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Out-of-hospital cardiac arrest is a major health problem, and immediate treatment is essential for improving the chances of survival. The development of technological solutions to detect out-of-hospital cardiac arrest and alert emergency responders is gaining momentum; multiple research consortia are currently developing wearable technology for this purpose. For the responsible design and implementation of this technology, it is necessary to attend to the ethical implications. This review identifies relevant ethical aspects of wearable-based out-of-hospital cardiac arrest detection according to four key principles of medical ethics. First, aspects related to beneficence concern the effectiveness of the technology. Second, non-maleficence requires preventing psychological distress associated with wearing the device and raises questions about the desirability of screening. Third, grounded in autonomy are empowerment, the potential reidentification from continuously collected data, issues of data access, bystander privacy, and informed consent. Finally, justice concerns include the risks of algorithmic bias and unequal technology access. Based on this overview and relevant legislation, we formulate design recommendations. We suggest that key elements are device accuracy and reliability, dynamic consent, purpose limitation, and personalization. Further empirical research is needed into the perspectives of stakeholders, including people at risk of out-of-hospital cardiac arrest and their next-of-kin, to achieve a successful and ethically balanced integration of this technology in society. [ABSTRACT FROM AUTHOR]

Background--Heart failure (HF) is a prevalent and deadly disease, and preventive strategies focused on at-risk individuals are needed. Current HF prediction models have not examined HF subtypes. We sought to develop and validate risk prediction models for HF with preserved and reduced ejection fraction (HFpEF, HFrEF). Methods and Results--Of 28,820 participants from 4 community-based cohorts, 982 developed incident HFpEF and 909 HFrEF during a median follow-up of 12 years. Three cohorts were combined, and a 2:1 random split was used for derivation and internal validation, with the fourth cohort as external validation. Models accounted for multiple competing risks (death, other HF subtype, and unclassified HF). The HFpEF-specific model included age, sex, systolic blood pressure, body mass index, antihypertensive treatment, and previous myocardial infarction; it had good discrimination in derivation (c-statistic 0.80; 95% confidence interval [CI], 0.78-0.82) and validation samples (internal: 0.79; 95% CI, 0.77-0.82 and external: 0.76; 95% CI: 0.71-0.80). The HFrEF-specific model additionally included smoking, left ventricular hypertrophy, left bundle branch block, and diabetes mellitus; it had good discrimination in derivation (c-statistic 0.82; 95% CI, 0.80-0.84) and validation samples (internal: 0.80; 95% CI, 0.78-0.83 and external: 0.76; 95% CI, 0.71-0.80). Age was more strongly associated with HFpEF, and male sex, left ventricular hypertrophy, bundle branch block, previous myocardial infarction, and smoking with HFrEF (P value for each comparison =0.02). Conclusions--We describe and validate risk prediction models for HF subtypes and show good discrimination in a large sample. Some risk factors differed between HFpEF and HFrEF, supporting the notion of pathogenetic differences among HF subtypes. [ABSTRACT FROM AUTHOR]

The article discusses a study on the relationship of myocardial microinjury with collagen metabolism markers. Participants in the Cardiovascular Health Study (CHS) where collagen metabolism markers and serial cTnT levels were measured as part of a nested case-control study of heart failure (HF) were included in the study. It indicates an association between myocardial injury at the microlevel with pathophysiological processes that are critically involved in tissue repair and fibrosis.

The article discusses a study on the relationship of serum markers of collagen turnover with cardiovascular (CV) outcomes in elderly people. The study's subjects were divided into groups of patients with heart failure (HF) and control subjects. The serum markers, amino-terminal peptide of procollagen type III (PIIINP) and carboxyl-terminal telopeptide of collagen type I (CITP) were found to be associated with adverse CV outcomes such as myocardial infarction, HF and death.

The article offers a Cardiovascular Health Study which examines the link between fibrosis biomarkers and heart failure (HF) in the elderly. It notes that the study compares participants with systolic HF and with controls using a nested case-control design. It mentions the findings of the study that fibrosis markers are critically advanced in elderly individuals having diastolic or systolic HF and the links are essential when adjusting for covariates associated to the aging process.

Background: It is not known how carbohydrate and fat intake affect the development of left ventricular (LV) hypertrophy and contractile dysfunction in response to pressure overload. We hypothesized that a low-carbohydrate/high-fat diet prevents LV hypertrophy and dysfunction compared with high-carbohydrate diets.Methods and Results: Rats were fed high-carbohydrate diets composed of either starch or sucrose, or a low-carbohydrate/high-fat diet, and underwent abdominal aortic banding (AAB) for 2 months. AAB increased LV mass with all diets. LV end-diastolic and systolic volumes and the ratio of the mRNA for myosin heavy chain beta/alpha were increased with both high-carbohydrate diets but not with the low-carbohydrate/high-fat diet. Circulating levels of insulin and leptin, both stimulants for cardiac growth, were lower, and free fatty acids were higher with the low-carbohydrate/high-fat diet compared with high-carbohydrate diets. Among animals that underwent AAB, LV volumes were positively correlated with insulin and LV mass correlated with leptin.Conclusion: A low-carbohydrate/high-fat diet attenuated pressure overload-induced LV remodeling compared with high-carbohydrate diets. This effect corresponded to lower insulin and leptin concentrations, suggesting they may contribute to the development of LV hypertrophy and dysfunction under conditions of pressure overload. [ABSTRACT FROM AUTHOR]

Abstract: Background: It is not known how carbohydrate and fat intake affect the development of left ventricular (LV) hypertrophy and contractile dysfunction in response to pressure overload. We hypothesized that a low-carbohydrate/high-fat diet prevents LV hypertrophy and dysfunction compared with high-carbohydrate diets. Methods and Results: Rats were fed high-carbohydrate diets composed of either starch or sucrose, or a low-carbohydrate/high-fat diet, and underwent abdominal aortic banding (AAB) for 2 months. AAB increased LV mass with all diets. LV end-diastolic and systolic volumes and the ratio of the mRNA for myosin heavy chain β/α were increased with both high-carbohydrate diets but not with the low-carbohydrate/high-fat diet. Circulating levels of insulin and leptin, both stimulants for cardiac growth, were lower, and free fatty acids were higher with the low-carbohydrate/high-fat diet compared with high-carbohydrate diets. Among animals that underwent AAB, LV volumes were positively correlated with insulin and LV mass correlated with leptin. Conclusion: A low-carbohydrate/high-fat diet attenuated pressure overload-induced LV remodeling compared with high-carbohydrate diets. This effect corresponded to lower insulin and leptin concentrations, suggesting they may contribute to the development of LV hypertrophy and dysfunction under conditions of pressure overload. [Copyright &y& Elsevier]

Background: Depression is frequently observed in patients with heart failure and is associated with poor quality of life and adverse prognosis. However, the prevalence of depression in heart failure could be overestimated because symptoms of depression overlap with those of heart failure. Similarly, the importance of depression may be overestimated if depression merely reflects worse heart failure. Because the response to depression treatment has not been evaluated in this patient population, we evaluated the efficacy of controlled-release paroxetine (paroxetine CR), a selective serotonin reuptake inhibitor, on depression and quality of life in chronic heart failure. Methods: A double-blind, randomized, placebo-controlled design was used to evaluate reductions in depression following 12 weeks of treatment with paroxetine CR (n = 14, age 62.1 ± 12.3 years) or placebo (n = 14, age = 61.9 ± 9.0 years). Patients with symptomatic congestive heart failure and a score of at least 10 on the Beck Depression Inventory (BDI) were eligible. Beck Depression Inventory was obtained at baseline and 4, 8, and 12 weeks of follow-up. Quality of life was assessed using the Medical Outcomes Study Short Form and the Minnesota Living with Heart Failure Questionnaire. Results: Controlled-release paroxetine resulted in significantly more recovery from depression (BDI <10) than placebo (69% vs 23%, P = .018) and resulted in lower continuous BDI scores throughout the intervention (P = .024). Controlled-release paroxetine was associated with higher general health levels compared with placebo on the Medical Outcomes Study 36-Item Short Form survey (38 ± 10 vs 30 ± 6, P = .016) at 12 weeks of follow-up. Reductions in depression were correlated with improvements in psychological aspects of quality of life (P < .05) but not with physical quality of life measures (P > .10). Conclusion: Antidepressant therapy with paroxetine CR results in significant reductions in depression among patients with heart failure. The reductions in depression with paroxetine CR are accompanied by improvements in psychological aspects of quality of life. Larger controlled trials are needed to further document the effectiveness of paroxetine CR and other selective serotonin reuptake inhibitors in patients with heart failure and to determine patient subgroups that are most likely to benefit from antidepressive interventions. [Copyright &y& Elsevier]

Objective: Acute physical and psychological stressors affect blood coagulation and fibrinolysis, but little is known about hemostatic factors associated with chronic psychological stress. Prolonged psychological stress may end in a state of vital exhaustion, which has been shown to be a risk factor for first myocardial infarction and recurrent events after coronary angioplasty. The present study tested the hypothesis that vital exhaustion resulting from chronic psychological stress is associated with impaired fibrinolytic capacity and increased coagulation factors.Methods: On the basis of a validated questionnaire and subsequent structured interview, a well-defined group of otherwise healthy exhausted men was recruited (N = 15) and compared with age-matched not-exhausted controls (N = 15). Fibrinolytic measures included tissue plasminogen activator (TPA) antigen and plasminogen activator inhibitor (PAI-1) activity, and as coagulation factors we examined factors VIIc, factor VIIIc, and fibrinogen. Control variables were: blood pressure, smoking status, triglycerides, cholesterol, and standard hematological measures. Samples were collected twice to correct for intraindividual fluctuations. Statistical analyses were performed using 2 x 2 mixed model analysis of variance with subsequent univariate testing.Results: Vital exhaustion was associated with significantly elevated levels of PAI-1 activity (p = .023). The higher PAI-1 activity in exhausted subjects (median = 13.0 U/ml vs. 6.0 U/ml) was not accounted for by smoking status or serum lipids. No significant differences were observed in TPA antigen, factor VIIc, factor VIIIc, and fibrinogen. The groups did not differ in blood pressure, smoking status, triglycerides, cholesterol, or standard hematological measures.Conclusion: These data suggest a reduced fibrinolytic capacity in exhausted individuals. Therefore, the relationship between vital exhaustion and risk of myocardial infarction may be mediated in part by an imbalance between blood coagulation and fibrinolysis. [ABSTRACT FROM AUTHOR]

Background: Subjective Cognitive Complaints (SCC) are common after stroke. This study documents the prevalence and course of SCC in the first year after stroke and determines which patient characteristics in the first 3 months predict subsequent SCC at 1-year follow-up.Methods: Using a longitudinal design, 155 patients (mean age 64.0 ± 11.9 years; 69.7% men) were assessed at 3 and 12 months after stroke. SCC were assessed using the Checklist for Cognitive and Emotional consequences following stroke (CLCE) inventory (content component [CLCE-c] and worry component [CLCE-w]). Potential predictors of 12 months SCC included demographics, stroke severity, objective cognitive impairment, psychological factors (depression, anxiety, perceived stress, fatigue, personality traits, coping style), and activities of daily life functioning assessed at 3 months poststroke. Multiple hierarchical linear regression analyses were used to determine predictors of SCC at 12 months poststroke.Results: SCC remained stable from 3 to 12 months over time (CLCE-c from 3.3 ± 2.4 to 3.3 ± 2.6; CLCE-w: from 1.9 ± 2.2 to 2.1 2.5). Independent predictors of SCC at 12 months were baseline CLCE-c (β = 0.54) and perceived stress (β = 0.23) for content, and baseline CLCE-w (β = 0.57) and depressive symptoms (β = 0.23) for worry.Conclusions: Patients who report SCC at 3 months after stroke are likely to continue having these complaints at 1 year follow-up. Perceived stress and depressive symptoms additionally increase the likelihood of having SCC at 12 months, independent of SCC at 3 months poststroke. Rehabilitation programs that target reduction of stress and depression in the first months after stroke might reduce sustained SCC and improve well-being. [ABSTRACT FROM AUTHOR]