Ischaemic heart disease and Australian immigrants: the influence of birthplace and language skills on treatment and use of health services

Admission rates for ischaemic heart disease (IHD), and the use of invasive cardiovascular procedures, separation mode and length of stay (LOS) were compared between Australians from non-English speaking background (NESB; n=8627) and English speaking background (ESB; n=13162) aged 20 years and over admitted to Victorian urban public hospitals. The study covered the period from 1993 to 1998. It was found that, compared with their ESB counterparts, the incidence of admission for acute myocardial infarction was significantly higher for NESB men and women before and after controlling for confounding factors. The age-adjusted ratios for NESB women compared with their ESB counterparts ranged from 1.23 to 1.89 for cardiac catheterisation, from 0.23 to 0.27 for percutaneous transluminal coronary angioplasty (PTCA), and from 1.04 to 1.80 for coronary artery bypass grafting (CABG).
Procedure rates were comparable in men for cardiac catheterisation and CABG but higher for PTA rates in NESB men (OR: 1.29, 95%CI: 1.11-1.50) than their ESB counterparts. Both NESB men (β=0.04, 95%CI: 0.01-0.07) and women (β=0.03, 95%CI: 0.02-0.08) experienced significantly longer hospital stays than their ESB counterparts. These findings indicate there may be systematic differences in patients’ treatment and service utilisation in Victorian public hospitals. The extent to which physicians’ bias and
patients’ choice could explain these differences requires further investigation.

Intrinsic resistance of female hearts to an ischemic insult is abrogated in primary cardiac hypertrophy

Important sex differences in cardiovascular disease outcomes exist, including conditions of hypertrophic cardiomyopathy and cardiac ischemia. Studies of sex differences in the extent to which load-independent (primary) hypertrophy modulates the response to ischemia-reperfusion (I/R) damage have not been characterized. We have previously described a model of primary genetic cardiac hypertrophy, the hypertrophic heart rat (HHR). In this study the sex differences in HHR cardiac function and responses to I/R [compared to control normal heart rat (NHR)] were investigated ex vivo. The ventricular weight index was markedly increased in HHR female (7.82 ± 0.49 vs. 4.80 ± 0.10 mg/g; P < 0.05) and male (5.76 ± 0.22 vs. 4.62 ± 0.07 mg/g; P < 0.05) hearts. Female hearts of both strains exhibited a reduced basal contractility compared with strain-matched males [maximum first derivative of pressure (dP/dtmax): NHR, 4,036 ± 171 vs. 4,258 ± 152 mmHg/s; and HHR, 3,974 ± 160 vs. 4,540 ± 259 mmHg/s; P < 0.05]. HHR hearts were more susceptible to I/R (I = 25 min, and R = 30 min) injury than NHR hearts (decreased functional recovery, and increased lactate dehydrogenase efflux). Female NHR hearts exhibited a significantly greater recovery (dP/dtmax) post-I/R relative to male NHR (95.0 ± 12.2% vs. 60.5 ± 9.4%), a resistance to postischemic dysfunction not evident in female HHR (29.0 ± 5.6% vs. 25.9 ± 6.3%). Ventricular fibrillation was suppressed, and expression levels of Akt and ERK1/2 were selectively elevated in female NHR hearts. Thus the occurrence of load-independent primary cardiac hypertrophy undermines the intrinsic resistance of female hearts to I/R insult, with the observed abrogation of endogenous cardioprotective signaling pathways consistent with a potential mechanistic role in this loss of protection.

Elevated dietary sodium intake exacerbates myocardial hypertrophy associated with cardiac-specific overproduction of angiotensin II

Introduction/hypothesis
Cardiac hypertrophy is an independent risk factor predictive of cardiovascular disease and is significantly associated with morbidity and mortality. The mechanism by which angiotensin II (Ang II) and dietary sodium exert additive effects on the development of cardiac hypertrophy is unclear. The goal of this study was to evaluate the hypothesis that, where there is a genetic predisposition to Ang II-dependent hypertrophy, there is also an increased susceptibility to sodium-induced hypertrophy mediated by AT₁-receptor expression.

Methods
Diets of low sodium (LS, 0.3% w:w) and high sodium (HS, 4.0% w:w) content were fed to adult (age 25 weeks) control wild-type mice (WT) and to weeks) control wild-type mice (WT) and to transgenic mice exhibiting cardiac specific overexpression of angiotensinogen (TG). At the conclusion of a 40-day dietary treatment period, cardiac tissue weights were compared and the relative expression levels of Ang II receptor subtypes (AT_1A and AT₂) were evaluated using RT-PCR.

Results
WT and TG mice fed HS and LS diets maintained comparable weight gains during the treatment period. The normalised heart weights of TG mice were elevated compared to WT, and the extent of the increase was greater for mice maintained on the HS diet treatments (WT 12% vs. TG 41% increase in cardiac weight index). While a similar pattern of growth was observed for ventricular tissues, the atrial weight parameters demonstrated an additional significant effect of dietary sodium intake on tissue weight, independent of animal genetic type. No differences in the relative (GAPDH normalised) expression levels of AT_1A- and AT₂-receptor mRNA were observed between diet or animal genetic groups.

Conclusion
This study demonstrates that, where there is a pre-existing genetic condition of Ang II-dependent cardiac hypertrophy, the pro-growth effect of elevated dietary sodium intake is selectively augmented. In TG and WT mice, this effect was evident with a relatively short dietary treatment intervention (40 days). Evaluation of the levels of Ang II receptor mRNA further demonstrated that this differential growth response was not associated with an altered relative expression of either AT_1A- or AT₂-receptor subtypes. The cellular mechanistic bases for this specific Ang II-dietary sodium interaction remain to be elucidated.

General practitioners' nutrition promotion among cardiac patients

General practitioners fall into three categories in their pursuit of dietary counselling: little involvement, or provider of referrals, or they have strong involvement. The barriers to dietary counselling are inadequate partnerships with dietitians, patients suffering multiple medical conditions and the view that HMG-CoA-reductase-inhibitors (statins) reduce the need for dietary change.

The neuronal noradrenaline transporter, anxiety and cardiovascular disease

Panic disorder can serve as a clinical model for testing whether mental stress can cause heart disease. Potential neural mechanisms of cardiac risk are the sympathetic activation during panic attacks, continuing release of adrenaline as a co-transmitter in the cardiac sympathetic nerves, and impairment of noradrenaline neuronal reuptake, augmenting sympathetic neural respnses.

The phenotype of impaired neuronal reuptake of noradrenaline: an epigenetic mechanism? We suspect that this phenotype, in sensitizing people to heart symptom development, is a cause of panic disorder, and by magnifying the sympathetic neural signal in the heart, underlies increased cardiac risk. No loss of function mutations of the coding region of the norepinephrine transporter (NET) are evident, but we do detect hypermethylation of CpG islands in the NET gene promoter region. Chromatin immunoprecipitation methodology demonstrates binding of the inhibitory transcription factor, MeCP2, to promoter region DNA in panic disorder patients.

Cardiovascular illnesses co-morbid with panic disorder. Panic disorder commonly coexists with essential hypertension and the postural tachycardia syndrome. In both of these cardiovascular disorders the impaired neuronal noradrenaline reuptake phenotype is also present and, as with panic disorder, is associated with NET gene promoter region DNA hypermethylation. An epigenetic ‘co-morbidity’ perhaps underlies the clinical concordance.

Brain neurotransmitters. Using internal jugular venous sampling, in the absence of a panic attack we find normal norepinephrine turnover, but based on measurements of the overflow of the serotonin metabolite, 5HIAA, a marked increase (six to sevenfold) in brain serotonin turnover in patients with panic disorder. This appears to represent the underlying neurotransmitter substrate for the disorder. Whether this brain serotonergic activation is a prime mover, or consequential on other primary causes of panic disorder, including cardiac sensitization by faulty neuronal noradrenaline reuptake leading to cardiac symptoms and the enhanced vigilance which accompanies them, is unclear at present.

Nutrition care for adult cardiac patients : Australian general practitioners' perceptions of their role

Background. Australia has implemented systematic managed care for patients with chronic disease. Little is known about how GPs perceive their nutrition care role in this system.
Objective. To examine GPs’ perceptions of their roles in the nutrition care of cardiac patients and to identify factors that influence their role.
Methods. Multi-methods research design. Semi-structured interviews were conducted with a sample (n = 30) GPs Victoria, Australia. The resulting narratives were used to develop a quantitative questionnaire to survey a random sample of GPs. Principal components analysis was conducted to reduce the role items to a small number of underlying dimensions. The association between roles and demographic variables were examined using stepwise multiple regressions.
Results. In all, 248 GPs (30% response) participated. Three main roles were established: Influencing, Coordinating and Nutrition Educator role. Together, the roles explained 54% of the total variance. Demographic variables were not associated with these roles. The majority (mean = 88%) endorsed the items which loaded on to the Influencing and Coordinating (mean = 49%) roles. Short consultation time, use of prescribed medications and perception of patient attendance at cardiac rehabilitation reduced the priority for nutrition education.
Conclusions. This study highlights the importance of developing more effective team care arrangements for patients with chronic disease and working with the medical education colleges to develop education resources for doctors that include an explanation of the non-pharmaceutical as well as the pharmaceutical treatment for each chronic disease condition.

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.

Development and validation of the Diet Quality Tool for use in cardiovascular disease prevention settings

The aim of this study was to develop and evaluate a dietary screening tool for use in a secondary cardiovascular disease (CVD) prevention setting to identify an individual’s overall dietary quality. The Diet Quality Tool (DQT) was validated against a 4-day food diary for 37 individuals with established CVD attending cardiac rehabilitation. Construct validity was demonstrated for % energy from saturated fat (P = 0.002, r = –0.500), dietary fibre (P < 0.001, r = 0.559) and omega-3 fatty acids (P = 0.048, r = 0.327). Criterion validity was established with a significant difference found between mean (95% CI) dietary intakes of fibre (28.2 g, 4.4 to 17.3) and % total energy from saturated fat (10.6%, –4.8 to –0.8) for those with better DQT scores (>60%) versus those with poorer scores (≤60%) when compared with 4-day food diary nutrient values. The usefulness of the DQT was confirmed by both patients (n = 25) and cardiac rehabilitation health professionals (n = 8). The DQT was found to be a valid and useful dietary assessment tool with potential for use in a secondary CVD prevention setting. The tool has the capacity to be used in a wider variety of settings and further refinement of the tool would enable a greater amount of nutrients to be reliably screened.

Best practice for prevention and treatment of cardiovascular disease through an equity lens : a review

Background Despite declining rates of cardiovascular disease (CVD) mortality in developed countries, lower socioeconomic groups continue to experience a greater burden of the disease. There are now many evidence-based treatments and prevention strategies for the management of CVD and it is essential that their impact on the more disadvantaged group is understood if socioeconomic inequalities in CVD are to be reduced.

Aims To determine whether key interventions for CVD prevention and treatment are effective among lower socioeconomic groups, to describe barriers to their effectiveness and the potential or actual impact of these interventions on the socioeconomic gradient in CVD.

Methods Interventions were selected from four stages of the CVD continuum. These included smoking reduction strategies, absolute risk assessment, cardiac rehabilitation, secondary prevention medications, and heart failure self-management programmes. Electronic searches were conducted using terms for each intervention combined with terms for socioeconomic status (SES).

Results Only limited evidence was found for the effectiveness of the selected interventions among lower SES groups and there was little exploration of socioeconomic-related barriers to their uptake. Some broad themes and key messages were identified. In the majority of findings examined, it was clear that the underlying material, social and environmental factors associated with disadvantage are a significant barrier to the effectiveness of interventions.

Conclusion Opportunities to reduce socioeconomic inequalities occur at all stages of the CVD continuum. Despite this, current treatment and prevention strategies may be contributing to the widening socioeconomic-CVD gradient. Further research into the impact of best-practice interventions for CVD upon lower SES groups is required.

Co-morbid cardiovascular disease and depression : sequence of disease onset is linked to mental but not physical self-rated health. Results from a cross-sectional, population-based study

Purpose: Self-rated health has been linked to important health and survival outcomes in individuals with co-morbid depression and cardiovascular disease (CVD). It is not clear how the timing of depression onset relative to CVD onset affects this relationship. We aimed to first identify the prevalence of major depressive disorder (MDD) preceding CVD and secondly determine whether sequence of disease onset is associated with mental and physical self-rated health. Methods: This study utilised cross-sectional, populationbased data from 224 respondents of the 2007 Australian National Survey of Mental Health and Wellbeing (NSMHWB). Participants were those diagnosed with MDD and reported ever having a heart/circulatory condition over their lifetime. Age of onset was reported for each condition. Logistic regression was used to explore differences in self-rated mental and physical health for those reporting pre-cardiac and post-cardiac depression. Results: The proportion of individuals in whom MDD preceded CVD was 80.36% (CI: 72.57-88.15). One-fifth (19.64%, CI: 11.85-27.42) reported MDD onset at the time of, or following, CVD. After controlling for covariates, the final model demonstrated that those reporting post-cardiac depression were significantly less likely to report poor selfrated mental health (OR:0.36, CI: 0.14-0.93) than those with pre-existing depression. No significant differences were found in self-rated physical health between groups (OR:0.90 CI: 0.38-2.14). Conclusions: MDD is most common prior to the onset of CVD. Further, there is an association between pre-morbid MDD and poorer self-rated mental health. To our knowledge, this is the first time this has been demonstrated in a national, population-based survey. As self-rated health has been shown to predict important outcomes such as survival, we recommend that those with MDD be identified as vulnerable to CVD onset and poorer health outcomes

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.

Concordance with phase-one cardiac rehabilitation guidelines in the inpatient setting

The aim of the paper was to examine concordance with phase-one cardiac rehabilitation (CR) guidelines, undertake an intervention that might optimise adherence to the guidelines, and establish a benchmark for practice in the coronary care unit (CCU) setting.

Screening, referral and treatment for depression in patients with coronary heart disease: a consensus statement from the National Heart Foundation of Australia

In 2003, the National Heart Foundation of Australia position statement on “stress” and heart disease found that depression was an important risk factor for coronary heart disease (CHD). This 2013 statement updates the evidence on depression (mild, moderate and severe) in patients with CHD, and provides guidance for health professionals on screening and treatment for depression in patients with CHD.

The prevalence of depression is high in patients with CHD and it has a significant impact on the patient’s quality of life and adherence to therapy, and an independent effect on prognosis. Rates of major depressive disorder of around 15% have been reported in patients after myocardial infarction or coronary artery bypass grafting.

To provide the best possible care, it is important to recognise depression in patients with CHD. Routine screening for depression in all patients with CHD is indicated at first presentation, and again at the next follow-up appointment. A follow-up screen should occur 2–3 months after a CHD event. Screening should then be considered on a yearly basis, as for any other major risk factor for CHD.

A simple tool for initial screening, such as the Patient Health Questionnaire-2 (PHQ-2) or the short-form Cardiac Depression Scale (CDS), can be incorporated into usual clinical practice with minimum interference, and may increase uptake of screening.

Patients with positive screening results may need further evaluation. Appropriate treatment should be commenced, and the patient monitored. If screening is followed by comprehensive care, depression outcomes are likely to be improved.

Patients with CHD and depression respond to cognitive behaviour therapy, collaborative care, exercise and some drug therapies in a similar way to the general population. However, tricyclic antidepressant drugs may worsen CHD outcomes and should be avoided.

Coordination of care between health care providers is essential for optimal outcomes for patients. The benefits of treating depression include improved quality of life, improved adherence to other therapies and, potentially, improved CHD outcomes.

Altered cardiac autonomic nervous function in depression

Background:
Depression is an independent risk factor for coronary artery disease. Autonomic instability may play a mediating or moderating role in this relationship; however this is not well understood. The objective of this study was to explore cardiac autonomic function and cardiac arrhythmia in depression, the correlation between depression severity and Heart Rate Variability (HRV) related indices, and the prevalence of arrhythmia.

Methods:
Individuals (n = 53) with major depression as assessed by the Diagnostic and Statistical Manual of Mental Disorders, who had a Hamilton Rating Scale for Depression (HAMD) score ≥20 and a Zung Self-Rating Depression Scale score > 53 were compared to 53 healthy individuals, matched for age and gender. Multichannel Electrocardiograph ECG-92C data were collected over 24 hours. Long-term changes in HRV were used to assess the following vagally mediated changes in autonomic tone, expressed as time domain indices: Standard deviation of the NN intervals (SDNN), standard deviation of 5 min averaged NN intervals (SDANN), Root Mean Square of the Successive Differences (RMSSD) and percentage of NN intervals > 50 ms different from preceding interval (pNN50). Pearson’s correlations were conducted to explore the strength of the association between depression severity (using the SDS and HRV related indices, specifically SDNN and low frequency domain / high frequency domain (LF/HF)).

Results:
The values of SDNN, SDANN, RMSSD, PNN50 and HF were lower in the depression group compared to the control group (P<.05). The mean value of the LF in the depression group was higher than the in control group (P<.05). Furthermore the ratio of LF/HF was higher among the depression group than the control group (P<.05). A linear relationship was shown to exist between the severity of the depression and HRV indices. In the depression group, the prevalence of arrhythmia was significantly higher than in the control group (P<.05), particularly supraventricular arrhythmias.

Conclusions:
Our findings suggest that depression is accompanied by dysfunction of the cardiac autonomic nervous system, and further, that depression severity is linked to severity of this dysfunction. Individuals with depression appear to be susceptible to premature atrial and/or ventricular disease.