Recovering from an acute cardiac event – the relationship between depression and life satisfaction

Aims. This study sought to measure the rates and trajectory of depression over six months following admission for an acute cardiac event and describe the relationship between depression and life satisfaction.
Background. Co-morbid depression has an impact on cardiac mortality and is associated with the significant impairment of quality of life and well-being, impairments in psychosocial function, decreased medication adherence and increased morbidity.
Design. This was a descriptive, correlational study.
Method. The study was undertaken at a large public hospital in Melbourne. Participants were asked to complete a survey containing the cardiac depression scale (CDS) and the Personal Well-being Index.
Results. This study mapped the course of depression over six months of a cohort of patients admitted for an acute cardiac event. Significant levels of depressive symptoms were found, at a level consistent with the literature. A significant correlation between depressive symptoms as measured by the CDS and the Personal Well-being Index was found.
Conclusions. Depression remains a significant problem following admission for an acute coronary event. The Personal Wellbeing Index may be a simple, effective and non-confrontational initial screening tool for those at risk of depressive symptoms in this population. Relevance to clinical practice. Despite the known impact of depression on coronary heart disease (CHD), there is limited research describing its trajectory. This study makes a compelling case for the systematic screening for depression in patients with CHD and the importance of the nursing role in identifying at risk individuals.

Cardiac structure and function in young endurance athletes and nonathletes

The purpose of this study was to examine, in male adolescents, the effects of long-term endurance training on cardiac structure and function, by adopting a cross-sectional comparison with a nonathletic control group. A total of 13 endurance-trained (EX) and seven untrained (CON) male adolescents (mean ± SE, age = 15.3 ± 0.3 and 15.2 ± 0.28 yrs, respectively) underwent echocardiography at rest to determine left ventricular enddiastolic dimension (LVD_d), left ventricular end-systolic dimension (LVD_s), left ventricular posterior wall thickness (LVPW), stroke volume (SV), and cardiac output (CO). On separate days, incremental exercise tests were conducted on a cycle ergometer to measure peak oxygen uptake (VO_2max) and anaerobic power. VO_2max was greater in the endurance group (54.4 ± 1.8 mL min^–1 kg^–1) than in the control group (45.8 ± 1.6 mL min^–1 kg^–1; p < 0.05). Mean exercise time was longer in EX (12.9 ± 0.7 min) than CON (10.4 ± 0.8 min; p < 0.05). No significant differences were noted between the two groups in resting heart rate, maximal heart rate, LVD_d, LVD_s, LVPW, SV, SV indexed, CO, and CO indexed, or in the anaerobic strength. These data provide evidence that endurance-trained adolescent males develop superior exercise performance before the cardiac remodeling that is evident in trained adult athletes.

Voluntary exercise does not affect stress-induced tachycardia, but improves resistance to cardiac arrhythmias in rats

1. It is currently unknown whether long-term voluntary exercise has enduring cardioprotective effects in animal models.

2. The present study was conducted in three groups of rats: (i) sedentary controls (n = 6); (ii) 24 h runners (n = 8; unlimited access to running wheels); and (iii) 2 h runners (n = 8; access to running wheels limited to 2 h daily). After termination of the 6 week exercise protocol, all rats were implanted with the telemetric electrocardiogram transmitters and were studied 1 week later.

3. Resting heart rate (HR) values in the control rats, 24 h runners and 2 h runners were 372 ± 7, 361 ± 9 and 298 ± 5 b.p.m., respectively (P < 0.05 for 2 h runners vs controls). The high-frequency spectral power in the control rats, 24 h runners and 2 h runners was 3.9 ± 0.2, 4.3 ± 0.3 and 5.3 ± 0.3 s2, respectively (P < 0.05 for 2 h runners vs controls), whereas intrinsic HR was 383 ± 3, 377 ± 2 and 346 ± 3 b.p.m., respectively (P < 0.001 for 2 h runners vs controls). Restraint stress provoked tachycardia of similar magnitude in all groups.

4. After completion of telemetric studies, haemodynamic indices and susceptibility to cardiac arrhythmias were assessed in anaesthetized animals, there were no major between-group differences in HR, arterial pressure, contractility indices or sensitivity to β-adrenoceptor stimulation (dobutamine) or blockade (atenolol). The effective refractory period in the control rats, 24 h runners and 2 h runners was 49 ± 2, 55 ± 2 and 60 ± 4 ms, respectively (P = 0.054 for 2 h runners vs controls). A significantly higher dose of aconitine was required to provoke ventricular arrhythmias in the 24 h and 2 h running groups compared with controls (489 ± 76, 505 ± 88 and 173 ± 33 μg, respectively; P < 0.05).

5. We conclude that, in rats, long-term voluntary exercise has enduring cardioprotective effects mediated at the level of both the central nervous system and the heart.

Clinical outcomes associated with screening and referral for depression in an acute cardiac ward

Aim.  The aim of this paper is to describe the implementation of a depression screening and referral tool in two cardiac wards of a major metropolitan public hospital. The tool consisted of two sections: (1) screening for depression risk (Cardiac Depression Scale-5) and (2) consequential referral actions.

Background.  Prior research has shown that depression in patients with heart disease is associated with significantly impaired quality of life, decreased medication adherence, increased morbidity and increased use of healthcare services.

Design.  A prospective in-patient study design.

Method.  A consecutive sample of 202 patients admitted to either the cardiac medical (n = 145) or surgical (n = 57) wards of a major Melbourne metropolitan hospital were recruited into the study over an 18-week period.

Results.  Just over half (54%) of the patients were identified as ‘at risk’ of depression. Of these, 19% were assessed as moderate risk and 35% high risk. Of those patients, 91% had the risk score documented in their medical history, 90% had engaged in discussions with clinicians regarding their risk score, 85% had their risk score communicated formally to the medical team and 25% were formally referred for appropriate follow-up – significantly more than prior to implementation of the screening and referral tool.

Conclusions.  By providing a formalised mechanism for detecting depression, documented screening and referral rates improved for those with comorbid depression and heart disease affording an opportunity for early intervention. These findings support a move towards integrated approaches to screening of depression to become standard practice in the acute cardiac setting.

Relevance to clinical practice.  Such mechanisms also have the potential to initiate the development of new models of care that acknowledge the complexity of comorbid depression and heart disease and provide pathways from speciality to primary care which integrate the physical and psychosocial domains inclusive of screening, referral, systematic monitoring and streamlined behavioural and physical care.

Impact of depression treatment on mental and physical health-related quality of life of cardiac patients : a meta-analysis

PURPOSE: To conduct a meta-analysis evaluating the effectiveness of depression treatment on mental and physical health-related quality of life (HRQOL) of cardiac patients.

METHODS: Studies were identified using medical, health, psychiatry, psychology, and social sciences databases. Inclusion criteria were (1) 1 or more control conditions, (2) random assignment to condition after admission for myocardial infarction (MI)/acute coronary syndrome, after recording positive results on a depression screener, (3) documentation of depression symptoms at baseline, (4) depression management as a component of the rehabilitation/intervention, (5) validated measure of HRQOL as an outcome, at minimum 6-month followup. For meta-analysis, mental and physical HRQOL were the end points studied, using standardized mean differences for continuous outcome measures, with 95% confidence intervals. Heterogeneity was explored by calculating I2 statistic.

RESULTS: Five randomized controlled trials included in the analysis represented 2105 participants (1058 intervention vs 1047 comparator). Compared with a comparator group at 6 months, a test for overall effect demonstrated statistically significant improvements in mental HRQOL in favor of the intervention (standardized mean differences = −0.29 [−0.38 to −0.20], [P < .00001]; I2 = 0%). Depression treatment had a modest yet significant impact on physical HRQOL (standardized mean differences = −0.14 [−0.24 to −0.04] [P = .009]; I2 = 15%).

CONCLUSION: While the impact of post-MI depression interventions on physical HRQOL is modest, treatment can improve mental HRQOL in a significant way. Future research is required to develop and evaluate a program that can achieve vital improvements in overall HRQOL, and potentially cardiovascular outcomes, of cardiac patients.

Metyrapone and fluoxetine suppress enduring behavioral but not cardiac effects of subchronic stress in rats

In humans, chronic stressors have long been recognized as potential causes for cardiac dysregulation. Despite this, the underlying mechanistic links responsible for this association are still poorly understood. The purpose of this study was to determine whether exposure to a paradigm of subchronic stress can provoke enduring changes on the heart rate of experimental rats and, if so, to reveal the autonomic and neural mechanisms that mediate these effects. The study was conducted on adult male Sprague-Dawley rats instrumented for telemetric recording of heart rate and locomotor activity. Animals were submitted to a subchronic stress protocol, consisting of a 1-h foot shock session on five consecutive days. Heart rate and locomotor activity were recorded continuously for 3 days before and for 6 days after the subchronic stress period. Subchronic foot shock produced significant and enduring reduction in heart rate both during the dark/active [Δ= −23 ± 3 beats per minute (bpm)] and light/inactive (Δ= −20 ± 3 bpm) phases of the circadian cycle, and a reduction in locomotor activity during the dark/active phase [Δ= −54 ± 6 counts per hour (cph)]. The bradycardic effect of subchronic stress was not related to a reduced locomotion. Selective sympathetic (atenolol) and vagal (methyl-scopolamine) blockades were performed to reveal which autonomic component was responsible for this effect. We found that the fall in heart rate persisted after subchronic stress in animals treated with atenolol (active phase Δ= −16 ± 3 bpm, inactive phase Δ= −19 ± 2 bpm), whereas vagal blockade with scopolamine transiently prevented this effect, suggesting that the bradycardia following subchronic stress was predominantly vagally mediated. Fluoxetine (selective serotonin reuptake inhibitor) and metyrapone (inhibitor of corticosterone synthesis) treatments did not affect heart rate changes but prevented the reduction in locomotion. We conclude that subchronic stress exposure in rats reduces heart rate via a rebound in vagal activation and that this effect is serotonin- and corticosterone-independent.