Predictors of outcome in patients with de novo diagnosis of heart failure with reduced ejection fraction: Role of combined myocardial and lung Iodine-123 Meta-Iodobenzylguanidine imaging.

BACKGROUND: The predictors of outcome in patients with de novo diagnosis of heart failure (HF) with reduced ejection fraction (HFrEF) are poorly known. METHODS AND RESULTS: All consecutive HFrEF patients admitted between October 2012 and November 2017 with their first episode of HF were scheduled for an outpatient follow-up. After 3 months, patients with confirmed HFrEF underwent Iodine-123 Meta-Iodobenzylguanidine imaging. We defined three study endpoints: HF rehospitalization, cardiac death and all-cause death. Eighty-four patients were enrolled. During follow-up (39.9 ± 18.6 months) HF rehospitalization occurred in 33 cases, cardiac death in 18 and all-cause death in 24. At multivariate analysis, systolic pulmonary arterial pressure (sPAP; HR: 1.047; p = .027) and Late lung to heart ratio (L/H; HR: 1.341; p < .001) independently predict HF rehospitalization; left ventricular end-systolic volume (LVESV; HR: 1.016; p = .017), sPAP (HR: 1.064; p = .034) and Late L/H (HR: 1.323; p = .009) were predictors of cardiac death; LVESV (HR: 1.013; p = .018) and Late L/H (HR: 1.245; p = .012) were independent predictors of all-cause death. Kaplan-Meier analysis of the individual predictors confirmed their prognostic ability during follow-up; of note, the Late L/H cut-off of 1.1 improved the risk stratification capability of echocardiographic parameters. CONCLUSIONS: Late L/H independently predicts HF rehospitalization, cardiac death and all-cause death in patients with de novo diagnosis of HFrEF and improves the prognostic stratification capability of conventional echocardiographic parameters.

Bipolar Disorder and Parkinson's Disease: A 123I-Ioflupane Dopamine Transporter SPECT Study.

Objectives: Bipolar disorder (BD) has been suggested to be a risk factor for the development of Parkinson's disease (PD). Standard treatment of BD includes drugs that are known to induce drug-induced parkinsonism (DIP). Clinical differentiation between PD and DIP is crucial and might be aided by functional neuroimaging of the dopaminergic nigrostriatal pathway. Methods: Twenty consecutive BD patients with parkinsonism were clinically assessed and underwent 123I-ioflupane dopamine transporter single-photon emission computer tomography (SPECT). Imaging data of BD patients with pathological scans were further compared to a population of 40 de novo PD patients. Results: Four BD patients had abnormal scans, but their clinical features and cumulative exposure to both antipsychotic drugs and lithium were similar to those of BD patients with normal dopamine transporter imaging. BD patients with pathological scans had putaminal binding ratio and putamen-to-caudate ratios higher than those of PD patients despite a similar motor symptom burden. Conclusions: Up to 20% of BD patients with parkinsonism might have an underlying dopaminergic deficit, which would not be due to cumulative exposure to offending drugs and is ostensibly higher than expected in the general population. This supports the evidence that BD represents a risk factor for subsequent development of neurodegenerative parkinsonism, the nature of which needs to be elucidated.