Background: Glucagon-like peptide 1 agonists differ in chemical structure, duration of action and in their effects on clinical outcomes. The cardiovascular effects of once-weekly albiglutide in type 2 diabetes are unknown. Methods: We randomly assigned patients with type 2 diabetes and cardiovascular disease to the addition of once-weekly subcutaneous injection of albiglutide (30 mg to 50 mg) or matching placebo to standard care. We hypothesized that albiglutide would be noninferior to placebo for the primary outcome of first occurrence of cardiovascular death, myocardial infarction, or stroke. If noninferiority was confirmed by an upper limit of the 95% confidence interval for the hazard ratio of less than 1.30, closed-testing for superiority was prespecified. Findings: Overall, 9463 participants were followed for a median of 1.6 years. The primary composite outcome occurred in 338 of 4731 patients (7.1%; 4.6 events per 100 person-years) in the albiglutide group and in 428 of 4732 patients (9.0%; 5.9 events per 100 person-years) in the placebo group (hazard ratio, 0.78; 95% confidence interval [CI ], 0.68 to 0.90), indicating that albiglutide, was superior to placebo (P<0.0001 for noninferiority, P=0.0006 for superiority). The incidence of acute pancreatitis (albiglutide 10 patients and placebo 7 patients), pancreatic cancer (6 and 5), medullary thyroid carcinoma (0 and 0), and other serious adverse events did not differ significantly between the two groups. Interpretation: In patients with type 2 diabetes and cardiovascular disease, albiglutide was superior to placebo with respect to major adverse cardiovascular events. (Funded by GlaxoSmithKline; Harmony Outcomes ClinicalTrials.gov number, NCT02465515.) noninferiority; P = 0.06 for superiority). There seems to be variation in the results of existing trials with GLP-1 receptor agonists, which if correct, might reflect drug structure or duration of action, patients studied, duration of follow-up or other factors.

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The results of this study strongly suggest that the impaired relaxation pattern observed in patients with CTEPH is not solely the result of geometric effects of RV enlargement and LV chamber distortion but is caused in large part by low LV preload and relative underfilling.

Spirituality and gratitude are associated with wellbeing. Few if any studies have examined the role of gratitude in heart failure (HF) patients or whether it is a mechanism through which spirituality may exert its beneficial effects on physical and mental health in this clinical population. This study examined associations bet ween gratitude, spiritual wellbeing, sleep, mood, fatigue, cardiac-specific self-efficacy, and inflammation in 186 men and women with Stage B asymptomatic HF (age 66.5 years ±10). In correlational analysis, gratitude was associated with better sleep (r=-.25, p<0.01), less depressed mood (r=-.41, p<0.01), less fatigue (r=-.46, p<0.01), and better self-efficacy to maintain cardiac function (r=.42, p<0.01). Patients expressing more gratitude also had lower levels of inflammatory biomarkers (r=-.17, p<0.05). We further explored relationships among these variables by examining a putative pathway to determine whether spirituality exerts its beneficial effects through gratitude. We found that gratitude fully mediated the relationship between spiritual wellbeing and sleep quality (z=−2.35, SE=.03, p=.02) and also the relationship between spiritual wellbeing and depressed mood (z=−4.00, SE=.075, p<.001). Gratitude also partially mediated the relationships between spiritual wellbeing and fatigue (z=−3.85, SE=.18, p<.001), and between spiritual wellbeing and self-efficacy (z=2.91, SE=.04, p=.003). In sum, we report that gratitude and spiritual wellbeing are related to better mood and sleep, less fatigue, and more self-efficacy, and that gratitude fully or partially mediates the beneficial effects of spiritual wellbeing on these endpoints. Efforts to increase gratitude may be a treatment for improving wellbeing in HF patients’ lives and be of potential clinical value.

These results demonstrate a correlation between RV Tei index and right heart hemodynamics (particularly PVR) in CTEPH. Because PVR is difficult to estimate noninvasively -- and yet correlates with disease severity -- the RV Tei index may be a valuable noninvasive parameter for monitoring disease severity in CTEPH and outcome after PTE.

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E/A is consistently abnormal in patients with CTEPH and increases post-PTE. Moreover, E/A varies inversely with mPAP and directly with CO. Following PTE, E/A >1.5 correlates with the absence of severe pulmonary hypertension (mPAP >35 mm Hg) and the presence of normal cardiac output (> 5.0 l/m).

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