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Objective: There is a reciprocal association between major depressive disorder (MDD) and coronary heart disease (CHD). These conditions are linked by a causal network of mechanisms. This causal network should be quantitatively studied and it is hypothesised that the investigation of vagal function represents a promising starting point. Heart rate variability (HRV) has been used to investigate cardiac vagal control in the context of MDD and CHD. This review aims to examine the relationship of HRV to both MDD and CHD in the context of vagal function and to make recommendations for clinical practice and research., Methods: The search terms 'heart rate variability', 'depression' and 'heart disease' were entered into an electronic multiple database search engine. Abstracts were screened for their relevance and articles were individually selected and collated., Results: Decreased HRV is found in both MDD and CHD. Both diseases are theorized to disrupt autonomic control feedback loops on the heart and are linked to vagal function. Existing theories link vagal function to both mood and emotion as well as cardiac function. However, several factors can potentially confound HRV measures and would thus impact on a complete understanding of vagal mechanisms in the link between MDD and CHD., Conclusions: The quantitative investigation of vagal function using HRV represents a reasonable starting point in the study of the relationship between MDD and CHD. Many psychotropic and cardiac medications have effects on HRV, which may have clinical importance. Future studies of HRV in MDD and CHD should consider antidepressant medication, as well as anxiety, as potential confounders.

Familial hypercholesterolaemia (FH) is a co-dominantly inherited disorder that causes marked elevation in plasma cholesterol and premature coronary heart disease. There are at least 45,000 people with FH in Australia and New Zealand, but most remain undiagnosed and undertreated. To bridge this gap in coronary prevention the FH Australasia Network has developed a model of care for FH. We present the executive summary, with a commentary contrasting the recommendations with other international guidelines and highlighting the role of the cardiologist., (Copyright © 2012 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

Objective: Major depressive disorder (MDD) and coronary heart disease (CHD) are both clinically important public health problems. Depression is linked with a higher incidence of ischaemic cardiac events and MDD is more prevalent in patients with CHD. No single comprehensive model has yet described the causal mechanisms linking MDD to CHD. Several key mechanisms have been put forward, comprising behavioural mechanisms, genetic mechanisms, dysregulation of immune mechanisms, coagulation abnormalities and vascular endothelial dysfunction, polyunsaturated omega-3 free fatty acid deficiency, and autonomic mechanisms. It has been suggested that these mechanisms form a network, which links MDD and CHD. The aim of this review is to examine the causal mechanisms underlying the relationship between MDD and CHD, with the aim of constructing a topological map of the causal network which describes the relationship between MDD and CHD., Methods: The search term 'depression and heart disease' was entered into an electronic multiple database search engine. Abstracts were screened for relevance and individually selected articles were collated., Results: This review introduces the first topological map of the causal network which describes the relationship between MDD and CHD., Conclusions: Viewing the causal pathways as an interdependent network presents a new paradigm in this field and provides fertile ground for further research. The causal network can be studied using the methodology of systems biology, which is briefly introduced. Future research should focus on the creation of a more comprehensive topological map of the causal network and the quantification of the activity between each node of the causal network.

Fully-developed one-dimensional Casson flow through a single vessel of varying radius is proposed as a model of low Reynolds number blood flow in small stenosed coronary arteries. A formula for the resistance-to-flow ratio is derived, and results for yield stresses of tau 0 = 0, 0.005 and 0.01 Nm-2, viscosities of mu = 3.45 x 10(-3), 4.00 x 10(-3) and 4.55 x 10(-3) Pa.s and fluxes of 2.73 x 10(-6), x 10(-5) and x 10(-4) m3 s-1 are determined for segment of 0.45 mm radius and 45 mm length, with 15 mm abnormalities at each end where the radius varies by up to +/- 0.225 mm. When tau 0 = 0.005 N m-2, mu = 4 x 10(-3) Pa.s and Q = 1, the numerical values of the resistance-to-flow ratio vary from lambda = 0.525, when the maximum radii of the two abnormal segments are both 0.675 mm, to lambda = 3.06, when the minimum radii are both 0.225 mm. The resistance-to-flow ratio moves closer to unity as yield stress increases or as blood viscosity or flux decreases, and the magnitude of these alterations is greatest for yield stress and least for flux.