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Introduction: Non-invasive methods to identify phenotype of pulmonary hypertension (PH) are essential to improve the diagnostic algorithm of PH. Hypothesis: Delayed tapering of pulmonary artery (PA) is a signature of pre-capillary PH, while in post-capillary PH, the PA tapers rapidly. This differential tapering pattern of PA can be detected on a chest CT-angiogram (CTA), and quantified as a ratio of main PA diameter to PA branch diameter (right or left) at 5.0 cm length after the PA bifurcation. Methods: We identified 30 subjects with chest CTA and PH confirmed with invasive right heart catheterization (RHC). We identified 3 PH phenotypes: 1. “PVD” (pulmonary vascular disease) = Pre-capillary PH (n=10, PVR>3.0 WU, PAWP 3.0 WU, PAWP >15mmHg), and 3. “PVH” (pulmonary venous hypertension) = post-capillary PH (n=10, PVR15mmHg). Results: The results are summarized in Table. Additional results are expressed as comparison among the three groups in order: PVD vs Mixed vs PVH (mean±SD, % or n, as appropriate). CTA-chest findings: RV basal diameter (mm)= 51.1±8.4 vs 51.0±5.4 vs 38.1±13.9, left ventricular (LV) basal diameter (mm)= 32.1±7.2 vs 31.6±13.3 vs 56.6±15.2*, PA:Ao ratio= 1.1±0.1 vs 1.1±0.2 vs 1.0±0.1. Echo findings: tricuspid annular plane systolic excursion (TAPSE, mm)= 16±3 vs 19±4 vs 22±10*. We performed ROC to identify predictive ability of PA:RPA-5 and PA:LPA-5 to predict PVR>3 WU. The AUC for PA:RPA-5 = 0.859 (p=0.03) and for PA:LPA-5 = 0.812 (p=0.01); with optimal cut-off for both parameters (PA:RPA-5 and PA:LPA-5) was 1.85. Among the overall cohort, the patients with PA:RPA3 and 11/16 were on PH meds. Conclusion: Pattern of PA tapering quantified with PA:RPA-5 or PA:LPA-5 can reliably identify elevated PVR (>3.0 WU). Pre-capillary PH imprints a signature morphological mark on the pattern of PA dilation that can be identified with a CTA-thorax.

Depressive disorders lack objective physiological measurements to characterize the affected population and facilitate study of relevant mechanisms. The melanopsin-mediated light signaling pathway may contribute to seasonal variation and can be measured non-invasively by pupillometry. We prospectively studied changes in melanopsin-mediated pupillary constriction in 19 participants with major depressive disorder (MDD) and 10 control across the summer and winter solstices. The melanopsin-mediated response, as measured by the pupil's sustained constriction six s after a high intensity blue light stimulus, was marginally attenuated in those with MDD relative to controls (p=0.071). The participants with MDD unexpectedly showed a significantly reduced transient pupillary response to low intensity red (p=0.011) and blue light (p=0.013), but not high intensity red and blue light. Sustained pupillary constriction in response to high intensity blue light was more pronounced with increasing daylight hours (p=0.037) and was more strongly related to objectively measured versus estimated light exposure. Melanopsin-mediated impairments in pupil response may serve as a biological marker for vulnerability to depression in low light conditions. Assessment of these and other responses to light stimuli, such as response to low intensity light, may be useful for the study of the neurobiology of MDD and related mood disorders.