Diabetes and poor glycaemic control in rural patients with coronary artery disease.

BACKGROUND: The burden of cardiovascular disease is higher in rural populations. Existing data on rural cardiovascular health is mainly based on community surveys. Regional differences are not well addressed. This study aims to identify regional inequalities in cardiovascular risk factors (CVRFs) in Australian patients with suspected coronary artery disease. METHODS AND RESULTS: 538 subjects (72% male; mean age 63years) were recruited from a single cardiac catheter laboratory over a 24-month period. Subjects were stratified into Remoteness Areas (RAs) according to the Australian Standard Geographical Classification (RA1 corresponds to Major Cities, RA2 to Inner Regional Areas, RA3 to Outer Regional Areas). Body-mass index, blood pressure, hypertension, dyslipidaemia, diabetes and smoking history were recorded. A blood sample taken before the angiogram was analysed for lipids and fasting blood glucose (FBG). Distribution of the study population across RA1, RA2 and RA3 was 34.8%, 46.1% and 19.1%. Only FBG (p=0.019) and diagnosed diabetes (p=0.009) were significantly different i.e. higher in RA1. Of those without known diabetes, RA3 had the highest prevalence of dysglycaemia (p=0.023) with two-thirds having either pre-diabetes or undiagnosed diabetes. Logistic regression showed that age and RA3 were the only statistically significant predictors of elevated FBG. CONCLUSION: CAD patients from remote Australia had higher rates of pre-diabetes, undiagnosed diabetes and poorer glycaemic control. Analysis of the main CVRFs revealed a regional inequality in the recognition and management of diabetes alone. Attention to this gap in rural and urban healthcare is crucial to future cardiovascular health outcomes in Australia.

Myocardial production and release of MCP-1 and SDF-1 following myocardial infarction: differences between mice and man.

BACKGROUND: Stem cell homing to the heart is mediated by the release of chemo-attractant cytokines. Stromal derived factor -1 alpha (SDF-1a) and monocyte chemotactic factor 1(MCP-1) are detectable in peripheral blood after myocardial infarction (MI). It remains unknown if they are produced by, and released from, the heart in order to attract stem cells to repair the damaged myocardium. METHODS: Murine hearts were studied for expression of MCP-1 and SDF-1a at day 3 and day 28 following myocardial infarction to determine whether production is increased following MI. In addition, we studied the coronary artery and coronary sinus (venous) blood from patients with normal coronary arteries, stable coronary artery disease (CAD), unstable angina and MI to determine whether these cytokines are released from the heart into the systemic circulation following MI. RESULTS: Both MCP-1 and SDF-1a are constitutively produced and released by the heart. MCP-1 mRNA is upregulated following murine experimental MI, but SDF-1a is suppressed. There is less release of SDF-1a into the systemic circulation in patients with all stages of CAD including MI, mimicking the animal model. However MCP-1 release from the human heart following MI is also suppressed, which is the exact opposite of the animal model. CONCLUSIONS: SDF-1a and MCP-1 release from the human heart are suppressed following MI. In the case of SDF-1a, the animal model appropriately reflects the human situation. However, for MCP-1 the animal model is the exact opposite of the human condition. Human observational studies like this one are paramount in guiding translation from experimental studies to clinical trials.