Focus on malignant ventricular premature contractions.

Premature ventricular contractions (PVCs) are common. Although often benign, they can also be associated with increased morbidity and mortality. The aim of this review was to assess the risk evaluation of PVCs in patients with or without structural heart disease and discuss the management of this arrhythmia. Reports published in English were searched in PubMed with the following search terms: premature ventricular contraction, ectopic ventricular beat, ventricular extrasystole, antiarrhythmic drugs, ablation, ventricular arrhythmia, ventricular tachycardia, ventricular fibrillation and torsade de pointe. This analysis suggests that all patients with frequent PVCs should be assessed for PVC burden, symptom status and the presence of structural heart disease. PVCs in patients with structurally normal hearts was once considered a benign phenomenon. Uncommonly, PVCs may provoke life-threatening arrhythmias. Ventricular fibrillation is the initial mode of malignant rapid ventricular arrhythmias (MRVAs). Patients with malignant PVC and PVC burden >10% are at increased risk of MRVA in case of myocardial infarction and heart failure. MRVA is the primary cause of sudden cardiac death in patients with and without structural heart disease. Therapeutic options include medical therapy and catheter ablation, the latter more effective and potentially curable, particularly in patients with left ventricular dysfunction. The timely recognition and effective treatment of malignant PVCs in symptomatic patients with underling cardiomyopathy are mandatory to initiate early therapies before the occurrence of adverse clinical outcomes and to improve the long-term prognosis.

Risk stratification in hypertrophic cardiomyopathy.

Sudden cardiac death (SCD) is the most devastating complication of hypertrophic cardiomyopathy (HCM). The greatest challenge in the management of HCM is identifying those at increased risk, since an implantable cardioverter-defibrillator (ICD) is a potentially life-saving therapy. We sought to summarize the available data on SCD in HCM and provide a clinical perspective on the current differing and somewhat conflicting data on risk stratification, with balanced guidance regarding rational clinical decision-making. Additionally, we sought to determine the status of the current implementation of guidelines compiled by HCM experts worldwide. The HCM Risk-SCD model helps improve the risk stratification of HCM patients for primary prevention of SCD by calculating an individual risk estimate that contributes to the clinical decision-making process. Improved risk stratification is important for decision-making before ICD implantation for the primary prevention of SCD.

Inherited primary arrhythmia disorders: cardiac channelopathies and sports activity.

Sudden cardiac death (SCD) in an apparently healthy individual is a tragedy. It is important to identify the cause of death and to prevent SCD in potentially at-risk family members. Inherited primary arrhythmia disorders are associated with exercise-related SCD. Despite the well-known benefits of exercise, exercise restriction has been a historical mainstay of therapy for these conditions. However, since familiarity with inherited arrhythmia conditions has increased and patients are often children and young adults, it is necessary to reassess the treatment guidelines regarding exercise constraints. The aim of this review is to analyze the risk of exercise-induced SCD in patients with inherited cardiac conditions and explore the challenges faced when advising patients about exercise limitations. We searched for publications on cardiac channelopathies in PubMed with the following medical subject headings (MeSH): "long QT syndrome"; "short QT syndrome"; "Brugada syndrome"; and "catecholaminergic polymorphic ventricular tachycardia". The abstracts of these articles were scanned, and articles of relevance, along with pertinent references, were read in full. The analysis was restricted to reports published in English. The findings of this analysis suggest that exercise with low-to-moderate cardiovascular demand may be possible under regular clinical follow-up in inherited primary arrhythmia disorders. Recent data show that patients with inherited primary arrhythmia disorders are at low risk for events once a comprehensive treatment program has been established. Recreational activity is likely safe for these individuals, with personalized management based on individual patient preferences and priorities.

Cellular and molecular etiology of hepatocyte injury in a murine model of environmentally induced liver abnormality.

Exposures to a wide variety of environmental substances are negatively associated with many biological cell systems both in humans and rodents. Trichloroethane (TCE), a ubiquitous environmental toxicant, is used in large quantities as a dissolvent, metal degreaser, chemical intermediate, and component of consumer products. This increases the likelihood of human exposure to these compounds through dermal, inhalation and oral routes. The present in vivo study was aimed to investigate the possible cellular and molecular etiology of liver abnormality induced by early exposure to TCE using a murine model. The results showed a significant increase in liver weight. Histopathological examination revealed a TCE-induced hepatotoxicity which appeared as heavily congested central vein and blood sinusoids as well as leukocytic infiltration. Mitotic figures and apoptotic changes such as chromatin condensation and nuclear fragments were also identified. Cell death analysis demonstrates hepatocellular apoptosis was evident in the treated mice compared to control. TCE was also found to induce oxidative stress as indicated by an increase in the levels of lipid peroxidation, an oxidative stress marker. There was also a significant decrease in the DNA content of the hepatocytes of the treated groups compared to control. Agarose gel electrophoresis also provided further biochemical evidence of apoptosis by showing internucleosomal DNA fragmentation in the liver cells, indicating oxidative stress as the cause of DNA damage. These results suggest the need for a complete risk assessment of any new chemical prior to its arrival into the consumer market.

Cutaneous squamous cell carcinoma in the lateral abdominal wall of local Libyan ewes.

Gross and histopathological features of surgically excised squamous cell carcinomas (SCC) observed in thirteen local Libyan ewes were reported. The age of the ewes enrolled in the current study ranged from 2 to 3 years. The cases were admitted to private veterinary clinics in south-western region of Tripoli, Libya, during the period between July 2014 and October 2015. All lesions were located in the right and left lateral abdominal wall (caudo-ventrally) with a size range of 8 to 11cm in diameter. The tumor masses have been removed by surgical excision. The histopathological examination of surgically excised masses has revealed the characteristic cell nests of SCC showing central keratinization and hyalinization with presence of apoptotic bodies, fattened keratinocytes, and a heavy interstitial infiltration of neutrophils and lymphocytes. The follow up of the cases showed no signs of tumor reoccurrence. In conclusion, SCC in Libyan sheep affects mainly the woolless areas and can be successfully removed by surgical excision.

[Utility of cardiovascular magnetic resonance in hypertrophic cardiomyopathy: when is it superior to echocardiography?]. / Imagerie par résonance magnétique dans la cardiomyopathie hypertrophique : qu'apporte-t-elle de plus par rapport à l'échocardiographie ?

The diagnosis of hypertrophic cardiomyopathy is usually established by echocardiography. Recently, there has been greatly increased use of cardiac magnetic resonance (CMR) because of its precise determination of myocardial anatomy and the depiction of myocardial fibrosis. In this review, we describe the role of echocardiography and magnetic resonance in the assessment of this complex disease. In conclusion, there is a complementarity between cardiovascular magnetic resonance imaging and echocardiography for the diagnosis and the management of HCM.

Comparative study of toxic effects of zearalenone and its two major metabolites alpha-zearalenol and beta-zearalenol on cultured human Caco-2 cells.

Zearalenone (ZEN) is a fusarotoxin converted predominantly into alpha-zearalenol (alpha-Zol) and beta-zearalenol (beta-Zol) by hepatic hydroxysteroid dehydrogenases. The feeding of naturally contaminated grains with ZEN was associated with hyperestrogenic and adverse effects on humans and animals. There is a lack of information on the attribution of the toxic effects of these toxins. One wonders if these effects are due to the parent molecule (ZEN) or to its major metabolites (alpha-Zol and beta-Zol). Using human Caco-2 cells, we looked for the molecular mechanisms of toxicity of ZEN, alpha-Zol, and beta-Zol. Toxicity effects were studied by MTT viability assay and oxidative stress induction by measuring malondialdehyde (MDA) generation. To check whether the oxidative stress induction was associated to DNA lesions, we looked for DNA fragmentation by means of the Comet and the diphenylamine assays. To specify cell death pathway, we investigated caspase-3 activation, confirmed by poly(ADP-ribose) polymerase cleavage and by Bcl-2 depletion. Our results clearly demonstrated that ZEN as well as its two metabolites presented variable toxic effects. They induced cell death and an increase in MDA generation. These effects were associated to DNA fragmentation as well as caspase-3 activation. The observed toxic effects seem to be relieved by the metabolism of ZEN into alpha-Zol and beta-Zol.