ABSTRACT
BACKGROUND: Anxiety and limited patient comprehension may pose significant barriers when informing elderly patients about complex procedures such as transcatheter aortic valve implantation (TAVI). OBJECTIVES: We aimed to evaluate the utility of medical graphics to improve the patient informed consent (IC) before TAVI. METHODS: In this prospective, randomized dual center study, 301 patients were assigned to a patient brochure containing medical graphics (Comic group, n = 153) or sham information (Control group, n = 148) on top of usual IC. Primary outcomes were patient understanding of central IC-related aspects and periprocedural anxiety assessed by the validated Spielberger State Trait Anxiety Inventory (STAI), both analyzed by cognitive status according to the Montreal Cognitive Assessment (MoCA). RESULTS: Patient understanding was significantly higher in the Comic group [mean number of correct answers 12.8 (SD 1.2) vs. 11.3 (1.8); mean difference 1.5 (95% CI 1.2-1.8); p < 0.001]. This effect was more pronounced in the presence of cognitive dysfunction (MoCA < 26) [12.6 (1.2) in the Comic vs. 10.9 (1.6) in the Control group; mean difference 1.8 (1.4-2.2), p < 0.001]. Mean STAI score declined by 5.7 (95% CI 5.1-6.3; p < 0.001) in the Comic and 0.8 points (0.2-1.4; p = 0.015) in the Control group. Finally, mean STAI score decreased in the Comic group by 4.7 (3.8-5.6) in cognitively impaired patients and by 6.6 (95% CI 5.8 to 7.5) in patients with normal cognitive function (p < 0.001 each). CONCLUSIONS: Our results prove beneficial effects for using medical graphics to inform elderly patients about TAVI by improving patient understanding and reducing periprocedural anxiety (DRKS00021661; 23/Oct/2020). Medical graphics entailed significant beneficial effects on the primary endpoints, patient understanding and periprocedural anxiety, compared to the usual patient informed consent (IC) procedure. Patient understanding of IC-related aspects was significantly higher in the Comic group, with a more pronounced benefit in patients with cognitive impairment (p for IC method and cognitive status < 0.001, respectively; p for IC method x MoCA category interaction = 0.017). There further was a significant decline of periprocedural anxiety in patients with and without cognitive impairment (p for IC method x measuring time point < 0.001; p for IC method x MoCA category x measuring time point interaction = 0.018).
ABSTRACT
In Germany more than 1.6â¯million patients suffer from atrial fibrillation (AF). Within the next decades this number will substantially increase due to current demographic trends with the increasing average age of the population. When untreated, patients with atrial fibrillation have a five times higher risk for stroke as compared with a control cohort. A potent stroke prevention therapy reducing the risk of stroke by approximately 70-80% is primarily treatment with new oral anticoagulants (NOACs). The risk scores for stroke (CHA2DS2-VASc) and major bleeding (HAS-BLED) in patients with atrial fibrillation share common variables, so that patients with the highest stroke risk often carry a very high bleeding risk. A significant number of patients (ca. 20-30%) are, however, not eligible for long-term anticoagulation, e.g. because of a high bleeding risk. For this population there is an urgent need for alternative stroke prevention strategies, such as catheter-based percutaneous left atrial appendage closure. Current data about the efficiency and safety of this treatment as well as a discussion of ongoing recruitment for randomized studies are discussed in this review.
Subject(s)
Atrial Appendage , Atrial Fibrillation , Stroke , Administration, Oral , Anticoagulants , Germany , HumansABSTRACT
In patients with nonvalvular atrial fibrillation, >90 % of thrombi are detected in the left atrial appendage (LAA). In particular these observations have resulted in the development of catheter-based LAA closure as an approach for stroke prevention in patients with nonvalvular atrial fibrillation in recent years. A preliminary randomized trial provided promising data with respect to efficacy and safety of this approach as compared to anticoagulation with warfarin. The safety of the procedure has been significantly improved in recent years due to procedural experience and refinement of implanted devices. In current clinical practice, this approach is particularly used for patients with nonvalvular atrial fibrillation, a significant ischemic risk (CHA2DS2-VASc score ≥2), and a high bleeding risk, i. e., in patients in whom there are relevant concerns with respect to long-term anticoagulation. The present article discusses the data from randomized clinical studies and registries, the present guideline recommendations, and the practical clinical use of LAA closure for stroke prevention.
Subject(s)
Atrial Appendage/surgery , Atrial Fibrillation/complications , Atrial Fibrillation/therapy , Stroke/etiology , Stroke/prevention & control , Vascular Closure Devices , Cardiac Catheters , Evidence-Based Medicine , Humans , Septal Occluder Device , Treatment OutcomeABSTRACT
Disorders of lipid metabolism play a major role in the development and progression of coronary artery disease. Dyslipidemia therefore plays a central role in therapeutic approaches for prevention and treatment of cardiovascular events associated with coronary artery disease. Epidemiological studies have shown an association between various lipid metabolism parameters, the risk of developing coronary artery disease and progression of a pre-existing disease. In particular, increased levels of low-density lipoprotein cholesterol (LDL-C), reduced levels of HDL cholesterol (HDL-C), as well as high levels of triglycerides and increased lipoprotein(a) [Lp(a)] levels can be taken into account when assessing the risk stratification of patients for primary prevention of coronary artery disease. Lifestyle and dietary changes, intensified statin therapy and possibly the addition of ezetimibe remain the major interventions in both primary and secondary prevention of coronary artery disease, as they improve the prognosis particularly by lowering levels of LDL-C. Recently, genetic studies have contributed to extending our understanding of the relationship between lipid metabolism and coronary artery disease. A causal role for progression of coronary artery disease could be demonstrated for LDL-C, Lpa and triglyceride-rich lipoproteins (TRL), which could not be demonstrated for HDL-C in various studies. Furthermore, the effect of reduction of LDL-C by proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition and by the cholesteryl ester transfer protein (CETP) inhibitor anacetrapib on cardiovascular events is currently being investigated in large clinical outcome study programs.
Subject(s)
Anticholesteremic Agents/therapeutic use , Coronary Artery Disease/blood , Coronary Artery Disease/epidemiology , Lipid Metabolism , Lipids/blood , Proprotein Convertase 9/blood , Coronary Artery Disease/prevention & control , Disease Progression , Evidence-Based Medicine , Humans , PCSK9 Inhibitors , Prevalence , Reproducibility of Results , Risk Factors , Sensitivity and Specificity , Treatment OutcomeABSTRACT
There is substantial evidence that patient compliance or rather adherence to medical measures and recommendations for lifestyle changes can pivotally influence the prognosis of the patients or disease progression. However, the scientific evaluation and the statistical analysis of "patient adherence" are extremely difficult due to the fact that the construct of "adherence" is complex and comprised of many layers, and varies greatly in different disease groups. With this paper, we describe the development and structure of this novel assessment tool that takes past and prospective information on different facets of drug and behavioural adherence into account, expected to result in considerably improved prediction of future cardiovascular risk. We suggest a simple scoring scheme and explore the psychometric properties and the higher order factorial structure. In this exploratory study the "Diabetes Cardiovascular Risk Evaluation Targets and Essential Data for Commitment of Treatment" (DETECT) adherence score revealed good psychometric properties in terms of internal consistency and factorial structure, suggesting that its further exploration in terms of external validity is promising. Findings also underline that it is useful and informative to cover within one score both, pharmacologic and non-pharmacologic interventions in primary care. Our combination in this respect is unique, as most studies conducted on this subject so far aimed at assessing solely drug adherence or behavioural adherence.
Subject(s)
Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/psychology , Patient Compliance/statistics & numerical data , Primary Health Care/statistics & numerical data , Psychometrics/methods , Age Factors , Aged , Cardiovascular Diseases/drug therapy , Factor Analysis, Statistical , Female , Humans , Male , Middle Aged , Patient Compliance/psychology , Physical Examination , Primary Health Care/methods , Psychometrics/statistics & numerical data , Risk Factors , Sex FactorsABSTRACT
Observations have been made linking the presence of psychosocial factors associated with elevated beta-endorphin concentrations with atherosclerosis. In this study, the authors assume an important role of the stress hormone beta-endorphin in several mechanisms that contribute to a dysbalance of human endothelial and monocytic endothelin (ET)-1 and nitric oxide (NO) release, mediated by mu1-opioid receptors. ET-1 and NO release were quantified via enzyme-linked immunosorbent assay (ELISA) or fluorometrically. mu1-Opioid receptors were identified by polymerase chain reaction (PCR) after stimulation with beta-endorphin. beta-Endorphin significantly increased endothelial and monocytic ET-1 release. The effect was mediated by mu1-opioid receptors and abolished by naloxonazine, a selective mu1-opioid receptor antagonist. In contrast, NO release was decreased under the influence of beta-endorphin. mu1-Opioid receptors on human monocytes and endothelial cells mediated a beta-endorphin-induced stimulation of ET-1 release, whereas NO release was decreased. Thus, the authors hypothesize a role of beta-Endorphin in the pathogenesis of stress-induced endothelial dysfunction through peripherally circulating beta-endorphin, which may offset the balance of vasoactive mediators, leading to an unopposed vasoconstriction. The data may also provide a new concept of mu1-opioid receptor antagonists, preventing beta-endorphin-induced disorders of vascular biology.