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Dietary Sodium Restriction in Patients with Heart FailureThis feature about a patient with heart failure offers a case vignette accompanied by two essays, one supporting recommendation of a low-sodium diet and the other recommending no sodium restriction.

The hippocampus has a well-documented role for spatial navigation across species, but its role for spatial memory in nonnavigational tasks is uncertain. In particular, when monkeys are tested in tasks that do not require navigation, spatial memory seems unaffected by lesions of the hippocampus. However, the interpretation of these results is compromised by long-term compensatory adaptation occurring in the days and weeks after lesions. To test the hypothesis that hippocampus is necessary for nonnavigational spatial memory, we selected a technique that avoids long-term compensatory adaptation. We transiently disrupted hippocampal function acutely at the time of testing by microinfusion of the glutamate receptor antagonist kynurenate. Animals were tested on a self-ordered spatial memory task, the Hamilton Search Task. In the task, animals are presented with an array of eight boxes, each containing a food reinforcer; one box may be opened per trial, with trials separated by a delay. Only the spatial location of the boxes serves as a cue to solve the task. The optimal strategy is to open each box once without returning to previously visited locations. Transient inactivation of hippocampus reduced performance to chance levels in a delay-dependent manner. In contrast, no deficits were seen when boxes were marked with nonspatial cues (color). These results clearly document a role for hippocampus in nonnavigational spatial memory in macaques and demonstrate the efficacy of pharmacological inactivation of this structure in this species. Our data bring the role of the hippocampus in monkeys into alignment with the broader framework of hippocampal function.

Complications of pregnancy present an opportunity to identify women at high risk of cardiovascular disease (CVD). Placental abruption is a severe and understudied pregnancy complication, and its relationship with CVD is poorly understood. The California Healthcare Cost and Utilization Project database was used to identify women with hospitalized pregnancies in California between 2005 and 2009, with follow-up through 2011. Pregnancies, exposures, covariates, and outcomes were defined by International Classification of Diseases Ninth Revision codes. Cox proportional-hazards regression was used to examine the association between placental abruption and myocardial infarction (MI), stroke, and heart failure (HF). Multivariate models controlling for age, race, medical co-morbidities, pregnancy complications, psychiatric and substance use disorders, and socioeconomic factors were employed. Among over 1.5 million pregnancies, placental abruption occurred in 14,881 women (1%). Median follow-up time from delivery to event or censoring was 4.87 (interquartile range 3.54 to 5.96) years. In unadjusted models, placental abruption was associated with risk of HF, but not MI or stroke. In fully-adjusted models, placental abruption remained significantly associated with HF (Hazard ratio 1.44; 95% confidence interval 1.09 to 1.90). Among women with placental abruptions, hypertensive disorders of pregnancy and preterm birth respectively modified and mediated the association between placental abruption and HF. In conclusion, placental abruption is a risk factor for HF, particularly in women who also experience hypertensive disorders of pregnancy and preterm birth. Placental abruption is a specific adverse pregnancy outcome associated with risk of HF.

Brain circuitry underlying defensive behaviors includes forebrain modulatory sites, e.g. the amygdala and hypothalamus, and midbrain effector regions, such as the deep/intermediate layers of the superior colliculus (DLSC). When disinhibited, this network biases behavior towards reflexive defense reactions. While well characterized in rodent models, little is known about this system in the primate brain. Employing focal pharmacological manipulations, we have previously shown that activation of the DLSC triggers reflexive defensive responses, including cowering, escape behaviors and defensive vocalizations. Here, we show that activation of the DLSC also disrupts normal dyadic social interactions between familiar pairs of monkeys. When the basolateral complex of the amygdala (BLA) was inhibited concurrent with DLSC activation, cowering behavior was attenuated, whereas escape behaviors and defensive vocalizations were not. Moreover, inhibition of the BLA, previously shown to produce a profound increase in dyadic social interactions, was unable to normalize the decrease in social behavior resulting from DLSC activation. Together these data provide an understanding of forebrain–midbrain interactions in a species and circuit with translational relevance for the psychiatry of anxiety and post-traumatic stress disorders.

Noninvasive assessment of pulmonary hemodynamics is often performed by echocardiographic estimation of the pulmonary artery systolic pressure (ePASP), despite limitations in the advanced lung disease population. Other noninvasive hemodynamic variables, such as echocardiographic pulmonary vascular resistance (ePVR), have not been studied in this population. We performed a retrospective analysis of 147 advanced lung disease patients who received both echocardiography and right heart catheterization for lung transplant evaluation. The ePVR was estimated by four previously described equations. Noninvasive and invasive hemodynamic parameters were compared in terms of correlation, agreement, and accuracy. The ePVR models strongly correlated with invasively determined PVR and had good accuracy with biases of <1 Wood units (WU), although with moderate precision and wide 95% limits of agreement varying from 5.9 to 7.8 Wood units. The ePVR models were accurate to within 1.9 WU in over 75% of patients. In comparison to the ePASP, ePVR models performed similarly in terms of correlation, accuracy, and precision when estimating invasive hemodynamics. In screening for pulmonary hypertension, ePVR models had equivalent testing characteristics to the ePASP. Mid‐systolic notching of the right ventricular outflow tract Doppler signal identified a subgroup of 11 patients (7%) with significantly elevated PVR and mean pulmonary artery pressures without relying on the acquisition of a tricuspid regurgitation signal. Analysis of ePVR and determination of the notching pattern of the right ventricular outflow tract Doppler flow velocity envelope provide reliable insights into hemodynamics in advanced lung disease patients, although limitations in precision exist.

Pulmonary hypertension (PH) is a known consequence of sickle cell disease (SCD) and is associated with increased mortality and more frequent episodes of acute chest syndrome (ACS). Pulmonary pressures are known to increase during ACS, and right ventricular (RV) failure has been described as a significant cause of mortality in this condition. Management of ACS includes exchange transfusion, pain control, and prevention of hypovolemia and hypoxemia. However, in patients with a history of precapillary PH in whom ACS is complicated by persistent RV failure and cardiogenic shock, RV afterload reduction with pulmonary vasodilators may be an effective treatment strategy. Here, we present a case of a young man with SCD-associated PH and ACS who was successfully managed with inhaled and oral pulmonary vasodilators in the setting of persistent elevations in pulmonary vascular resistance leading to acute RV failure and cardiogenic shock.

A recent clinical trial of people with near-daily methamphetamine use achieved >75% study-drug adherence via financial incentives and close follow-up.5 Bubble packs are useful, as is preferentially choosing once per day dosing options (eg, metoprolol succinate over carvedilol). A recently established inpatient consultation addiction care team at our hospital provides services such as motivational interviewing, discussion of safer use strategies, behavioural and pharmacological SUD treatment, and linkage to ongoing care in the community.6 To address social determinants of health, we established a multidisciplinary team (cardiology, primary care, palliative care, addiction medicine, social work, case management and street medicine), which meets monthly to discuss patients with HF, SUDs and frequent admissions. Directly observed therapy and reward-based incentives have been shown to be effective in chronic disease management in patients with SUDs and infectious diseases, but these strategies remain underexplored in HF.7 We developed a novel two times-per-week cardiology–addiction comanagement clinic for patients with co-occurring HF and stimulant use disorder which incorporates contingency management (figure 1). A systematic review of community-based interventions to improve oral chronic disease medication regimen adherence among individuals with substance use disorder.