A systematic review of the effectiveness of patient education through patient portals.

Objective: The objective of this study was to systematically review all literature studying the effect of patient education on patient engagement through patient portals. Introduction: Patient portals provide patients access to health records, lab results, medication refills, educational materials, secure messaging, appointment scheduling, and telehealth visits, allowing patients to take a more active role in their health care decisions and management. A debate remains around whether these additional aids actually improve patient engagement and increase their ability to manage their own health conditions. This systematic review looks specifically at the effect of educational materials included in patient portals. Materials and Methods: In accordance with PRISMA guidelines, the literature search was mapped across 5 databases (PubMed, CINAHL, Scopus, PsychINFO, Embase), and implemented on June 2, 2020. Results: Fifty-two studies were included in the review. Forty-six (88.5%) reported rates of patient utilization of educational resources in the patient portal. Thirty (57.9%) shared patients' perceptions of the usefulness of the education materials. Twenty-one (40.4%) reported changes in health outcomes following educational interventions through the patient portal. This review found that efforts are indeed being made to raise awareness of educational resources in patient portals, that patients are increasingly utilizing these resources, that patients are finding them useful, and that they are improving health outcomes. Conclusion: It seems that patient portals are becoming a powerful tool for patient education and engagement, and show promise as a means of achieving the quadruple aim of healthcare. Moving forward, research should establish more uniform methods of measurement in order to strengthen the literature surrounding the effectiveness of patient education through patient portals.

Utilization of EHR to Improve Support Person Engagement in Health Care for Patients With Chronic Conditions.

Innovations in electronic health record (EHR) systems invite new patient and family engagement methods and create opportunities to reduce healthcare disparities. However, many patients and their identified support persons (ie, proxies) are unsure how to interface with the technology. This phenomenological qualitative study served as a pilot study to investigate the patient, proxy, and provider lived experiences utilizing patient-facing EHR portals. Individual interviews and focus groups were utilized to collect qualitative data from 21 patient, proxy, and healthcare provider participants across 3 time points. Colaizzi's phenomenological data analysis method was utilized to interpret the data. Four themes emerged highlighting critical benefits and obstacles for patients and support persons interfacing with a patient portal: (a) agency, (b) connection, (c) support, and (d) technology literacy. Results help highlight strategies and dispel myths essential to advancing patient and family engagement using EHR patient portal systems. The study's outcomes reflect recommendations for onboarding proxies and improving patient/family engagement and family-centered care models.

Mast cell tryptase: a new biomarker in patients with stable coronary artery disease.

Mast cells may participate actively in the inflammatory process of atherosclerotic plaques by releasing proteolytic enzymes and various other pro-inflammatory substances. We hypothesized that increased levels of mast cell tryptase, could be an important biomarker in patients with stable coronary artery disease (CAD). We measured tryptase in 102 patients without acute coronary syndromes undergoing cardiac catheterization. Patients with significant CAD [> or =50% stenosis in > or =1 artery (n=66)] had significantly higher serum tryptase than patients with normal angiography (n=13) or non-significant CAD [<50% stenosis (n=23)]. The median, 25th and 75th percentiles for tryptase in these two groups were 8.38 (6.4 and 10.7)mug/L versus 6.78 (5.61 and 9.72) microg/L, p=0.014. Patients in the highest quartile of tryptase levels had a 4.3-fold risk for CAD [Odds ratio (OR): 4.3; 95% confidence interval (CI): 1.08-17.19; p=0.04]. In a multivariate regression analysis, tryptase remained an independent predictor for CAD along with age (OR: 1.178; 95% CI: 1.021-1.359, p=0.025). High circulating tryptase levels may be a result of chronic low-grade inflammatory activity present in atherosclerotic plaques. Tryptase measurements may emerge as a novel way of identifying asymptomatic patients with CAD, and represent a new biomarker of therapeutic efficacy in patients with CAD.

Relation of serum levels of mast cell tryptase of left ventricular systolic function, left ventricular volume or congestive heart failure.

BACKGROUND: Activated mast cells (MC) present in the myocardium of patients with cardiomyopathy may contribute to left ventricular dilatation and systolic dysfunction. We sought to determine whether peripheral levels of tryptase, an MC-specific protease, are related to indices of left ventricular size and function, as well as congestive heart failure (CHF) or coronary artery disease (CAD). METHODS AND RESULTS: Serum tryptase was measured in 85 patients undergoing cardiac catheterization with left ventriculography and coronary angiography and examined in relation to left ventricular ejection fraction (LVEF), left ventricular end-diastolic volume (LVEDV), congestive heart failure (CHF), and angiographically evident CAD. Systemic tryptase levels were lower in patients with increased (>90 mL) LVEDV (6.2 [5.3-8.0] mcg/L versus 8.3 [6.6-10.3] mcg/L, P=.01) and in patients with CHF (6.2 [3.6-7.3] mcg/L versus 8 [6.2-10] mcg/L, P=.02) and tended to be lower in patients with depressed (<55%) LVEF (6.8 [5.2-9] mcg/L versus 8 [6.3-9.9] mcg/L, P=NS). Linear regression did not show a significant relationship between tryptase levels with either LVEF or LVEDV. Finally, tryptase levels were consistently elevated in relation to the presence of CAD. CONCLUSION: Despite increased numbers of MC in the myocardium of patients with cardiomyopathy, systemic levels of MC tryptase appear to be lower in relation to LV systolic dysfunction, LV dilatation, or clinical CHF. In contrast, the presence of angiographically significant CAD is associated with elevated systemic tryptase levels.

Proteasome inhibition ablates activation of NF-kappa B in myocardial reperfusion and reduces reperfusion injury.

Both acute coronary occlusion and reperfusion of an infarct-related artery lead to significant myocardial cell death. Recent evidence has been presented that activation of the transcription factor nuclear factor-kappaB (NF-kappaB) plays a critical role in reperfusion injury. NF-kappaB is usually bound to its inhibitor, IkappaB, and classic activation of NF-kappaB occurs when the 20S proteasome degrades IkappaB that has been phosphorylated and ubiquitinated. In this study, activation of NF-kappaB was inhibited by systemic administration of a 20S proteasome inhibitor (PS-519) in a porcine model of myocardial reperfusion injury. The experimental protocol induced myocardial ischemia in the distribution of the left anterior descending coronary artery for 1 h with subsequent reperfusion for 3 h. A single systemic treatment with PS-519 reduced 20S proteasome activity; blocked activation of NF-kappaB induced by reperfusion; reduced creatine kinase, creatine kinase-muscle-brain fraction, and troponin I release from the myocardium; preserved regional myocardial function measured by segmental shortening; significantly reduced the size of myocardial infarction; and exhibited no acute toxicity. These data show that myocardial reperfusion injury can be inhibited by using proteasome inhibitors, which likely function through the inhibition of NF-kappaB activation.