Many advances have been made in the diagnosis and management of heart failure (HF) in recent years. Cardiac biomarkers are an essential tool for clinicians: point of care B-Type Natriuretic Peptide (BNP) and its N-terminal counterpart (NT-proBNP) levels help distinguish cardiac from non-cardiac causes of dyspnea and are also useful in the prognosis and monitoring of the efficacy of therapy. One of the major limitations of HF biomarkers is in obese patients where the relationship between BNP and NT-proBNP levels and myocardial stiffness is complex. Recent data suggest an inverse relationship between BNP and NT-proBNP levels and body mass index. Given the ever-increasing prevalence of obesity world-wide, it is important to understand the benefits and limitations of HF biomarkers in this population. This review will explore the biology, physiology, and pathophysiology of these peptides and the cardiac endocrine paradox in HF. We also examine the clinical evidence, mechanisms, and plausible biological explanations for the discord between BNP levels and HF in obese patients.

Background The genetic variation underlying many heritable forms of cardiovascular disease is incompletely understood, even in patients with strong family history or early age at onset. Methods and Results We used whole exome sequencing to detect pathogenic variants in 55 patients with suspected monogenic forms of cardiovascular disease. Diagnostic analysis of established disease genes identified pathogenic variants in 21.8% of cases, and variants of uncertain significance in 34.5% of cases. Three patients harbored heterozygous nonsense or splice-site variants in the nucleoporin genes NUP37, NUP43, and NUP188, which have not been implicated previously in cardiac disease. We also identified a heterozygous splice site variant in the nuclear envelope gene SYNE1 in a child with severe dilated cardiomyopathy that underwent transplant, as well as in his affected father. To confirm a cardiovascular role for these candidate genes in vivo, we used morpholinos to reduce SYNE1, NUP37, and NUP43 gene expression in zebrafish. Morphant embryos displayed cardiac abnormalities, including pericardial edema and heart failure. Furthermore, lymphoblasts from the patient carrying a SYNE1 splice-site variant displayed changes in nuclear morphology and protein localization that are consistent with disruption of the nuclear envelope. Conclusions These data expand the repertoire of pathogenic variants associated with cardiovascular disease, and validate the diagnostic and research utility of whole exome sequencing. We identify NUP37, NUP43, and NUP188 as novel candidate genes for cardiovascular disease, and suggest that dysfunction of the nuclear envelope may be an under-recognized component of inherited cardiac disease in some cases.

Background: Wireless implantable hemodynamic monitors assist cardiac care providers in tailoring medication regimens to reduce chronic heart failure hospital admissions and to improve patient quality of life. Previous research exists to support wireless implantable hemodynamic monitors favorable impact on medical endpoints but, however, their psychological and behavioral effects have not yet been established. The purpose of this pilot study was to investigate patient psychological and behavioral changes after receiving the wireless implantable hemodynamic monitor. Methods: Patients with heart failure ( n=26) who were implanted with wireless implantable hemodynamic monitor sensors completed the Cardiac Anxiety Questionnaire and Self-Care of Heart Failure Index version 6.2 at pre-implant and at one-month post-implant, as well as an initial demographic questionnaire. Results: Heart failure patients who received a wireless implantable hemodynamic monitor experienced a significant reduction in cardiac anxiety, t(25)=2.93, p=0.007, z=−0.46, d=0.58, driven by a reduction in fear of their condition, t(25)=2.26, p=0.03, z=−0.42, d=0.44. Increases in self-care behaviors fell short of significance t(25)=1.67, p=0.11, but showed a medium effect size, d=0.33. Conclusion: Heart failure patients who received a wireless implantable hemodynamic monitor reported significantly reduced cardiac fear, indicating that wireless implantable hemodynamic monitor technology may produce a collateral benefit in psychological effects. Patient self-care may also benefit but the current study was under-powered to reach statistical significance. Patient education about psychological and behavioral aspects of the wireless implantable hemodynamic monitor implant may yield increased patient engagement and broader health benefits if these results are confirmed in a larger study.

we found improvements in verbal memory 6 months and 12 months post-placement and in visual memory between 12 and 24 months. Objectives: The purpose of the current follow-up study was to assess the impact of an increased sample (n = 17) and additional follow-up testing. Methods: We again compared cognition pre-and post-LVAD placement across time points (A: 3-6 months; B: 6-12 months; C: 2 years) for individuals using paired samples t-tests. Individuals were administered the Repeatable Battery for the Assessment of Neuropsychological Status and the Trail Making Test. Patients' cognition was stable or improved up to 24 months post-placement. Results: In addition to the verbal and visual memory impairment previously observed, we now saw. Statistically significant improvement in cognition was observed on measures assessing processing speed (Pre to A) and verbal recognition memory (Pre to B). Trends toward significance were observed in visual memory (Pre to A), delayed list memory (Pre to B), and delayed story memory (A to C). Conclusions: Findings add to limited extant research showing stable or modest improvements in cognition and provide further understanding of the effects of LVAD placement on neurocognition.