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Percutaneous mitral valve repair has been increasingly performed worldwide after approval. We sought to investigate predictors of clinical outcome in patients with mitral regurgitation undergoing percutaneous valve repair. The MITRA-UMG study, a single-centre registry, retrospectively collected consecutive patients with symptomatic moderate-to-severe or severe MR undergoing MitraClip therapy. The primary endpoint was the composite of cardiovascular death or rehospitalization for heart failure. Between March 2012 and July 2018, a total of 150 consecutive patients admitted to our institution were included. Procedural success was obtained in 95.3% of patients. The composite primary endpoint of cardiovascular death or rehospitalization for HF was met in 55 patients (37.9%) with cumulative incidences of 7.6%, 26.2%, at 30 days and 1-year, respectively. In the Cox multivariate model, NYHA functional class and left ventricular end-diastolic volume index (LVEDVi), independently increased the risk of the primary endpoint at long-term follow-up. At Kaplan–Meier analysis, a LVEDVi > 92 ml/m2 was associated with an increased incidence of the primary endpoint. In this study, patients presenting with dilated ventricles (LVEDVi > 92 ml/m2) and advanced heart failure symptoms (NYHA IV) at baseline carried the worst prognosis after percutaneous mitral valve repair.

Subjects with Neurofibromatosis 1 (NF1) develop vascular complications. The protein product of the gene affected in NF1, neurofibromin, physiologically modulates endothelial function and preserves vascular and myocardial structure. Our study aimed to verify whether subjects with NF1 have early, preclinical abnormalities of carotid artery structure, brachial artery function, and cardiac function. We recruited 22 NF1 subjects without previous cardiovascular events and 22 healthy control subjects. All subjects underwent measurement of carotid artery intima-media thickness (IMT), evaluation of brachial artery endothelial function after ischemia and exercise, and cardiac function. Mean IMT was 543 ± 115 μ in NF1 subjects and 487 ± 70 μ in Controls (p p p p

Background Empagliflozin showed efficacy in controlling glycaemia, leading to reductions in HbA1c levels, weight loss and blood pressure, compared to standard treatment. Moreover, the EMPA-REG OUTCOME trial demonstrated a 14% reduction of major adverse cardiovascular events (MACE), a 38% reduction in cardiovascular (CV) death and a 35% reduction in the hospitalization rate for heart failure (HF). These beneficial effect on HF were apparently independent from glucose control. However, no mechanistic in vivo studies are available to explain these results, yet. We aimed to determine the effect of empagliflozin on left ventricular (LV) function in a mouse model of doxorubicin-induced cardiomyopathy (DOX-HF). Methods Male C57Bl/6 mice were randomly assigned to the following groups: controls (CTRL, n = 7), doxorubicin (DOX, n = 14), DOX plus empagliflozin (DOX + EMPA, n = 14), or DOX plus furosemide (DOX + FURO group, n = 7). DOX was injected intraperitoneally. LV function was evaluated at baseline and after 6 weeks of treatment using high-resolution echocardiography with 2D speckle tracking (Vevo 2100). Histological assessment was obtained using Haematoxylin and Eosin and Masson’s Goldner staining. Results A significant decrease in both systolic and diastolic LV function was observed after 6 weeks of treatment with doxorubicin. EF dropped by 32% (p = 0.002), while the LS was reduced by 42% (p Conclusion Empagliflozin attenuates the cardiotoxic effects exerted by doxorubicin on LV function and remodelling in nondiabetic mice, independently of glycaemic control. These findings support the design of clinical studies to assess their relevance in a clinical setting.

The inherited and acquired long QT is a risk marker for potential serious cardiac arrhythmias and sudden cardiac death. Smartwatches are becoming more popular and are increasingly used for monitoring human health. The present study aimed to assess the feasibility and reliability of evaluating the QT interval in lead I, lead II, and V2 lead using a commercially available Apple Watch. One hundred nineteen patients admitted to our Cardiology Division were studied. I, II, and V2 leads were obtained after recording a standard 12-lead ECG. Lead I was recorded with the smartwatch on the left wrist and the right index finger on the crown. Lead II was obtained with the smartwatch on the left lower abdomen and the right index finger on the crown. The V2 lead was recorded with the smartwatch in the fourth intercostal space left parasternal with the right index finger on the crown. There was agreement among the QT intervals of I, II, and V2 leads and the QT mean using the smartwatch and the standard ECG with Spearman’s correlations of 0.886; 0.881; 0.793; and 0.914 (p

Coronavirus disease 2019 (COVID-19) is a highly contagious disease that appeared in China in December 2019 and spread rapidly around the world. Several patients with severe COVID-19 infection can develop a coagulopathy according to the ISTH criteria for disseminated intravascular coagulopathy (DIC) with fulminant activation of coagulation, resulting in widespread microvascular thrombosis and consumption of coagulation factors. We conducted a meta-analysis in order to explore differences in coagulopathy indices in patients with severe and non-severe COVID-19. An electronic search was performed within PubMed, Google Scholar and Scopus electronic databases between December 2019 (first confirmed Covid-19 case) up to April 6th, 2020. The primary endpoint was the difference of D-dimer values between Non-Severe vs Severe disease and Survivors vs Non-Survivors. Furthermore, results on additional coagulation parameters (platelet count, prothrombin time, activated partial thromboplastin time) were also analyzed. The primary analysis showed that mean d-dimer was significantly lower in COVID-19 patients with non-severe disease than in those with severe (SMD − 2.15 [− 2.73 to − 1.56], I2 98%, P 2 98%, P 2 96%, P 2 97%, P 2 98%, P 2 98%, P

Quantitative analysis of biochemical parameters is crucial for a correct diagnosis and prognosis of patients subject to acute myocardial infarction (AMI). In order to achieve a quantitative understanding of the dynamics of cardiac biomarkers, we have developed a mathematical model that can be exploited to extrapolate the release curve of cardiac troponin T (cTnT) into the plasma from few experimental acquisitions. The present work introduces a novel approach, based on the cTnT-release model, aimed at the identification of the infarct onset time. Indeed, in spite of the clinical importance of such information, in many cases, it is not easy to establish the exact time of occurrence of the ischemic event. We show that using a model-based optimization approach, the infarct onset time can be reliably estimated using the cTnT concentration acquisitions taken in the first few hours post-AMI. The assessment of the proposed approach is conducted on an experimental dataset, in which the infarct has been artificially induced and, therefore, the onset time is exactly known. In particular, the effectiveness of the devised estimation algorithm has been tested under several scenarios, with the first cTnT acquisition taken up to 12 h after AMI. Altogether, the proposed model-based approach provides a useful tool to help the clinicians in the quantitative estimation of important clinical parameters from the release curves of the cardiac biomarkers.

AimsTo investigate the changes in left atrial strain (LAS) after correction of severe aortic stenosis (AS) with transcatheter aortic valve replacement (TAVR) and assess its prognostic impact.Methods and resultsOne hundred consecutive patients with severe symptomatic AS who underwent TAVR at the Magna Graecia University of Catanzaro underwent echocardiographic examination including assessment of LAS before and after TAVR. Independent investigators collected outcome data and information. The primary study outcome was the difference in ΔLAS (postTAVR–preTAVR) between patients those met the main clinical endpoint (a composite of cardiovascular mortality and heart failure hospitalisation) and those not meeting the endpoint.During a median follow-up of 31 months, 35 patients (35%) met the combined clinical endpoint. The difference between LAS post-TAVR and LAS pre-TAVR (ΔLAS) was significantly larger in patients who met the combined endpoint (HR=0.76 (0.67–0.86); pConclusionsA lower reduction in ΔLAS after TAVR was an independent predictor of the primary composite outcome of cardiovascular death and hospitalisation for heart failure.

The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) exert pleiotropic effects on cardiac cell biology which are not yet fully understood. Here we tested whether statin treatment affects resident endogenous cardiac stem/progenitor cell (CSC) activation in vitro and in vivo after myocardial infarction (MI). Statins (Rosuvastatin, Simvastatin and Pravastatin) significantly increased CSC expansion in vitro as measured by both BrdU incorporation and cell growth curve. Additionally, statins increased CSC clonal expansion and cardiosphere formation. The effects of statins on CSC growth and differentiation depended on Akt phosphorylation. Twenty-eight days after myocardial infarction by permanent coronary ligation in rats, the number of endogenous CSCs in the infarct border zone was significantly increased by Rosuvastatin-treatment as compared to untreated controls. Additionally, commitment of the activated CSCs into the myogenic lineage (c-kitpos/Gata4pos CSCs) was increased by Rosuvastatin administration. Accordingly, Rosuvastatin fostered new cardiomyocyte formation after MI. Finally, Rosuvastatin treatment reversed the cardiomyogenic defects of CSCs in c-kit haploinsufficient mice, increasing new cardiomyocyte formation by endogenous CSCs in these mice after myocardial infarction. In summary, statins, by sustaining Akt activation, foster CSC growth and differentiation in vitro and in vivo. The activation and differentiation of the endogenous CSC pool and consequent new myocyte formation by statins improve myocardial remodeling after coronary occlusion in rodents. Similar effects might contribute to the beneficial effects of statins on human cardiovascular diseases.

Recently, two randomized trials, the PARTNER 3 and the Evolut Low Risk Trial, independently demonstrated that transcatheter aortic valve replacement (TAVR) is non-inferior to surgical aortic valve replacement (SAVR) for the treatment of severe aortic stenosis in patients at low surgical risk, paving the way to a progressive extension of clinical indications to TAVR. We designed a meta-analysis to compare TAVR versus SAVR in patients with severe aortic stenosis at low surgical risk. The study protocol was registered in PROSPERO (CRD42019131125). Randomized studies comparing one-year outcomes of TAVR or SAVR were searched for within Medline, Scholar and Scopus electronic databases. A total of three randomized studies were selected, including nearly 3000 patients. After one year, the risk of cardiovascular death was significantly lower with TAVR compared to SAVR (Risk Ratio (RR) = 0.56, 95% CI 0.33&ndash, 0.95, p = 0.03). Conversely, no differences were observed between the groups for one-year all-cause mortality (RR = 0.67, 95% CI 0.42&ndash, 1.07, p = 0.10). Among the secondary endpoints, patients undergoing TAVR have lower risk of new-onset of atrial fibrillation compared to SAVR (RR = 0.26, 95% CI 0.17&ndash, 0.39, p &lt, 0.00001), major bleeding (RR = 0.30, 95% CI 0.14&ndash, 0.65, 0.002) and acute kidney injury stage II or III (RR = 0.28, 0.58, p = 0.0005). Conversely, TAVR was associated to a higher risk of aortic regurgitation (RR = 3.96, 95% CI 1.31&ndash, 11.99, p = 0.01) and permanent pacemaker implantation (RR = 3.47, 95% CI 1.33&ndash, 9.07, p = 0.01) compared to SAVR. No differences were observed between the groups in the risks of stroke (RR= 0.71, 95% CI 0.41&ndash, 1.25, p = 0.24), transient ischemic attack (TIA, RR = 0.98, 95% CI 0.53&ndash, 1.83, p = 0.96), and MI (RR = 0.75, 95% CI 0.43&ndash, 1.29, p = 0.29). In conclusion, the present meta-analysis, including three randomized studies and nearly 3000 patients with severe aortic stenosis at low surgical risk, shows that TAVR is associated with lower CV death compared to SAVR at one-year follow-up. Nevertheless, paravalvular aortic regurgitation and pacemaker implantation still represent two weak spots that should be solved.

13 pages, 11 figures, Cardiovascular diseases represent, to date, the major cause of mortality worldwide. Diagnosis of the most frequent of such disease, acute myocardial infarction (AMI), requires the evaluation of time-series measurement of specific cardiac biomarkers concentration. The aim of this paper is to provide the clinicians with a quantitative tool to analyze such time-series, with the final goal of enhancing the diagnostic and prognostic procedures. The proposed approach is based on a novel dynamical model, which synthetically describes the basic mechanisms underlying cardiac troponin (cTnT) release into the plasma after the onset of AMI. Leveraging tools of system identification and a data set of AMI patients treated at our University Hospital, the model has been assessed as an effective tool to quantify the characteristic release curves observed under different conditions. Furthermore, it has been shown how the devised approach is also suitable in those cases where only partial measurements are available to the clinician to recover important clinical information. Finally, an optimal experimental design analysis has been performed in order to gain insights on how to optimize the experimental data collection phase with potentially relevant implications on both the quality and cost of the diagnosis procedure, M.R.G. acknowledges financial support from the Spanish Government and the European Regional Development Fund through the project DPI2014-54085-JIN

Background During ischemia a close relationship exists between sub-endocardial blood flow and myocardial function. Strain parameters can capture an impairment of regional longitudinal function but are load dependent. Recently, a novel non-invasive method to calculate Myocardial Work (MW) showed a strong correlation with invasive work measurements. Our aim was to investigate the ability of non-invasive MW indices to identify the ischaemic risk area during transient acute coronary occlusion (TACO). Methods and results The study population comprises 50 individuals with critical coronary stenosis (CCS). Echocardiography recordings were obtained before coronary angiography, during TACO and after revascularization to measure global longitudinal strain (GLS), Myocardial Work Index (MWI), Myocardial Constructive Work (MCW), Myocardial Wasted work (MWW), Myocardial work efficiency (MWE). Compared to baseline, we found a significant reduction of GLS (p = 0.005), MWI, MCW and MWE (p Conclusions The non-invasive measurement of MW parameters is a sensitive and early marker of myocardial ischemia during TACO.

Background. The pandemic of Novel Coronavirus Disease 2019 (COVID-19) is challenging, given the large number of hospitalized patients. Cardiovascular co-morbidities are linked to a higher mortality risk. Thus, patients with Congenital Heart Disease (CHD) might represent a high-risk population. Nevertheless, no data about them are available, yet. Hence, we conducted a nationwide survey to assess clinical characteristics and outcomes in patients with congenital heart disease affected by COVID-19. Methods and Results. This is a multi-centre, observational, nationwide survey, involving high-volume Italian CHD centres. COVID-19 diagnosis was defined as either &ldquo, clinically suspected&rdquo, or &ldquo, confirmed&rdquo, where a severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) test had been performed and was positive. Cardiovascular comorbidities were observed among adult patients&mdash, atrial fibrillation (seven, 9%), hypertension (five, 7%), obesity (seven, 9%) and diabetes (one, 1%)&mdash, but were absent among children. Cardiovascular complications were mainly observed in the &ldquo, COVID-19+ group, consisting of heart failure (9%), palpitations/arrhythmias (3%), stroke/TIA (3%) and pulmonary hypertension (3%). Cardiovascular symptoms such as chest pain (1%), myocardial injury (1%) and pericardial effusion (1%) were also recorded. On the contrary, CHD patients from the clinically suspected COVID-19 group presented no severe symptoms or complications. Conclusions. Despite previous reports pointing to a higher case-fatality rate among patients with cardiovascular co-morbidities, we observed a mild COVID-19 clinical course in our cohort of CHD patients. Although these results should be confirmed in larger cohorts to investigate the underlying mechanisms, the findings of low cardiovascular complications rates and no deaths are reassuring for CHD patients.

The recent outbreak of 2019 severe acute respiratory syndrome coronavirus-2 is having major repercussions on healthcare services provision in Italy and worldwide. Data suggest the virus has a strong impact on the cardiovascular system, and cardiac imaging will play an important role in patients affected by coronavirus disease-2019. Although paediatric patients are mildly affected, they represent a clear accelerator in spreading the virus, and healthcare workers are at higher risk of infection. The aim of this position paper is to provide clinical recommendation regarding the execution of imaging investigations for the cardiac diagnostic work-up of paediatric patients with suspected or confirmed infection.

Aortic valve tissue is largely exposed to high blood flow. Cells belonging to aortic valve tissues are able to detect and respond to flow conditions changes. Bicuspid aortic valve (BAV) presents altered morphology, with only two abnormal cusps instead of three. This results in an alteration of blood flow dynamics on valve cusps and aortic wall, which may, in turn, increase the risk to develop aortic stenosis and/or regurgitation, endocarditis, aortopathy and/or aortic dissection. MicroRNAs (miRNAs) are short RNA strands regulating gene expression mainly through the inhibition of their target mRNAs. They are largely involved in cardiovascular pathophysiology and heart disease. More recently, it has been observed that the expression of specific miRNAs can be modulated in response to changes in hemodynamic conditions. Using a bioinformatic approach, this article analyses available scientific evidence about the differential expression of miRNAs in the bicuspid aortic valve, with a focus on the differential modulation compared to the calcific-degenerative tricuspid aortic valve.

Up to 15% of coronavirus disease 2019 (COVID-19) patients experience severe clinical presentation, resulting in acute respiratory distress (ARDS) and finally death. N-terminal natriuretic peptide (NT-proBNP) is associated with a worse prognosis in patients with ARDS. However, whether or not this peptide can help discriminate high-risk COVID-19 patients remains unclear. Therefore, in this meta-analysis, we summarized the available evidence on NT-proBNP in patients admitted for COVID-19. Pooled mean, mean differences (MD) and standardized mean difference (SMD) were the summary metrics. Thirteen studies were finally selected for this analysis with a total of 2248 patients, of which 507 had a severe condition (n = 240) or died (n = 267). Pooled mean NT-proBNP levels on admission were 790.57 pg/mL (95% confidence intervals (CIs): 532.50 to 1048.64) in patients that experienced a severe clinical condition or died, and 160.56 pg/mL (95% CI: 118.15 to 202.96) in non-severe patients (SMD: 1.05; 95% (CI): 0.83 to 1.28; p < 0.001; I2 74%; and MD was 645.84 pg/mL (95% CI: 389.50–902.18). Results were consistent in studies categorizing patients as non-survivors versus survivors (SMD: 1.17; 95% CI 0.95 to 1.40; p < 0. 001; I2: 51%), and in those classifying populations in severe versus non-severe clinical condition (SMD: 0.94 95% CI 0.56 to 1.32; p < 0.001; I2: 81%; pinteraction = 0.30). In conclusion, our results suggest that assessing NT-proBNP may support physicians in discriminating high-risk COVID-19 patients.

Background: It is unclear whether or not ultrasound-guided cannulation (UGC) of the femoral artery is superior to the standard approach (SA) in reducing vascular complications and improving access success. Objective: We sought to compare procedural and clinical outcomes of femoral UGC versus SA in patients undergoing percutaneous cardiovascular intervention (PCvI). Methods: We searched EMBASE, MEDLINE, Scopus and web sources for randomized trials comparing UGC versus SA. We estimated risk ratio (RR) and standardized mean differences (SMDs) with 95% confidence intervals (CIs) for categorical and continuous variables, respectively. Primary efficacy endpoint was the success rate at the first attempt, while secondary efficacy endpoints were access time and number of attempts. Primary safety endpoints were the rates of vascular complications, while secondary endpoints were major bleeding, as well as access site hematoma, venepuncture, pseudoaneurysms and retroperitoneal hematoma. This meta-analysis has been registered on Centre for Open Science (OSF) (osf.io/fy82e). Results: Seven trials were included, randomizing 3180 patients to UGC (n = 1564) or SA (n = 1616). Efficacy between UGC and SA was the main metric assessed in most of the trials, in which one third of the enrolled patients underwent interventional procedures. The success rate of the first attempt was significantly higher with UGC compared to SA, (82.0% vs. 58.7%, RR: 1.36, 95% CI: 1.17 to 1.57, p &lt, 0.0001, I2 = 88%). Time to access and number of attempts were significantly reduced with UGC compared to SA (SMD: &minus, 0.19, 95% CI: &minus, 0.28 to &minus, 0.10, I2 = 22%) and (SMD: &minus, 0.40, 0.58 to &minus, 0.21, I2 = 82%), respectively. Compared with SA, use of UGC was associated with a significant reduction in vascular complications (1.3% vs. 3.0%, RR: 0.48, CI 95%: 0.25 to 0.91, p = 0.02, I2 = 0%) and access-site hematoma (1.2% vs. 3.3%, RR: 0.41, CI 95%: 0.20 to 0.83, p = 0.01, I2 = 27%), but there were non-significant differences in major bleeding (0.7% vs. 1.4%, RR: 0.57, CI 95%: 0.24 to 1.32, p = 0.19, I2 = 0%). Rates of venepuncture were lower with UGC (3.6% vs. 12.1%, RR: 0.32, CI 95%: 0.20 to 0.52, 0.00001, I2 = 55%). Conclusion: This study, which included all available data to date, demonstrated that, compared to a standard approach, ultrasound-guided cannulation of the femoral artery is associated with lower access-related complications and higher efficacy rates. These results could be of great clinical relevance especially in the femoral cannulation of high risk patients.

Background. Aortic stenosis (AS) is the most common heart valve disease in developed countries. The advent of transcatheter aortic valve implantation (TAVI) significantly improved patients’ outcome but made clinical management more complex. The aim of the present study was to describe TAVIApp, a mobile app we developed to guide the management of AS, and test its efficacy. Methods and Results. Clinical cases comprising 42 patients with AS were blindly evaluated by (A) an interventional cardiologist, assisted by the Heart Team (EXPERT), (B) young residents in cardiology, and (C) a young resident supported by TAVIApp. There was poor concordance between Group A and Group B with low performance by young residents (k=0.52; p<0.001). However, concordance increased to an optimal value when young residents were supported by TAVIApp (k=1.0; p<0.001) for the diagnosis of severe AS and eligibility assessment. Furthermore, regarding the selection of the most appropriate prosthesis size, concordance to Group A was poor without TAVIApp support (Group B) (k=0.78; p=0.430), but excellent with TAVIApp (k=1.0; p<0.001). Conclusions. This study is the first describing and validating a new mobile application to support the management of AS. TAVIApp supports cardiologists in the evaluation of stenosis severity, eligibility for TAVI or AVR, and selection of the most appropriate prosthesis size in individual patients.

Background. Circulating microRNAs are appealing biomarkers to monitor several processes underlying cardiovascular diseases. Platelets are a major source for circulating microRNAs. Interestingly, the levels of specific microRNAs were reported to correlate with the level of platelet activation. The aim of the present study was to test whether the treatment with the novel antiplatelet agent, ticagrelor, is associated with modulation in the levels of key platelet-derived microRNAs.Methods and Results. Patients were randomly selected from those participating in the SHIFT-OVER study, in which we had previously evaluated the effect of the therapeutic switch from clopidogrel to ticagrelor on platelet aggregation. Circulating levels of selected microRNAs were measured before and after the therapeutic switch from a dual antiplatelet therapy including acetylsalicylic acid (ASA) and clopidogrel to the more potent ticagrelor. Interestingly, the circulating levels of miR-126 (p=0.030), miR-223 (p=0.044), and miR-150 (p=0.048) were significantly reduced, while the levels of miR-96 were increased (p=0.038). No substantial differences were observed for the remaining microRNAs.Conclusions. Switching from a dual antiplatelet treatment with clopidogrel to ticagrelor is associated with significant modulation in the circulating levels of specific microRNAs. If confirmed in larger, independent cohorts, our results pave the way for the use of circulating microRNAs as biomarkers of platelets activity in response to specific pharmacological treatments.

Background Adenosine administration is currently required for evaluation of stenosis severity with fractional flow reserve (FFR). The instantaneous wave-free ratio (iFR) was recently introduced as an adenosine-free alternative in patients with stable CAD. The aim of the present study was to replicate the findings of previous iFR studies using an independent calculation algorithm and to evaluate the iFR for the assessment of non-culprit vessels in patients with acute coronary syndrome (ACS).Methods and results 53 patients with ACS (65%) and at least one non-culprit intermediate lesion and 29 (35%) with stable CAD were included. A total of 123 stenoses were evaluated with both FFR and iFR. Classification match of iFR in ACS was not inferior to stable CAD (79.5% in ACS and 84.4% in CAD; p = 0.497). Accordingly, no difference was observed in iFR/FFR correlation between ACS and stable CAD (r = 0.66 in ACS vs. r = 0.69 in CAD). Overall, a significant correlation was found between iFR and FFR (r = 0.68; p < 0.001) with a good diagnostic efficiency at ROC analysis (area under the curve: 0.87). In addition, neither the localization of the stenosis within the coronary tree (p = 0.147) nor the time interval from the acute event (p = 0.550) significantly influenced the concordance of iFR with FFR.Conclusions The iFR is a promising method for the assessment of non-culprit lesion severity in patients with acute coronary syndrome.

Background Adequate expansion is critical to achieve optimal Bioresorbable Vascular Scaffolds (BVS) apposition to the vessel wall. However, compared to metallic stents, BVS present different mechanical properties. Hence, slow deployment and maintenance of balloon inflation for at least 30” is recommended for BVS implantation. However, since no evidences are available demonstrating the superiority of a longer balloon dilatation time, the implantation technique is highly variable among different centers. Methods A total of 24 BVS-treated lesions were included in the present analysis. After BVS deployment at 12 atmosphere (ATM) the balloon was rapidly deflated and scaffold expansion was documented with an angiogram. The same balloon was then inflated again and kept at 12 ATM for 30”. Finally, a further angiogram was obtained to evaluate BVS expansion. Quantitative coronary angiography (QCA) was performed at each step. Results A significant increase of minimal luminal diameter (MLD)-to-reference scaffold diameter (RSD) ratio (MLD to RSD Ration, MR-Ratio) from 0.70 ± 0.10 after initial stent deployment to 0.79 ± 0.10 after the 30”-long balloon dilation was observed (p

The role of miR-92a on vascular remodelling after injury is currently unknown. Thus, the aim of the present study was to evaluate the role of miR-92a on rat endothelial and vascular smooth muscle cells proliferation and migration in vitro as well as after balloon injury or arterial stenting in vivo. MiR-92a was highly expressed in RAO-ECs and vascular endothelium, but not in RAOSMCs or medial smooth muscle as assessed by real-time RT-PCR. Importantly, BrdU incorporation and wound healing assay provide evidence that functional inhibition of miR-92a resulted in an increased RAO-ECs proliferation and migration, but had no effect on RAO-SMCs proliferation or migration in vitro. Immunoblotting analysis revealed an increased phosphorylation of ERK1/2, JNK/ SAPK as well as eNOS and phospho-eNOS increased expression level in RAO-ECs as a consequence of miR-92a inhibition. Using gain and loss of function experiments, we showed that miR-92a modulates regulation of KLF4 and MKK4 expression level in endothelial cells. Finally, in vivo administration of antagomiR-92a significantly enhanced re-endothelialization in injured carotid arteries and reduced neointimal formation after balloon injury or arterial stenting. These data provide the first evidence that inhibition of miR-92a may represent a novel strategy to improve endothelial regeneration and reduce restenosis after vascular injury.