Introduction. Cardiac magnetic resonance imaging (CMR) is considered the reference diagnostic method for quantifying right ventricular size and function, and pulmonary regurgitation in patients with tetralogy of Fallot surgery. The aim of this paper is to confirm the importance of magnetic resonance continuous postoperative monitoring of right and left heart function parameters as a diagnostic method that provides the most precise and accurate assessment. Methods. The prospective observational study included subjects with TOF surgery who were diagnosed with residual morphological and/or functional disorders on control postoperative echocardiographic examinations. All subjects underwent magnetic resonance imaging of the heart on a 1.5 T scanner with dedicated coils for the heart surface according to the standard protocol for a period of one year from the beginning of the study. Criteria for exclusion from the study were: significant residual pulmonary stenosis, condition after pulmonary valve replacement, existence of residual shunt lesions, contraindications for cardiac magnetic resonance imaging (pacemaker, ICD, claustrophobia). Depending on the time elapsed since the tetralogy of Fallot surgery, the subjects were divided into groups: more than 15 years, 11-15 years, 6-10 years, less than 5 years. Results. The study included 131 subjects with an average age of 24.18 ± 11.57 years with complete correction of TOF. Intergroup differences in values of right ventricular end-diastolic volume, right ventricular ejection fraction, and left ventricular ejection fraction were demonstrated, but there was no statistically significant intergroup difference in values of pulmonary regurgitation fraction. The negative interaction of the right and left ventricles intensifies during the years of follow-up of patients after TOF surgery, which is especially true fifteen years after surgery. Conclusion. CMR has the most significant role in research efforts aimed at improving the outcomes of operated patients with tetralogy of Fallot.

Cancer-related cognitive dysfunction is an important clinical problem that can interfere with the daily functioning, work productivity, childcare, and other responsibilities of women with a history of breast cancer. Risks of cancer-related cognitive impairment include cancer and cancer treatment, as well as patient-related vulnerabilities. There is no established standard of neuroprotective care or treatment for breast cancer-related cognitive impairment.

BACKGROUND Patients with Huntington disease (HD) develop diabetes mellitus more often than do matched healthy controls. Recent studies in neurodegenerative diseases suggested that insulin resistance constitutes a metabolic stressor that interacts with a preexisting neurobiological template to induce a given disorder. OBJECTIVE To investigate possible changes in insulin sensitivity and secretion, major determinants of glucose homeostasis, in a group of consecutive normoglycemic patients with HD. DESIGN Metabolic investigations. PARTICIPANTS Twenty-nine untreated, nondiabetic patients with HD and 22 control participants matched by age, sex, and socioeconomic background. MAIN OUTCOME MEASURES Glucose tolerance, assessed by means of the glucose curve during oral glucose challenge; insulin sensitivity, assessed using homeostasis model assessment and minimal model analysis based on frequent sampling of plasma glucose and plasma insulin during the intravenous glucose tolerance test; and insulin secretion, determined by means of the acute insulin response and the insulinogenic index. RESULTS The evaluation of insulin sensitivity using homeostasis model assessment demonstrated higher homeostasis model assessment insulin resistance indices, and a lower sensitivity index when the minimal model approach was used, in patients with HD compared with controls (P = .03 and P = .003, respectively). In the assessment of early-phase insulin secretion, the acute insulin response and the insulinogenic index were lower in patients with HD compared with controls (P = .02). The number of CAG repeats correlated significantly only with acute insulin response (P = .003). CONCLUSIONS Besides impairment in insulin secretion capacity, a simultaneous decrease in insulin sensitivity, with an increase in the insulin resistance level, was found in normoglycemic patients with HD compared with controls. These data imply that progression of the insulin secretion defect in HD may lead to a failure to compensate for insulin resistance.