Physical activity and sedentary behavior thresholds for identifying childhood hypertension and its phenotypes: The Healthy Growth Study

Hypertension phenotypes may represent differential pathophysiologic mechanisms and clinical impact, yet they have been poorly investigated. The study aimed to examine the associations of physical activity and sedentary behavior with hypertension phenotypes in a large group of Greek children and to identify thresholds regarding risk of hypertension. This was a cross-sectional study with a regionally representative sample of 2473 schoolchildren aged 9–13 years, with full data on physical activity and sedentary behavior indices, as well as arterial blood pressure measurements, physical examination, and anthropometry. Hypertensive children of both sexes had lower levels of physical activity (steps/d). Hypertensive girls had lower moderate-to-vigorous physical activity (MVPA), whereas hypertensive boys with isolated systolic hypertension (ISH) had more screen time than their normotensive counterparts. Increased levels of physical activity was associated with 33%–54% lower risk of all hypertension phenotypes in both sexes, whereas increased MVPA was associated with 41%–65% lower risk of all phenotypes in girls and with ISH and systolic and diastolic hypertension (SDH) in boys. In boys, higher sedentary time was associated with 11%–13% higher risk for SDH and ISH. Cutoff points of 12,378 steps/d, 47.3 min/d of MVPA, and 2.9 h/d of sedentary behavior were determined for identifying children at increased risk of hypertension. Physical activity is inversely associated with all hypertension phenotypes, whereas sedentary behavior is positively associated with ISH and SDH in boys. More studies should confirm the hypertension-specific cutoff values identified to be used in future prevention programs for childhood hypertension.     

The ARVD/C Genetic Variants Database: 2014 Update

Arrhythmogenic cardiomyopathy (ACM) is an inherited cardiac disease characterized by myocardial atrophy, fibro‐fatty replacement, and a high risk of ventricular arrhythmias that lead to sudden death. In 2009, genetic data from 57 publications were collected in the arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) Genetic Variants Database (freeware available at http://www.arvcdatabase.info ), which comprised 481 variants in eight ACM‐associated genes. In recent years, deep genetic sequencing has increased our knowledge of the genetics of ACM, revealing a large spectrum of nucleotide variations for which pathogenicity needs to be assessed. As of April 20, 2014, we have updated the ARVD/C database into the ARVD/C database to contain more than 1,400 variants in 12 ACM‐related genes (PKP2, DSP, DSC2, DSG2, JUP, TGFB3, TMEM43, LMNA, DES, TTN, PLN, CTNNA3) as reported in more than 160 references. Of these, only 411 nucleotide variants have been reported as pathogenic, whereas the significance of the other approximately 1,000 variants is still unknown. This comprehensive collection of ACM genetic data represents a valuable source of information on the spectrum of ACM‐associated genes and aims to facilitate the interpretation of genetic data and genetic counseling.     

Detection and Significance of Occult Axillary Metastatic Disease in Breast Cancer Patients

▪ Abstract: After clinical staging, the single most important prognostic factor for patients with newly diagnosed primary breast cancer is the presence or absence of detectable metastases to axillary lymph nodes when examined by conventional light microscopy. More sensitive methods of determination of lymph node status, such as evaluation of serial sections, immunohistochemical staining, and use of molecular biological assays increase the rate of detection of micrometastases. Although the feasibility of enhanced detection of occult axillary metastatic disease is well established, the prognostic significance of such detection is only recently starting to emerge. Furthermore, the enormous recent interest in the application of sentinel lymph node biopsy as an alternative to the evaluation of the entire axilla in patients with breast cancer makes the first-time detailed evaluation for micrometastases practically feasible. In this review the different methods of detecting micrometastatic disease in the axilla and the significance of such findings are discussed. ▪     

Focused echocardiography in cardio-oncology

Transthoracic echocardiography (TTE) is the cornerstone of imaging in patients with a malignancy in all stages of their treatment—before, during, and after the completion of it—to identify most of the cardiotoxic complications. However, the restricted time and resources of cardio-oncology services and the high volume of oncological patients and survivors on the other hand limit the access of this population to this modality. Focused Echo in Cardio-Oncology (FECO) in proportion to other focused cardiac protocols is proposed as a valuable tool after the initial standard complete TTE to: (a) identify the potential toxicity expected by the specific cancer therapy applied; (b) assess sequentially the pre-existing abnormality, if any, in relation to therapy; (c) assess the effect of any cardio-protective intervention; (d) identify any cardiac origin of patient complaints during or after therapy; (e) assess cardiac function in asymptomatic patients who develop significant changes in cardiac biomarkers during cancer therapy. Four different protocols of FECO are proposed according to the type of cardiotoxicity anticipated: FECOm (in patients on chemotherapeutics that cause myocardial dysfunction), FECOv (in patients at risk of valvular heart disease), FECOpd (in patients at risk of pericardial disease), and FECOph (in patients at risk of pulmonary hypertension). The application of FECO protocols is aimed to ensure accuracy, reliability, and effectiveness in the early identification of cardiovascular complications, improving quality of life, and being at the same time cost-effective.     

Lipoprotein profile,glycemic control and physical fitness after strength and aerobic training in post-menopausal women with type 2 diabetes

We studied the effects on blood lipids and physical fitness after a training program that combined strength and aerobic exercise in postmenopausal women with type 2 diabetes. Ten patients (55.0 ± 5.2 years) followed four exercise sessions per week, two strength and two aerobic, and ten (59.4 ± 3.2 years) served as a control group. Lipid profile, glycated hemoglobin (HbA_1c), HOMA2 index, exercise stress and muscular testing were assessed at the beginning and after 16 weeks of training program. Exercise training increased significantly HDL-C (17.2%; P < 0.001) and decreased triglycerides (18.9%), HbA_1c (15.0%), fasting plasma glucose (5.4%), insulin resistance (HOMA2 25.2%) and resting blood pressure (P < 0.01). After 16 weeks of training, exercise time (17.8%) and muscular strength increased significantly (P < 0.001). The results indicated that a combined strength and aerobic training program could induce positive adaptations on lipid profile, glycemic control, insulin resistance, cardiovascular function, and physical fitness in post-menopausal women with type 2 diabetes. An erratum to this article can be found at     

Sudden cardiac death with normal heart:: molecular autopsy

Several culprits may be identified at postmortem in sudden death (SD) victims, including coronary artery, myocardial, valve, conduction system, and congenital heart diseases. However, particularly in young people, the heart can be found grossly and histologically normal in a not-so-minor amount of cases (the so-called unexplained SD or “mors sine materia”) and inherited ion channel diseases are implicated (long and short QT syndromes, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia). These channelopathies are due to defective genes encoding for proteins of sodium and potassium ion channels at the sarcolemma level or for receptors regulating intracellular calcium release at the sarcoplasmic reticulum level. Postmortem investigation may still represent the first opportunity to make the proper diagnosis also in the setting of a structurally normal heart and the employment of molecular biology techniques is of help to solve the puzzle of such “silent” autopsies. For these reasons, autopsy investigation of cardiac SD should always include sampling for genetic testing to search for the invisible inherited arrhythmogenic disorders, as recommended in the recent guidelines by the Association for European Cardiovascular Pathology.     

Prevalence and clinical significance of anticardiolipin antibodies in patients with type 1 autoimmune hepatitis

There are few case reports on the association between autoimmune hepatitis (AIH) and anticardiolipin antibodies (anti-CLAbs) and/or antiphospholipid syndrome (APLS). We studied the anti-CLAbs prevalence in AIH and other hepatic diseases. We also investigated whether anti-CLAbs are co-factor dependent and which is their avidity since co-factor dependency or increased resistance is associated with APLS. Fifty-nine AIH patients, 228 HCV, 50 HBV, 123 with other non-viral and non-autoimmune liver disorders (nV-nALD) and 267 healthy people were investigated for anti-CLAbs and antibodies against beta-2-glycoprotein I (anti-beta2-GPI). Resistance of IgG anti-CLAbs was evaluated using 2 M urea. IgG anti-CLAbs detected in 39% of AIH, 19.7% of HCV (p=0.006), 14% of HBV (p=0.01), 8.1% of nV-nALD (p=0.000) and 1.1% of healthy (p=0.000). IgG anti-CLAbs were associated with the presence of cirrhosis and active AIH while their resistance to urea was high. Anti-beta2-GPI was detected in two AIH patients. We demonstrated a significantly higher prevalence of anti-CLAbs in patients with AIH compared to other diseases and healthy people. Anti-CLAbs were associated with AIH stage but no association was found with APLS clinical manifestations (thrombosis, pregnancy morbidity, thrombocytopenia). However, their avidity was comparable with that of APLS indicating the need for prospective studies in order to address whether anti-CLAbs in AIH may contribute to the progression of liver disease or APLS development.