (MAPRE2) protein degradation. Our results indicated that the loss of ASB14 decreased the degradation of MAPRE2 protein, subsequently promoting cardiomyocyte nuclear proliferation and enhancing cardiac repair after myocardial infarction (MI). In conclusion, our study provides evidence that inhibition of ASB14-mediated MAPRE2 ubiquitination promotes cardiomyocyte nuclear proliferation, which may serve as a potential target for treating heart failure induced by MI injury.

Comparison of Drug-Coated Balloon and Drug-Eluting Stent for the Treatment of Small Vessel Disease (from the Dissolve SVD Randomized Trial).

The Dissolve drug-coated balloons (DCBs) is a new-generation DCB coated with paclitaxel of balloon surface, with midchain triglyceride excipient. Although the use of DCBs is a promising technique, little is known about the the clinical efficacy of the novel Dissolve DCB in coronary small vessel disease. This study was a prospective, randomized, multicenter, noninferiority trial comparing the Dissolve DCB with the Resolute drug-eluting stent (DES) in patients with a reference vessel diameter ≥2.25 and ≤2.75 mm. Patients with a reference vessel diameter ≥2.00 and <2.25 mm were enrolled in the very small vessel registry. The angiographic and clinical follow-up were planned at 9 months and 1 year in all patients, respectively. The primary end point was 9-month in-segment percentage diameter stenosis. A total of 247 patients with small vessel disease from 10 Chinese sites were included (Dissolve DCB, n = 118; Resolute DES, n = 129); 30 patients were treated with the DCB in the very small vessel cohort. The 9-month in-segment percentage diameter stenosis was 31.2 ± 2.0% with Dissolve DCB versus 26.1 ± 2.1% with Resolute DES; the 1-sided 97.5% upper confidence limit of the difference was 10.3% (p for noninferiority = 0.0002). At 12 months, the DCB and DES groups were associated with similar rates of target lesion failure (8.5% vs 6.1%, p = 0.28) and major adverse cardiac and cerebrovascular events (20.9% vs 13.6%, p = 0.12). In conclusion, the Dissolve DCB was noninferior to the Resolute DES for the primary end point of 9-month in-segment percentage diameter stenosis in this multicenter, head-to-head, randomized trial (a safety and efficacy study of Dissolve In Treatment Of Coronary Small Vessel Disease; NCT03376646).

Biolimus-coated versus paclitaxel-coated balloons for coronary in-stent restenosis (BIO ASCEND ISR): a randomised, non-inferiority trial.

BACKGROUND: The treatment of in-stent restenosis (ISR) after drug-eluting stent (DES) implantation remains challenging in current clinical practice. AIMS: The study was conducted to investigate a novel biolimus-coated balloon (BCB) for the treatment of coronary DES-ISR compared with the best-investigated paclitaxel-coated balloon (PCB). METHODS: This was a prospective, multicentre, randomised, non-inferiority trial comparing a novel BCB with a clinically proven PCB for coronary DES-ISR. The primary endpoint was in-segment late lumen loss (LLL) at 9 months assessed by an independent core laboratory. Baseline and follow-up optical coherence tomography were performed in a prespecified subgroup of patients. RESULTS: A total of 280 patients at 17 centres were randomised to treatment with a BCB (n=140) versus a PCB (n=140). At 9 months, LLL in the BCB group was 0.23±0.37 mm compared to 0.25±0.35 mm in the PCB group; the mean difference between the groups was -0.02 (95% confidence interval [CI]: -0.12 to 0.07) mm; p-value for non-inferiority<0.0001. Similar clinical outcomes were also observed for both groups at 12 months. In the optical coherence tomography substudy, the neointimal area at 9 months was 2.32±1.04 mm2 in the BCB group compared to 2.37±0.93 mm2 in the PCB group; the mean difference between the groups was -0.09 (95% CI: -0.94 to 0.76) mm2; p=non-significant. CONCLUSIONS: This head-to-head comparison of a novel BCB shows similar angiographic outcomes in the treatment of coronary DES-ISR compared with a clinically proven PCB. (ClinicalTrials.gov: NCT04733443).

Effectiveness and Safety of a Novel Intravascular Lithotripsy System for Severe Coronary Calcification: The CALCI-CRACK Trial.

BACKGROUND: Intravascular lithotripsy is effective and safe for managing coronary calcification; however, available devices are limited, and complex lesions have been excluded in previous studies. This study aimed to investigate the effectiveness and safety of a novel intravascular lithotripsy system for severe calcification in a population with complex lesions. METHODS: CALCI-CRACK (ChiCTR2100052058) was a prospective, single-arm, multicentre study. The primary end point was the procedural success rate. Major safety end points included major adverse cardiovascular events (MACE) and target lesion failure (TLF) at 30 days and 6 months, and severe angiographic complications. Calcification morphology was assessed in the optical coherence tomography (OCT) subgroup. RESULTS: In total, 242 patients from 15 high-volume Chinese centres were enrolled, including 26.45% of patients with true bifurcation lesions, 3.31% with severely tortuous vessels, and 2.48% with chronic total occlusion, respectively. The procedural success rate was 95.04% (95% confidence interval 91.50%-97.41%), exceeding the prespecified performance goal of 83.4% (P < 0.001). The 30-day and 6-month MACE rates were 4.13% and 4.55%, respectively. TLF rates at those time points were 1.24% and 1.65%, respectively. Severe angiographic complications occurred in 0.42% of patients. In the OCT subgroup (n = 93), 93.55% of calcified lesions were fractured, and minimal lumen area increased from 1.55 ± 0.55 mm2 to 4.91 ± 1.22 mm2 after stent implantation, with acute gain rate of 245 ± 102%. CONCLUSIONS: The novel intravascular lithotripsy system is effective and safe for managing severely calcified coronary lesions in a cohort that included true bifurcation lesions, severely tortuous vessels, and chronic total occlusion. CLINICAL TRIAL REGISTRATION: Chinese Clinical Trial Registry (ChiCTR), number ChiCTR2100052058.

[The expression and clinical implication of plasma miR-328 in patients with atrial fibrillation].

OBJECTIVE: To observe the expression and clinical implication of plasma miR-328 in patients with atrial fibrillation (AF). METHODS: Fifty-eight patients with AF (AF group: 17 paroxysmal AF, 21 persistent AF, and 20 permanent AF) and 15 healthy volunteers (Control group) were included. General clinical data and related biochemical parameters were collected. Plasma miR-328 levels were detected with quantitative real-time polymerase chain reaction (qRT-PCR) analysis. The correlation between plasma miR-328 and AF risk factors was analyzed. RESULTS: (1) Compared with the control group, the expression level of plasma miR-328 was significantly elevated in AF group (fold 7.72 ± 9.32) (P < 0.05). (2) In AF group, the expression of plasma miR-328 was significantly different in different type of AF[paroxysmal AF with (1.98 ± 0.81), persistent AF with (6.57 ± 5.82) and permanent AF with (13.47 ± 12.29)] (P < 0.05), and which was increased in proportion to the duration of AF. (3) There was a positive correlation between plasma miR-328 level and left atrial diameter in the AF group (r = 0.310, P < 0.05). CONCLUSION: miR-328 expression is significantly increased in patients with AF, which may be involved in the atrial remodeling process of AF.

Incidence, risk factors, and clinical sequelae of incomplete stent apposition after sirolimus-eluting stent.

Incomplete stent apposition has been documented after sirolimus-eluting stent implantation. However, its clinical sequelae remain controversial. To identify the incidence and its clinical consequences of ISA, IVUS was performed on 78 patients. In spite of well apposition immediately after the deployment, late stent malapposition occurred after 6-months follow-up. A total of 7 patients who received SES showed ISA. There were no significant differences in IVUS measurements between patients with or without ISA. However, there was an increase in external elastic membrane area in ISA group than non-ISA group (19.69 ± 3.50 vs. 15.05 ± 2.56 mm2, P<0.05). There were positive clinical events for ISA cases at 6-months clinical follow-up. Univariate and multivariable analyses indicated that hs-CRP, miR-21, and MMP-2 were risk factor for ISA. ISA was observed in 9% of patients after SES implantation, which was related to vessel positive remodeling. The incidence of MACEs in patients with ISA was higher than those without ISA. However, careful long-term follow-up remains to be clarified.

A Randomized Comparison of 2 Different Drug-Coated Balloons for In-Stent Restenosis.

BACKGROUND: Although use of drug-coated balloons (DCB) is a promising technique, little is known about the clinical efficacy of the Dissolve DCB in drug-eluting stent (DES) in-stent restenosis (ISR). OBJECTIVES: This study sought to evaluate the efficacy and safety of the Dissolve DCB in patients with DES ISR. METHODS: This was a prospective, multicenter, randomized, noninferiority trial comparing Dissolve DCB with SeQuent Please DCB in patients with DES ISR. Angiographic and clinical follow-up was planned at 9 months in all patients. The primary endpoint was 9-month in-segment late loss. RESULTS: A total of 260 patients with ISR from 10 Chinese sites were included (Dissolve DCB, n = 128; SeQuent Please DCB, n = 132). Nine-month in-segment late loss was 0.50 ± 0.06 mm with Dissolve DCB vs 0.47 ± 0.07 mm with SeQuent Please DCB; the 1-sided 97.5% upper confidence limit of the difference was 0.18 mm (P for noninferiority = 0.03). Rates of target lesion failure and binary restenosis were numerical higher in the Dissolve DCB cohort compared with the SeQuent Please DCB cohort at 9 months (17.5% vs 10.7%; P = 0.12; 23.4% vs 16.4%; P = 0.19, respectively). At 9 months, major adverse cardiac and cerebrovascular events occurred in 36 patients (28.3%) vs 30 patients (22.9%) in the Dissolve DCB and SeQuent Please DCB groups, respectively. CONCLUSIONS: In this head-to-head randomized trial, the Dissolve DCB was noninferior to the SeQuent Please DCB for 9-month in-segment late loss. However, Dissolve DCB with its numerical increase in target lesion failure and binary restenosis warrants assessment in larger clinical trials (A Safety and Efficacy Study of Dissolve™ in Treatment of Coronary In-Stent Restenosis; NCT03373695).

Short-term outcomes of drug-coated balloon versus drug-eluting stent for de novo saphenous vein graft lesions in coronary heart disease.

Background: As a device for percutaneous coronary intervention, drug-coated balloon (DCB) is widely used to treat in-stent restenosis. However, data regarding the use of DCB in treating de novo saphenous vein graft (SVG) lesions are limited. This study aimed to explore the outcomes of using the DCB in the treatment of de novo SVG lesions of coronary heart disease (CHD). Methods: This retrospective and observational study analyzed CHD patients with de novo SVG lesions treated with DCB or the new-generation drug-eluting stent (DES) between January 2018 and December 2020. Restenosis was the primary endpoint, whereas target lesion revascularization (TLR), major adverse cardiac events, restenosis, cardiac death, target vessel revascularization, and myocardial infarction were the secondary outcomes. Results: We enrolled 31 and 23 patients treated with DCB and DES, respectively. The baseline clinical data, lesion characteristics, and procedural characteristics were similar between the two groups. Twenty-eight (90.3%) patients in the DCB group and 21 (91.3%) in the DES group completed follow-up angiography after 1 year. The quantitative coronary angiography measurements at angiographic follow-up showing late lumen loss were -0.07 ± 0.95 mm for the DCB group and 0.86 ± 0.71 mm for the DES group (P = 0.039), and the rates of restenosis were 13.3% and 21.7% for the DCB and DES groups, respectively (P = 0.470). No significant differences were observed in the rates of MACE (16.7% vs. 26.1%, P = 0.402) and TLR (13.3% vs. 4.3%, P = 0.374) during clinical follow-up. Conclusion: Our findings suggest that when pre-dilatation was successful, DCB might be safe and effective in treating de novo SVG lesions.