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- Enhancing Cardiac Rehabilitation With Stress Management Training: A Randomized, Clinical Efficacy Trial
- Gait Speed Predicts 30-Day Mortality After Transcatheter Aortic Valve Replacement: Results From the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy Registry
- Conditional Deletion of Hsd11b2 in the Brain Causes Salt Appetite and Hypertension
- Potassium Channel Subfamily K Member 3 (KCNK3) Contributes to the Development of Pulmonary Arterial Hypertension
- Duration of Prehospital Resuscitation Efforts After Out-of-Hospital Cardiac Arrest
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Enhancing Cardiac Rehabilitation With Stress Management Training: A Randomized, Clinical Efficacy Trial
Cardiac rehabilitation (CR) represents the standard of care for patients with coronary heart disease. Despite considerable epidemiological evidence that high levels of stress are associated with worse prognosis, there is limited evidence that reducing stress improves clinical outcomes. Enhancing Standard Cardiac Rehabilitation With Stress Management Training in Patients With Coronary Heart Disease (ENHANCED) was a randomized, clinical trial in which patients referred to CR completed a psychometric stress battery and underwent evaluation of coronary heart disease biomarkers, including measures of endothelial dysfunction, heart rate variability, baroreflex sensitivity, and inflammation, before and after a 12-week treatment program of comprehensive CR alone (n=75) or comprehensive CR enhanced by stress management training (SMT; n=76). SMT consisted of 12 weekly 1.5-hour sessions that provided education, group support, and instruction in methods for coping more effectively with stress (eg, time management, progressive muscle relaxation training, cognitive restructuring, communication skills). A nonrandom sample of CR-eligible patients who declined to engage in CR formed a no-CR comparison group. Results showed that although both CR groups reported less stress, CR enhanced by SMT achieved greater reductions in stress compared with CR alone. Compared with the matched no-CR comparison group, both CR groups had fewer clinical events (all-cause mortality, fatal and nonfatal myocardial infarction, coronary or peripheral artery revascularization, stroke/transient ischemic attack, and unstable angina requiring hospitalization). Moreover, combining stress management training with CR (ie, CR+SMT) resulted in better clinical outcomes compared with CR alone. These findings confirm the value of CR in reducing the risk for adverse clinical events. Furthermore, SMT provided incremental value to standard CR by further reducing stress and improving clinical outcomes. Including SMT as a routine component of standard CR, regardless of patients’ reported levels of stress, should be encouraged. See p 1341.
Gait Speed Predicts 30-Day Mortality After Transcatheter Aortic Valve Replacement: Results From the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy Registry
Previous studies have established that patients undergoing transcatheter aortic valve replacement are frail and at increased risk for adverse outcomes, but no study to date has focused on gait speed alone as an indicator of frailty. We examined data on 8039 patients from 256 sites registered in the national Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy Registry to describe the association between preprocedural gait speed and outcomes in those undergoing transcatheter aortic valve replacement. We found that the majority of patients undergoing transcatheter aortic valve replacement are considered frail by gait speed cut points used to identify frailty in community-dwelling older populations and that gait speed is independently associated with adverse outcomes in this large cohort of patients with severe aortic valve disease. To anticipate and improve clinical care, clinicians need to become familiar with the gait speed test because implementation of screening in all patients with severe aortic stenosis would identify those at greatest risk. Future research should also consider preprocedural frailty status in comparisons of the treatment and outcomes of patients being considered for transcatheter aortic valve replacement. See p 1351.
Conditional Deletion of Hsd11b2 in the Brain Causes Salt Appetite and Hypertension
For the majority of people in industrialized societies, dietary salt intake habitually exceeds the recommended upper tolerable limit. This sustained high salt intake is associated with hypertension and with increased risk of cardiovascular disease. Reducing sodium intake may be beneficial for a large number of people, particularly those with hypertension or heart failure. However, compliance to restricted salt intake is poor, which may in part reflect enhanced salt appetite. The central pathways controlling salt intake are incompletely defined, but it is known that certain neurons in the brain stem are activated by salt depletion. We genetically modified mice, removing a gene in the brain stem to amplify local aldosterone signaling. Basal blood pressure and systemic electrolyte and hormonal status were not affected by this genetic modification. However, ad libitum salt intake increased 3-fold and this caused hypertension. We were able to partially block salt appetite with the mineralocorticoid antagonist spironolactone. This study demonstrates an important role for brain stem pathways in the control of sodium homeostasis and blood pressure. Mineralocorticoid antagonists could help improve compliance to restricted salt regimens during the management of cardiovascular disease. See p 1360.
Potassium Channel Subfamily K Member 3 (KCNK3) Contributes to the Development of Pulmonary Arterial Hypertension
Pulmonary arterial hypertension (PAH) is a severe cardiopulmonary condition leading to right-sided heart failure and ultimately death. In the last 20 years, the development of drugs that specifically target pathways involved in disease pathogenesis has led to improvements in the quality of life and clinical outcomes in patients with PAH, but there is still no cure for this devastating disease. Recently, the identification of loss-of-function mutations in the gene encoding the potassium channel subfamily K member 3 (KCNK3) in some patients with PAH has highlighted a novel dysfunctional pathway and a potential therapeutic target. In the present study, we demonstrate that loss of function of KCNK3 is a hallmark of idiopathic and heritable PAH and experimental pulmonary hypertension. Moreover, we show that in vivo pharmacological activation of KCNK3 with the phospholipase A2 inhibitor ONO-RS-082 alleviates monocrotaline-induced pulmonary hypertension in rats when KCNK3 is still expressed in pulmonary arteries. This suggests that this strategy might be of interest in patients with PAH who retain a residual level of KCNK3 expression, possibly within the frame of personalized therapy. A major limitation of the ONO-RS-082 compound is its phospholipase A2 inhibitory activity, which can have deleterious side effects. Identification or development of more specific molecules is thus needed to envision KCNK3 activation in humans. Alternatively, targeted gene therapy allowing KCNK3 re-expression in affected pulmonary arteries could be another possible approach. See p 1371.
Duration of Prehospital Resuscitation Efforts After Out-of-Hospital Cardiac Arrest
Since 1992, all cardiopulmonary resuscitation guidelines have stated that the chain of survival (early access, early basic life support, early defibrillation, and early advanced cardiovascular life support) is an essential series of actions designed to reduce the mortality associated with out-of-hospital cardiac arrest. Recent cardiopulmonary resuscitation guidelines state that termination of resuscitation (TOR) rules are an important component of cardiopulmonary resuscitation, but TOR rules have not specified the minimum duration for prehospital resuscitation efforts. Furthermore, TOR rules are difficult to define objectively because community systems of emergency care vary around the world and ethical and cultural norms must be considered. It is clear that field termination reduces transport to the hospital, but the optimal prehospital cardiopulmonary resuscitation duration to maximize the number of patients with good neurological outcome has not previously been established. From the All-Japan Utstein Registry, in which emergency medical service responders do not implement TOR rules, we demonstrate that prehospital resuscitation efforts to achieve favorable neurological outcome should be continued for at least 40 minutes from call receipt, inclusive of bystander and emergency medical service responder resuscitation efforts, and for at least 33 minutes from scene arrival for emergency medical service responder resuscitation efforts exclusively. We believe that this study will help optimize treatment for patients with out-of-hospital cardiac arrest to maximize the number of neurologically intact survivors of cardiac arrest and will inform the development of future TOR rules. The costs and benefits of prolonging prehospital resuscitation efforts must be taken into consideration when these results are translated into clinical practice, and further studies are needed. See p 1386.
- © 2016 American Heart Association, Inc.
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Jump to
- Article
- Enhancing Cardiac Rehabilitation With Stress Management Training: A Randomized, Clinical Efficacy Trial
- Gait Speed Predicts 30-Day Mortality After Transcatheter Aortic Valve Replacement: Results From the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy Registry
- Conditional Deletion of Hsd11b2 in the Brain Causes Salt Appetite and Hypertension
- Potassium Channel Subfamily K Member 3 (KCNK3) Contributes to the Development of Pulmonary Arterial Hypertension
- Duration of Prehospital Resuscitation Efforts After Out-of-Hospital Cardiac Arrest
- Info & Metrics
- eLetters
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