Patterns of scheduled follow-up appointments following hospitalization for heart failure: insights from an urban medical center in the United States.

OBJECTIVES: Although postdischarge outpatient follow-up appointments after a hospitalization for heart failure represent a potentially effective strategy to prevent heart failure readmissions, patterns of scheduled follow-up appointments upon discharge are poorly described. We aimed to characterize real-world patterns of scheduled follow-up appointments among adult patients with heart failure upon hospital discharge. PATIENTS AND METHODS: This was a retrospective cohort study performed at a large urban academic center in the United States among adults hospitalized with a principal diagnosis of congestive heart failure between January 1, 2013, and December 31, 2014. Patient demographics, administrative data, clinical parameters, echocardiographic indices, and scheduled postdischarge outpatient follow-up appointments were collected. RESULTS: Of the 796 patients hospitalized for heart failure, just over half of the cohort had a scheduled follow-up appointment upon discharge. Follow-up appointments were less likely among patients who were white and had heart failure with preserved ejection fraction and more likely among patients with Medicaid and chronic obstructive pulmonary disease. In an adjusted multivariable regression model, age ≥65 years was inversely associated with a scheduled follow-up appointment upon hospital discharge, despite higher rates of several cardiovascular and noncardiovascular comorbidities. CONCLUSION: Just half of the patients discharged home following a hospitalization for heart failure had a follow-up appointment scheduled, representing a missed opportunity to provide a recommended care transition intervention. Despite a greater burden of both cardiovascular and noncardiovascular comorbidities, older adults (age ≥65 years) were less likely to have a follow-up appointment scheduled upon discharge compared with younger adults, revealing a disparity that warrants further investigation.

Therapeutic delivery of hydrogen sulfide for salvage of ischemic skeletal muscle after the onset of critical ischemia.

BACKGROUND: Recent evidence suggests that hydrogen sulfide is capable of mitigating the degree of cellular damage associated with ischemia-reperfusion injury (IRI). METHODS: This study evaluated the potential utility of hydrogen sulfide in preventing IRI in skeletal muscle by using in vitro (cultured myotubes subjected to sequential hypoxia and normoxia) and in vivo (mouse hind limb ischemia, followed by reperfusion) models to determine whether intravenous hydrogen sulfide delivered after the ischemic event had occurred (pharmacologic postconditioning) conferred protection against IRI. Injury score and apoptotic index were determined by analysis of specimens stained with hematoxylin and eosin and terminal deoxynucleotide transferase-mediated deoxy-uridine triphosphate nick-end labeling, respectively. RESULTS: In vitro, hydrogen sulfide reduced the apoptotic index after 1, 3, or 5 hours of hypoxia by as much as 75% (P = .002), 80% (P = .006), and 83% (P < .001), respectively. In vivo, hydrogen sulfide delivered after the onset of hind limb ischemia and before reperfusion resulted in protection against IRI-induced cellular changes, which was validated by significant decreases in the injury score and apoptotic index. The timing of hydrogen sulfide delivery was crucial: when delivered 20 minutes before reperfusion, hydrogen sulfide conferred significant cytoprotection (P < .001), but treatment 1 minute before reperfusion did not provide protection (P = NS). CONCLUSIONS: These findings confirm that hydrogen sulfide limits IRI-induced cellular damage in myotubes and skeletal muscle, even when delivered after the onset of ischemia in this murine model. These data suggest that when given in the appropriate dose and within the proper time frame, hydrogen sulfide may have significant therapeutic applications in multiple clinical scenarios.

Steroid profiles of transgenic tobacco expressing an Actinomyces 3-hydroxysteroid oxidase gene.

Previously, we have shown that the expression of a 3-hydroxysteroid-oxidase gene in transgenic tobacco initiated a series of biochemical events leading to the conversion of sterol to stanol. As a result, the plants maintained a diminished sterol pool and a modified relative sterol ratio but demonstrated no observable morphological abnormalities. The maintenance of normal higher plant physiology in the absence of particular sterols or in the presence of modified sterol ratios is controversial. In this report, we present additional biochemical and physiological characteristics of transgenic tobacco expressing an Actinomyces 3-hydroxysteroid-oxidase gene. The total steroid accumulated in the transgenic plants is 6-fold higher than in control plants and consists of sterol, 3-ketosteroid and stanol. The relative abundance of sterols within whole plant and individual organs is grossly altered as ethylated side chain sterols account for 99% of the total sterol pool in the transgenic tobacco. Stigmasterol is readily apparent in all tissues and cholesterol is found at measurable levels in specific organs, while campesterol and sitosterol are detected at trace levels in the transgenic plants. Stanols and 3-ketosteroids accumulate in all tissues and represent 77% of the measurable steroid pool in the transgenic plants. The sum of sterol, the respective 3-ketosteroid plus stanol provide a relative abundance of steroid, which is similar to the abundance of sterol accumulated in control tissue. In vitro photosynthetic electron transport measurements demonstrate altered activity of chloroplasts under a variety of reaction conditions, indicating a link between the modified steroid pool and a modulation of chloroplast membrane function.