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Indications for cardiac implantable electronic devices (CIEDs) are increasing. Almost one-third of device-related infections are endocarditis. Transvenous lead extraction (TLE) has emerged as an effective and safe approach for treating device-related infections and complications. Multiple types of extraction tools are being used worldwide. Our goal is to evaluate the safety and effectiveness of TLE using non-powered extraction tools. The study included patients between October 2018 and July 2022 requiring TLE according to EHRA expert consensus recommendations on lead extraction. A total of 88 consecutive patients were included. Indications for TLE included device-related infections in 74% of the patients. Of those, 32% had device-related endocarditis with or without sepsis. Staphylococcus Aureus was the most frequent pathogen in patients with endocarditis and positive bacteremia, and 57% had negative bloodstream cultures. A total of 150 cardiac pacing and defibrillator leads were targeted for extraction. The mean dwell time for leads was 6.92 ± 4.4 years; 52.8% were older than 5 years, 15.8% were older than ten years, and the longest lead dwell time was 26 years. Patients' age varied between 18 and 98, with a mean age of 66 ± 16 years. Sixty-seven percent of patients were males. Using only non-powered extraction tools, we report 93.3% complete lead removal and 99% clinical success with partial extraction. We report no procedure-related death nor major complications. Minor complication incidence was 6.8%, and all complications resolved spontaneously. The 30-day mortality rate was 3.4%. TLE using non-powered extraction tools is safe and effective even without surgical backup on site. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) impacts hundreds of millions of people each year and is the main cause of death worldwide, with atherosclerosis being its most frequent form of manifestation. Low-density lipoproteins (LDL) have already been established as a significant cardiovascular risk factor, but more recent studies have shown that small, dense LDLs are the ones more frequently associated with a higher overall risk for developing atherosclerotic cardiovascular disease. Ever since atherogenic phenotypes were defined for the first time, LDL subfractions have been continuously analyzed in order to identify those with a higher atherogenic profile that could further become not only high-accuracy, effective prognostic biomarkers, but also treatment targets for novel lipid-lowering molecules. This review sets out to comprehensively evaluate the association between various LDL-subfractions and the risk of further developing major adverse cardiovascular events, by assessing both genetical and clinical features and focusing on their physiopathological characteristics, chemical composition, and global ability to predict long-term cardiovascular risk within the general population. Further research is required in order to establish the most beneficial range of LDL-C levels for both primary and secondary prevention, as well as to implement LDL subfraction testing as a routine protocol, separately from the general assessment of the other traditional cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

Cardiac resynchronization therapy (CRT) restores ventricular dyssynchrony, improving left ventricle (LV) systolic function, symptoms, and outcome in patients with heart failure, systolic dysfunction, and prolonged QRS interval. The left atrium (LA) plays tremendous roles in maintaining cardiac function, being often inflicted in various cardiovascular diseases. LA remodeling implies structural—dilation, functional—altered phasic functions, and strain and electrical—atrial fibrillation remodeling. Until now, several important studies have approached the relationship between LA and CRT. LA volumes can predict responsiveness to CRT, being also associated with improved outcome in these patients. LA function and strain parameters have been shown to improve after CRT, especially in those who were positive responders to it. Further studies still need to be conducted to comprehensively characterize the impact of CRT on LA phasic function and strain, and, also, in conjunction with its impact on functional mitral regurgitation and LV diastolic dysfunction. The aim of this review was to provide an overview of current available data regarding the relation between CRT and LA remodeling. [ABSTRACT FROM AUTHOR]

Hypertrophic cardiomyopathy (HCM) is an inherited primary myocardial disease characterized by asymmetrical/symmetrical left ventricle (LV) hypertrophy, with or without LV outflow tract (LVOT) dynamic obstruction, and poor prognosis. Cardiac resynchronization therapy (CRT) has emerged as a minimally invasive tool for patients with heart failure (HF) with decreased LV ejection fraction (LVEF) and prolonged QRS duration of over 120 ms with or without left bundle branch block (LBBB). Several HCM patients are at risk of developing LBBB because of disease progression or secondary to septal myomectomy, while others might develop HF with decreased LVEF, alleged end-stage/dilated HCM, especially those with thin myofilament mutations. Several studies have shown that patients with myectomy-induced LBBB might benefit from left bundle branch pacing or CRT to relieve symptoms, improve exercise capacity, and increase LVEF. Otherwise, patients with end-stage/dilated HCM and prolonged QRS interval could gain from CRT in terms of NYHA class improvement, LV systolic performance increase and, to some degree, LV reverse remodeling. Moreover, several electrical and imaging parameters might aid proper selection and stratification of HCM patients to benefit from CRT. Nonetheless, current available data are scarce and further studies are still required to accurately clarify the view. This review reassesses the importance of CRT in patients with HCM based on current research by contrasting and contextualizing data from various published studies. [ABSTRACT FROM AUTHOR]

Background: The prevalence of chronic kidney disease (CKD) correlates with the prevalence of hypertension (HT). We studied the prevalence and predictors of CKD in a representative sample of the Romanian adult population. Methods: A sample of 1470 subjects were enrolled in the SEPHAR IV (Study for the Evaluation of Prevalence of Hypertension and Cardiovascular Risk) survey. All subjects were evaluated for blood pressure (BP) and extensive evaluations of target organ damage, blood, and urine samples were undertaken. Results: A total of 883 subjects were included in the statistical analysis. Those experiencing CKD with an eGFR < 60 mL/min/1.73 m2 were older at 71.94 ± 7.4 years (n = 19, 2.15%) compared with those without renal impairment at 50.3 ± 16.21 years (n = 864, 97.85%), p < 0.0001. The prevalence of CKD among hypertensives (379 from 883) was 4.49% (17/379), while 17 out of 19 subjects with CKD had HT (89.47%). After adjusting for age, sex, and diabetic status, only serum uric acid (SUR) > 6.9 mg/dL (OR: 6.61; 95% CI: 2.063, 10.83; p = 0.004) was an independent risk factor and a predictor of CKD. Conclusions: The prevalence of CKD in hypertensive Romanian adults was more than ten times higher than in the normotensive population. Levels of SUR > 6.9 mg/dL were predictors of CKD. [ABSTRACT FROM AUTHOR]

Myocardial infarction is one of the leading causes of death worldwide, despite numerous efforts to find efficient prognostic biomarkers and treatment targets. In the present study, we aimed to assess the potential of six microRNAs known to be involved in cardiovascular diseases, cell-free DNA (cfDNA), and mitochondrial DNA (mtDNA) circulating in plasma to be used as prognostic tools for the occurrence of unfavorable outcomes such as major adverse cardiovascular events (MACE) after acute ST-segment elevation myocardial infarction (STEMI). Fifty STEMI patients were enrolled and monitored for 6 months for the occurrence of MACE. Plasma was collected at three time points: upon admission to hospital (T0), at discharge from hospital (T1), and 6 months post-STEMI (T6). Plasma levels of miR-223-3p, miR-142-3p, miR-155-5p, miR-486-5p, miR-125a-5p, and miR-146a-5p, as well as of cfDNA and mtDNA, were measured by RT-qPCR. Results showed that the levels of all measured miRNAs, as well as of cfDNA and mtDNA, were the most increased at T1, compared to the other two time points. In the plasma of STEMI patients with MACE compared to those without MACE, we determined increased levels of miRNAs, cfDNA, and mtDNA at T1. Hence, we used the levels of all measured parameters at T1 for further statistical analysis. Statistical analysis demonstrated that all six miRNAs and cfDNA plus mtDNA levels, respectively, were associated with MACE. The minimal statistical model that could predict MACE in STEMI patients was the combination of mtDNA and miR-142-3p levels, as evidenced by ROC analysis (AUC = 0.97, p < 0.001). In conclusion, the increased plasma levels of mtDNA, along with miR-142-3p, could be used to predict unfavorable outcomes in STEMI patients. [ABSTRACT FROM AUTHOR]

Ischemic heart disease is one of the most important causes of mortality and morbidity worldwide. Revascularization of coronary stenosis inducing ischemia, either by percutaneous or surgical intervention, significantly reduces major adverse cardiovascular events and improves quality of life. However, in cases of intermediate lesions, classified by a diameter stenosis between 50 and 90% by European guidelines and 40–70% in American counterparts with no clear evidence of ischemia, the indication of revascularization and impact is determined using various methods that altogether comprehensively evaluate the lesions. This review will discuss the various techniques to assess intermediate stenoses, highlighting indications and advantages, but also drawbacks. Fractional flow rate (FFR) and instantaneous wave-free ratio (iFR) are the gold standard for the functional evaluation of intermediate lesions, but there are clinical circumstances in which these pressure-wire-derived indices are not accurate. Complementary invasive investigations, mainly intravascular ultrasound and/or optical coherence tomography, offer parameters that can be correlated with FFR/iFR and additional insights into the morphology of the plaque guiding the eventual percutaneous intervention in terms of length and size of stents, thus improving the outcomes of the procedure. The development of artificial intelligence and machine learning with advanced algorithms of prediction will offer multiple scenarios for treatment, allowing real-time selection of the best strategy for revascularization. [ABSTRACT FROM AUTHOR]

Background: Visual estimation (VE) of coronary stenoses is the first step during invasive coronary angiography. The aim of this study was to evaluate the accuracy of VE together with invasive functional assessment (IFA) in defining the functional significance (FS) of coronary stenoses based on the opinion of multiple operators. Methods: Fourteen independent operators visually evaluated 133 coronary lesions which had a previous FFR measurement, indicating the degree of stenosis (DS), FS and IFA intention. We determined the accuracy of FS prediction using several scenarios combining individual and group decision, considering IFA as deemed necessary by the operator or only in intermediate lesions. Results: The accuracy of VE in predicting FS was largely variable between operators (average 66.1%); it improved significantly when IFA was used either as per operator's opinion (86.3%; p < 0.0001) or only in intermediate DS (82.9; p < 0.0001). There was no significant difference between using IFA per observer's opinion or only in intermediate DS lesions (p = 0.166). The poorest accuracy of VE for FS was obtained in intermediate DS lesions (59.1%). Conclusions: There are significant inter-observer differences in reporting the degree of DS, while the accuracy of VE prediction of FS is also largely dependent on the operator, and the worst performance is obtained in the evaluation of intermediate DS. [ABSTRACT FROM AUTHOR]

References 1 Popescu S., Preda M., Marinescu C., Simionescu M., Burlacu A. Dual Stem Cell Therapy Improves the Myocardial Recovery Post-Infarction through Reciprocal Modulation of Cell Functions. Extracellular vesicles (EV) are recently discovered cell-derived elements encompassing apoptotic bodies, ectosomes and exosomes. We designed this Special Issue with the belief that biomedical research will pave the road which in the near future will lead us to find remedies and cures for the cardiovascular diseases. Cardiovascular diseases have attracted our full attention not only because they are the main cause of mortality and morbidity in many countries but also because the therapy for and cure of these maladies are among the major challenges of the medicine in the 21st century. [Extracted from the article]

Familial hypercholesterolemia (FH) is increasingly associated with inflammation, a phenotype that persists despite treatment with lipid lowering therapies. The alternative C3 complement system (C3), as a key inflammatory mediator, seems to be involved in the atherosclerotic process; however, the relationship between C3 and lipids during plaque progression remains unknown. The aim of the study was to investigate by a systems biology approach the role of C3 in relation to lipoprotein levels during atherosclerosis (AT) progression and to gain a better understanding on the effects of C3 products on the phenotype and function of human lipid-loaded vascular smooth muscle cells (VSMCs). By mass spectrometry and differential proteomics, we found the extracellular matrix (ECM) of human aortas to be enriched in active components of the C3 complement system, with a significantly different proteomic signature in AT segments. Thus, C3 products were more abundant in AT-ECM than in macroscopically normal segments. Furthermore, circulating C3 levels were significantly elevated in FH patients with subclinical coronary AT, evidenced by computed tomographic angiography. However, no correlation was identified between circulating C3 levels and the increase in plaque burden, indicating a local regulation of the C3 in AT arteries. In cell culture studies of human VSMCs, we evidenced the expression of C3, C3aR (anaphylatoxin receptor) and the integrin αMβ2 receptor for C3b/iC3b (RT-PCR and Western blot). C3mRNA was up-regulated in lipid-loaded human VSMCs, and C3 protein significantly increased in cell culture supernatants, indicating that the C3 products in the AT-ECM have a local vessel-wall niche. Interestingly, C3a and iC3b (C3 active fragments) have functional effects on VSMCs, significantly reversing the inhibition of VSMC migration induced by aggregated LDL and stimulating cell spreading, organization of F-actin stress fibers and attachment during the adhesion of lipid-loaded human VSMCs. This study, by using a systems biology approach, identified molecular processes involving the C3 complement system in vascular remodeling and in the progression of advanced human atherosclerotic lesions. [ABSTRACT FROM AUTHOR]

Endothelium has a rich vesicular network that allows the exchange of macromolecules between blood and parenchymal cells. This feature of endothelial cells, along with their polarized secretory machinery, makes them the second major contributor, after platelets, to the particulate secretome in circulation. Extracellular vesicles (EVs) produced by the endothelial cells mirror the remarkable molecular heterogeneity of their parent cells. Cargo molecules carried by EVs were shown to contribute to the physiological functions of endothelium and may support the plasticity and adaptation of endothelial cells in a paracrine manner. Endothelium-derived vesicles can also contribute to the pathogenesis of cardiovascular disease or can serve as prognostic or diagnostic biomarkers. Finally, endothelium-derived EVs can be used as therapeutic tools to target endothelium for drug delivery or target stromal cells via the endothelial cells. In this review we revisit the recent evidence on the heterogeneity and plasticity of endothelial cells and their EVs. We discuss the role of endothelial EVs in the maintenance of vascular homeostasis along with their contributions to endothelial adaptation and dysfunction. Finally, we evaluate the potential of endothelial EVs as disease biomarkers and their leverage as therapeutic tools. [ABSTRACT FROM AUTHOR]

The novel protein ADTRP, identified and described by us in 2011, is androgen-inducible and regulates the expression and activity of Tissue Factor Pathway Inhibitor, the major inhibitor of the Tissue Factor-dependent pathway of coagulation on endothelial cells. Single-nucleotide polymorphisms in ADTRP associate with coronary artery disease and myocardial infarction, and deep vein thrombosis/venous thromboembolism. Some athero-protective effects of androgen could exert through up-regulation of ADTRP expression. We discovered a critical role of ADTRP in vascular development and vessel integrity and function, manifested through Wnt signaling-dependent regulation of matrix metalloproteinase-9. ADTRP also hydrolyses fatty acid esters of hydroxy-fatty acids, which have anti-diabetic and anti-inflammatory effects and can control metabolic disorders. Here we summarize and analyze the knowledge on ADTRP and try to decipher its functions in health and disease. [ABSTRACT FROM AUTHOR]

During the last decade, studies have raised awareness of the crucial role that the right ventricle plays in various clinical settings, including diseases primarily linked to the left ventricle. The assessment of right ventricular performance with conventional echocardiography is challenging. Novel echocardiographic techniques improve the functional assessment of the right ventricle and they show good correlation with the gold standard represented by cardiac magnetic resonance. This review summarizes the traditional and innovative echocardiographic techniques used in the functional assessment of the right ventricle, focusing on the role of right ventricular dysfunction in heart failure with reduced ejection fraction and providing a perspective on recent evidence from literature. [ABSTRACT FROM AUTHOR]

Pediatric inherited cardiomyopathies (CMPs) and channelopathies (CNPs) remain important causes of death in this population, therefore, there is a need for prompt diagnosis and tailored treatment. Conventional evaluation fails to establish the diagnosis of pediatric CMPs and CNPs in a significant proportion, prompting further, more complex testing to make a diagnosis that could influence the implementation of lifesaving strategies. Genetic testing in CMPs and CNPs may help unveil the underlying cause, but needs to be carried out with caution given the lack of uniform recommendations in guidelines about the precise time to start the genetic evaluation or the type of targeted testing or whole-genome sequencing. A very diverse etiology and the scarce number of randomized studies of pediatric CMPs and CNPs make genetic testing of these maladies far more particular than their adult counterpart. The genetic diagnosis is even more puzzling if the psychological impact point of view is taken into account. This review aims to put together different perspectives, state-of-the art recommendations—synthetizing the major indications from European and American guidelines—and psychosocial outlooks to construct a comprehensive genetic assessment of pediatric CMPs and CNPs. [ABSTRACT FROM AUTHOR]

Despite significant progress in treating ischemic cardiac disease and succeeding heart failure, there is still an unmet need to develop effective therapeutic strategies given the persistent high-mortality rate. Advances in stem cell biology hold great promise for regenerative medicine, particularly for cardiac regeneration. Various cell types have been used both in preclinical and clinical studies to repair the injured heart, either directly or indirectly. Transplanted cells may act in an autocrine and/or paracrine manner to improve the myocyte survival and migration of remote and/or resident stem cells to the site of injury. Still, the molecular mechanisms regulating cardiac protection and repair are poorly understood. Stem cell fate is directed by multifaceted interactions between genetic, epigenetic, transcriptional, and post-transcriptional mechanisms. Decoding stem cells' "panomic" data would provide a comprehensive picture of the underlying mechanisms, resulting in patient-tailored therapy. This review offers a critical analysis of omics data in relation to stem cell survival and differentiation. Additionally, the emerging role of stem cell-derived exosomes as "cell-free" therapy is debated. Last but not least, we discuss the challenges to retrieve and analyze the huge amount of publicly available omics data. [ABSTRACT FROM AUTHOR]

The concepts underlying hypertrophic cardiomyopathy (HCM) pathogenesis have evolved greatly over the last 60 years since the pioneering work of the British pathologist Donald Teare, presenting the autopsy findings of "asymmetric hypertrophy of the heart in young adults". Advances in human genome analysis and cardiac imaging techniques have enriched our understanding of the complex architecture of the malady and shaped the way we perceive the illness continuum. Presently, HCM is acknowledged as "a disease of the sarcomere", where the relationship between genotype and phenotype is not straightforward but subject to various genetic and nongenetic influences. The focus of this review is to discuss key aspects related to molecular mechanisms and imaging aspects that have prompted genotype-phenotype correlations, which will hopefully empower patient-tailored health interventions.