Cardiovascular diseases (CVDs) continue to represent the number one cause of death and disability in industrialized countries. The most severe form of CVD is acute myocardial infarction (AMI), a devastating disease associated with high mortality and disability. In a substantial proportion of patients who survive AMI, loss of functional cardiomyocytes as a result of ischaemic injury leads to ventricular failure, resulting in significant alteration to quality of life and increased mortality. Therefore, many attempts have been made in recent years to identify new tools for the regeneration of functional cardiomyocytes. Regenerative therapy currently represents the ultimate goal for restoring the function of damaged myocardium by stimulating the regeneration of the infarcted tissue or by providing cells that can generate new myocardial tissue to replace the damaged tissue. Stem cells (SCs) have been proposed as a viable therapy option in these cases. However, despite the great enthusiasm at the beginning of the SC era, justified by promising initial results, this therapy has failed to demonstrate a significant benefit in large clinical trials. One interesting finding of SC studies is that exosomes released by mesenchymal SCs (MSCs) are able to enhance the viability of cardiomyocytes after ischaemia/reperfusion injury, suggesting that the beneficial effects of MSCs in the recovery of functional myocardium could be related to their capacity to secrete exosomes. Ten years ago, it was discovered that exosomes have the unique property of transferring miRNA between cells, acting as miRNA nanocarriers. Therefore, exosome-based therapy has recently been proposed as an emerging tool for cardiac regeneration as an alternative to SC therapy in the post-infarction period. This review aims to discuss the emerging role of exosomes in developing innovative therapies for cardiac regeneration as well as their potential role as candidate biomarkers or for developing new diagnostic tools.
Introduction: In patients with out-of-hospital cardiac arrest (OHCA) complicating an ST-segment elevation myocardial infarction (STEMI), the survival depends largely on the restoration of coronary flow in the infarct related artery. The aim of this study was to determine clinical and angiographic predictors of in-hospital mortality in patients with OHCA and STEMI, successfully resuscitated and undergoing primary percutaneous intervention (PCI). Methods: From January 2013 to July 2015, 78 patients with STEMI presenting OHCA, successfully resuscitated, transferred immediately to the catheterization unit and treated with primary PCI, were analyzed. Clinical, laboratory and angiographic data were compared in 28 non-survivors and 50 survivors. Results:The clinical baseline characteristics of the study population showed no significant differences between the survivors and non-survivors in respect to age (p=0.06), gender (p=0.8), the presence of hypertension (p=0.4), dyslipidemia (p=0.09) obesity (p=1), smoking status (p=0.2), presence of diabetes (p=0.2), a clinical history of acute myocardial infarction (p=0.7) or stroke (p=0.17). Compared to survivors, the non-survivor group exhibited a significantly higher incidence of cardiogenic shock (50% vs 24%, p=0.02), renal failure (64.3% vs 30.0%, p=0.004) and anaemia (35.7% vs 12.0%, p=0.02). Three-vessel disease was significantly higher in the non-survivor group (42.8% vs. 20.0%, p=0.03), while there was a significantly higher percentage of TIMI 3 flow postPCI in the infarct-related artery in the survivor group (80.% vs. 57.1%, p=0.03). The time from the onset of symptoms to revascularization was significantly higher in patients who died compared to those who survived (387.5 +/-211.3 minutes vs 300.8 +/-166.1 minutes, p=0.04), as was the time from the onset of cardiac arrest to revascularization (103.0 +/-56.34 minutes vs 67.0 +/-44.4 minutes, p=0.002). Multivariate analysis identified the presence of cardiogenic shock (odds ratio [OR]: 3.17, p=0.02), multivessel disease (OR: 3.0, p=0.03), renal failure (OR: 4.2, p=0.004), anaemia (OR: 4.07, p=0.02), need for mechanical ventilation >48 hours (OR: 8.07, p=0.0002) and a duration of stay in the ICU longer than 5 days (OR: 9.96, p=0.0002) as the most significant independent predictors for mortality in patients with OHCA and STEMI. Conclusion: In patients surviving an OHCA in the early phase of a myocardial infarction, the presence of cardiogenic shock, renal failure, anaemia or multivessel disease, as well as a longer time from the onset of symptoms or of cardiac arrest to revascularization, are independent predictors of mortality. However, the most powerful predictor of death is the duration of stay in the ICU and the requirement of mechanical ventilation for more than forty-eight hours.
Introduction:Interventional ablation has been demonstrated to represent an effective therapy in patients with atrial fibrillation (AF), leading to restoration and maintenance of sinus rhythm in the majority of cases. However, recurrence of AF is encountered in 35% to 40% of cases, and the causes for this frequent complication have not been elucidated so far.Material and methods:Here we present the study protocol of the FIBRO-RISK trial, a prospective, single-center, cohort study which aims to investigate the impact of inflammatory-mediated myocardial fibrosis on the risk of recurrence after successful catheter ablation of atrial fibrillation. The level of systemic inflammation in the pre-ablation and immediate post-ablation period will be assessed on the basis of serum levels of inflammatory biomarkers (hsCRP, matrix metalloproteases, interleukin-6), while the level of cardiac fibrosis will be determined based on cardiac magnetic resonance imaging associated with complex post-processing techniques for mapping myocardial fibrosis at the level of left atrium and left ventricle. At the same time, the amount of epicardial fat will serve as an indirect marker of localized inflammation and will be determined at different levels in the heart (surrounding left atrium, right atrium or the entire heart), while ventricular function will be assessed on the basis of serum levels of NT-proBNP prior to the procedure. All these parameters will be investigated in patients with successful ablation of AF, who will be divided into 2 groups: group 1 – patients who develop AF recurrence at 1-year, and group 2 – patients with no recurrence of AF at 1-year. In all patients, the following biomarkers will be determined: serum levels of inflammatory biomarkers and NT-proBNP at 24 hours and 1-year post procedure, the amount of myocardial fibrosis at the level of left atrium and left ventricle at baseline +/− 7 days, and the amount of epicardial fat surrounding left atrium, right atrium and the entire heart at baseline +/− 7 days.The primary endpoint of the study will be represented by the rate of AF recurrence at 1-year post ablation, documented by either ECG or Holter monitoring. The secondary endpoints of the study will consist in:the rate of re-hospitalization,the rate of survival without relapse, andthe rate of major adverse cardiovascular events (MACE rate, including cardiovascular death or stroke).In conclusion, FIBRO-RISK will be the first CMR-based study that will investigate the impact of inflammation-mediated myocardial fibrosis and ventricular remodeling on the risk of recurrence after successful ablation of AF, aiming to validate inflammatory biomarkers and myocardial fibrosis as predictors for AF recurrence.
Atrial fibrillation (AF) is the most frequent form of supraventricular arrhythmia in medical practice. It is characterized by chaotic electrical activity in the atria, which often leads to irregular and fast ventricular contractions. Pulmonary veins (PV) play an essential part in the genesis of AF. There are a series of risk factors that trigger the development and recurrence of AF after PV isolation. Despite advanced medical technology, the success rate of AF ablation is not satisfactory. The purpose of this study is to assess the preprocedural imaging and serum biomarkers linked to an increased recurrence of AF after PV isolation. The primary endpoint is represented by AF recurrence after PV isolation. In addition, the rate of cardiovascular death and the rate of major adverse cardiovascular events will be assessed in relation to the enlargement of the left atrium and the volume of epicardial adipose tissue surrounding the heart.
Recent studies demonstrated that despite restoration of the sinus rhythm, patients with a positive history of atrial fibrillation (AF) are still at risk of thromboembolic events. The primary objective of this study is to identify new imaging-derived biomarkers provided by modern imaging technologies, such as cardiac computed tomography angiography, delayed enhancement magnetic resonance imaging, or speckle tracking echocardiography, as well as hematological biomarkers, associated with the risk of intracavitary thrombosis in patients with AF, in order to identify the imaging-derived characteristics associated with an increased risk of cardioembolic events. Imaging data collected will be post-processed using advanced techniques of computational modeling, in order to fully characterize the degree of structural remodeling and the amount of atrial fibrosis. The primary endpoint of the study is represented by the rate of thromboembolic events. The rate of cardiovascular death, the rate of major adverse cardiovascular events, and the rate of AF recurrence will also be determined in relation to the degree of structural remodeling and atrial fibrosis.
Atrial fibrillation is the most frequent arrhythmia in adults, becoming more frequent with age. Recent clinical studies demonstrated that epicardial fat is linked with atrial fibrillation induction and recurrence. The arrhythmogenic mechanism consists in the fact that the epicardial adipose tissue is metabolically active, inducing local inflammation and enhancing the oxidative stress, which lead to atrial fibrillation as well as atherosclerosis. Having metabolic activity and secreting various anti- and pro-inflammatory biomarkers, the fat surrounding the heart has been linked to the complex process of coronary plaque vulnerabilization. This clinical update aims to summarize the role of epicardial adipose tissue in the pathogenesis, persistence, and severity of atrial fibrillation.
Introduction: We present the case of a patient suffering from inferior vena cava hypoplasia complicated with Phlegmasia cerulean dolens. Imaging techniques allow precise diagnosis of inferior vena cava hypoplasia, providing essential structural details on the degree of damage of the vena cava and for the other branches. Case presentation: A 58 years old, obese and diabetic male patient presented with intense pain in the lower limbs, with the onset 24h before presentation. The patient presented generalized edema, cyanosis and functional impotence. Angio CT examination revealed hypoplasia of the inferior vena cava, with extensive DVT (deep vein thrombosis). In emergency conditions, with the agreement of the patient, we initiated the thrombolytic therapy (streptokinase for 72h) associated with anticoagulants (heparin). The evolution was favorable: a significant reduction in leg circumference was recorded, together with pain relief and reduction of local inflammation in the lower limbs. Conclusion: Severe cases of inferior vena cava hypoplasia complicated with deep vein thrombosis can present a good prognosis if appropriate treatment with anticoagulants and thrombolytics is initiated in time.
Funding Acknowledgements Plaqueimage Background Atrial fibrillation (AF) is the most common supraventricular rhythm disturbance and pulmonary vein (PV) isolation has an important role in rhythm control treatment strategies of this disease. Various anatomical and clinical characteristics have been well established as predictors of the risk of recurrence following ablation procedures, but the role of epicardial fat tissue (EFT) in the recurrence of AF has not been elucidated so far. Purpose To investigate the influence of left atrial size and EFT volume in the recurrence of AF after pulmonary vein ablation, during a 6-month follow-up. Methods A total of 40 patients, 52.5% with paroxysmal and 47.5% with chronic AF underwent PV isolation using radiofrequency and cryoablation techniques. EFT was determined using cardiac computed tomography angiography (CCTA) associated with advanced image post-processing techniques. Results In patients who developed AF recurrence at 6 months after AF ablation, the volume of EFT and of left atrium were significantly larger than in the group who maintained sinus rhythm (202.5 ± 64.56 ml vs. 138 ± 55.74 ml, p = 0.01 for EFT, and 149.3 ± 4.66 ml vs. 90.63 ± 5.19 ml, p <0.0001 for left atrial volume, respectively). The left ventricular ejection fraction was significantly lower in patients with AF recurrence (50.25 ± 6.54% vs. 54.22 ± 3.95%, p = 0,04). The analysis of AF recurrence between the two different ablation techniques did not show any difference in recurrence rates between radiofrequency and cryoablation methods (29% vs. 23%, respectively p = 0.73). At the same time, recurrence rates after AF ablation were not influenced by the main cardiovascular risk factors (age, hypertension, dyslipidemia and smoking) and was not associated with different risk scores (CHA2DS2-VASc and HAS-BLED). Conclusion Patients with AF recurrence after pulmonary vein ablation present significantly higher EFT or left atrial volumes compared to patients who maintained sinus rhythm. This indicates the inflammatory mediated response, usually accompanied by an increased amount of EFT, could be associated with the risk of AF recurrence following catheter ablation of the pulmonary veins.
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