Current and state of the art on the electrophysiologic characteristics and catheter ablation of arrhythmogenic right ventricular dysplasia/cardiomyopathy

AbstractArrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an inherited genetic disease caused by defective desmosomal proteins, and it has typical histopathological features characterized by predominantly progressive fibro-fatty infiltration of the right ventricle. Clinical presentations of ARVD/C vary from syncope, progressive heart failure (HF), ventricular tachyarrhythmias, and sudden cardiac death (SCD). The 2010 modified Task Force criteria were established to facilitate the recognition and diagnosis of ARVD/C. An implantable cardiac defibrillator (ICD) remains to be the cornerstone in prevention of SCD in patients fulfilling the diagnosis of definite ARVD/C, especially among ARVD/C patients with syncope, hemodynamically unstable ventricular tachycardia (VT), ventricular fibrillation, and aborted SCD. Further risk stratification is clinically valuable in the management of patients with borderline or possible ARVD/C and mutation carriers of family members. However, given the entity of heterogeneous penetrance and non-uniform phenotypes, the standardization of clinical practice guidelines for at-risk individuals will be the next frontier to breakthrough.Antiarrhythmic drugs are prescribed frequently to patients experiencing frequent ventricular tachyarrhythmias and/or appropriate ICD shocks. Amiodarone is the recommended drug of choice. Radiofrequency catheter ablation (RFCA) has been demonstrated to effectively eliminate the drug-refractory VT in patients with ARVD/C. However, the efficacy and clinical prognosis of RFCA via endocardial approach alone was disappointing prior to the era of epicardial approach. In recent years, it has been proven that the integration of endocardial and epicardial ablation by targeting the critical isthmus or eliminating abnormal electrograms within the diseased substrates could yield higher acute success and lower recurrence of ventricular tachyarrhythmias during long-term follow-up. Heart transplantation is the final option for patients with extensive disease, biventricular HF with uncontrollable hemodynamic compromise, and refractory ventricular tachyarrhythmias despite aggressive medical and ablation therapies

Women with endometriosis have higher comorbidities: Analysis of domestic data in Taiwan

AbstractEndometriosis, defined by the presence of viable extrauterine endometrial glands and stroma, can grow or bleed cyclically, and possesses characteristics including a destructive, invasive, and metastatic nature. Since endometriosis may result in pelvic inflammation, adhesion, chronic pain, and infertility, and can progress to biologically malignant tumors, it is a long-term major health issue in women of reproductive age. In this review, we analyze the Taiwan domestic research addressing associations between endometriosis and other diseases. Concerning malignant tumors, we identified four studies on the links between endometriosis and ovarian cancer, one on breast cancer, two on endometrial cancer, one on colorectal cancer, and one on other malignancies, as well as one on associations between endometriosis and irritable bowel syndrome, one on links with migraine headache, three on links with pelvic inflammatory diseases, four on links with infertility, four on links with obesity, four on links with chronic liver disease, four on links with rheumatoid arthritis, four on links with chronic renal disease, five on links with diabetes mellitus, and five on links with cardiovascular diseases (hypertension, hyperlipidemia, etc.). The data available to date support that women with endometriosis might be at risk of some chronic illnesses and certain malignancies, although we consider the evidence for some comorbidities to be of low quality, for example, the association between colon cancer and adenomyosis/endometriosis. We still believe that the risk of comorbidity might be higher in women with endometriosis than that we supposed before. More research is needed to determine whether women with endometriosis are really at risk of these comorbidities

Metronomic chemotherapy prevents therapy-induced stromal activation and induction of tumor-initiating cells

Although traditional chemotherapy kills a fraction of tumor cells, it also activates the stroma and can promote the growth and survival of residual cancer cells to foster tumor recurrence and metastasis. Accordingly, overcoming the host response induced by chemotherapy could substantially improve therapeutic outcome and patient survival. In this study, resistance to treatment and metastasis has been attributed to expansion of stem-like tumor-initiating cells (TICs). Molecular analysis of the tumor stroma in neoadjuvant chemotherapy–treated human desmoplastic cancers and orthotopic tumor xenografts revealed that traditional maximum-tolerated dose chemotherapy, regardless of the agents used, induces persistent STAT-1 and NF-κB activity in carcinoma-associated fibroblasts. This induction results in the expression and secretion of ELR motif–positive (ELR(+)) chemokines, which signal through CXCR-2 on carcinoma cells to trigger their phenotypic conversion into TICs and promote their invasive behaviors, leading to paradoxical tumor aggression after therapy. In contrast, the same overall dose administered as a low-dose metronomic chemotherapy regimen largely prevented therapy-induced stromal ELR(+) chemokine paracrine signaling, thus enhancing treatment response and extending survival of mice carrying desmoplastic cancers. These experiments illustrate the importance of stroma in cancer therapy and how its impact on treatment resistance could be tempered by altering the dosing schedule of systemic chemotherapy

Additional file 1: of Rhodiola crenulata extract counteracts the effect of hypobaric hypoxia in rat heart via redirection of the nitric oxide and arginase 1 pathway

HPLC profiling data of salidroside (a) and RCE (b). (DOCX 120 kb