Echocardiography and Other Noninvasive Imaging Techniques in the Selection and Management of Patients with Cardiac Resynchronization Therapy

Cardiac resynchronization therapy has become a widely used procedure for the treatment of patients with heart failure and severely impaired systolic function who associate left bundle branch block and remain symptomatic, in New York Heart Association II to IV functional class, despite maximum tolerated medical therapy. Imaging evaluation of these patients is complex, aiming to provide an accurate and extensive assessment before and after implantation, although a standardized protocol is yet to be implemented. Extensive research has been conducted to assess the ability of different imaging techniques and parameters to identify and quantify mechanical dyssynchrony, assess myocardial remodeling, provide prognostic information, or help guide lead placement and pacing parameters optimization in this category of patients. For these purposes, ultrasound-based imaging techniques, as well as cardiac magnetic resonance imaging, multislice cardiac computed tomography and nuclear ventriculography have been and are currently used, for research, as well as for clinical purposes. The aim of the current paper was to provide some insights into the imaging assessment of candidates and patients who have undergone cardiac resynchronization therapy

Plasma homocysteine and the severity of heart failure in patients with previous myocardial infarction

Background: Homocysteine is considered to be a risk factor, or an indicator of risk, for the development of cardiovascular disease. Little data is available on its significance in patients with previous myocardial infarction. The aim of our study was to assess the plasma level of homocysteine and its relationship with the severity of heart failure in patients with chronic myocardial infarction. Methods: We studied 144 patients with previous myocardial infarction. Patients were divided into two groups according to the presence or absence of heart failure, as certified by clinical evidence of heart failure and by echocardiographic criteria for left ventricular systolic dysfunction. Results: Of the patients with prior myocardial infarction (144; 63.6 ± 9.6 years) included in the study, 65 had heart failure. The mean level of homocysteine was significantly higher in the heart failure group (18.9 mmol/L) than in the non-heart failure group (14.1 mmol/L; p ≤ 0.001). Our study demonstrated that there is a statistically significant correlation between homocysteine plasma levels and the severity of heart failure in patients with prior myocardial infarction. Homocysteine levels have proved to become higher with NYHA class progression. A significant cross-sectional correlation has been assessed between homocysteine and tissue Doppler echocardiography parameters. Conclusions: Increased plasma homocysteine levels independently correlate with the severity of heart failure in patients with chronic myocardial infarction. We suggest that homocysteine can be used in clinical practice as a valuable heart failure risk marker in patients with chronic myocardial infarction. (Cardiol J 2011; 18, 1: 55-62

Biomarkers in Metabolic Syndrome

Nowadays, biomarkers are useful in the early detection and risk stratification of metabolic syndrome (MetS) patients. Studies confirmed the implication of adipokines, neuropeptides, inflammatory cytokines, prothrombotic factors, and others in MetS pathogenesis. Leptin:adiponectin ratio is useful in predicting insulin resistance and MetS severity; leptin is correlated with obesity and waist size and adiponectin is inversely related with MetS components. Ghrelin is inversely correlated with MetS components, and studies confirmed its role in MetS prediction. Regarding the pro-inflammatory cytokines, studies confirmed that interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha are positively correlated with hypertriglyceridemia, hypertension, fasting glucose levels, insulin resistance, and in postmenopausal women with central obesity. Oxidized low-density lipoprotein (LDL) levels could be implicated in insulin resistance. Recent studies also confirmed that novel biomarkers such as pentraxin-3 are positively correlated with MetS severity and the presence of vascular lesions, and it could bring new data on the MetS mechanism. Within this chapter, we review data on the contribution of biomarkers as well as on the stratification of MetS patients, discussing their key contribution for creating a risk assessment algorithm

Enhanced laser thermal ablation for the in vitro treatment of liver cancer by specific delivery of multiwalled carbon nanotubes functionalized with human serum albumin

The main goal of this investigation was to develop and test a new method of treatment for human hepatocellular carcinoma (HCC). We present a method of carbon nanotube-enhanced laser thermal ablation of HepG2 cells (human hepatocellular liver carcinoma cell line) based on a simple multiwalled carbon nanotube (MWCNT) carrier system, such as human serum albumin (HSA), and demonstrate its selective therapeutic efficacy compared with normal hepatocyte cells. Both HepG2 cells and hepatocytes were treated with HSA–MWCNTs at various concentrations and at various incubation times and further irradiated using a 2 W, 808 nm laser beam. Transmission electron, phase contrast, and confocal microscopy combined with immunochemical staining were used to demonstrate the selective internalization of HSA–MWCNTs via Gp60 receptors and the caveolin-mediated endocytosis inside HepG2 cells. The postirradiation apoptotic rate of HepG2 cells treated with HSA–MWCNTs ranged from 88.24% (for 50 mg/L) at 60 sec to 92.34% (for 50 mg/L) at 30 min. Significantly lower necrotic rates were obtained when human hepatocytes were treated with HSA–MWCNTs in a similar manner. Our results clearly show that HSA–MWCNTs selectively attach on the albondin (aka Gp60) receptor located on the HepG2 membrane, followed by an uptake through a caveolin-dependent endocytosis process. These unique results may represent a major step in liver cancer treatment using nanolocalized thermal ablation by laser heating

Nanoparticles Targeting the Molecular Pathways of Heart Remodeling and Regeneration

Cardiovascular diseases are the main cause of death worldwide, a trend that will continue to grow over the next decade. The heart consists of a complex cellular network based mainly on cardiomyocytes, but also on endothelial cells, smooth muscle cells, fibroblasts, and pericytes, which closely communicate through paracrine factors and direct contact. These interactions serve as valuable targets in understanding the phenomenon of heart remodeling and regeneration. The advances in nanomedicine in the controlled delivery of active pharmacological agents are remarkable and may provide substantial contribution to the treatment of heart diseases. This review aims to summarize the main mechanisms involved in cardiac remodeling and regeneration and how they have been applied in nanomedicine

Is galectin-3 a promoter of ventricular dysfunction?

Heart failure is nowadays a common condition associated with high mortality and increased healthcare-related costs. Over the years, the research on heart failure management has been extensive in order to better diagnose and treat the condition. Since the progression of left ventricular dysfunction is a consequence of myocardial inflammation, apopotosis, and fibrosis leading to myocardium remodelling, several molecules that are involved in the inflammation pathways have been explored as possible biomarkers for the condition. The study of biomarkers and their key roles in inflammation could allow early identification of patients with heart failure, improve prognostic assessment, and provide a target for future therapies. Among currently studied biomarkers, extensive research has been conducted on galectin-3, a galactoside-binding lectin, which is synthetised and secreted when cardiomyocytes and fibroblasts are submitted to mechanical stress. Accordingly, it has been hypothesised that galectin-3 could be a promoter of left ventricular dysfunction. Galectin-3 has been shown to mediate inflammation by several different pathways which are further detailed in the current review. Also, we aimed to provide a comprehensive overview of existing evidence on the utility of galectin-3 in clinical settings associated with heart failure