A comparison of age-standardised event rates for acute and chronic coronary heart disease in metropolitan and regional/remote Victoria: a retrospective cohort study

Abstract Background Acute and chronic coronary heart disease (CHD) pose different burdens on health-care services and require different prevention and treatment strategies. Trends in acute and chronic CHD event rates can guide service implementation. This study evaluated changes in acute and chronic CHD event rates in metropolitan and regional/remote Victoria. Methods Victorian hospital admitted episodes with a principal diagnosis of acute CHD or chronic CHD were identified from 2005 to 2012. Acute and chronic CHD age-standardised event rates were calculated in metropolitan and regional/remote Victoria. Poisson log-link linear regression was used to estimate annual change in acute and chronic CHD event rates. Results Acute CHD age-standardised event rates decreased annually by 2.9 % (95 % CI, −4.3 to −1.4 %) in metropolitan Victoria and 1.7 % (95 % CI, −3.2 to −0.1 %) in regional/remote Victoria. In comparison, chronic CHD age-standardised event rates increased annually by 4.8 % (95 % CI, +3.0 to +6.5 %) in metropolitan Victoria and 3.1 % (95 % CI, +1.3 to +4.9 %) in regional/remote Victoria. On average, age-standardised event rates for regional/remote Victoria were 30.3 % (95 % CI, 23.5 to 37.2 %) higher for acute CHD and 55.3 % (95 % CI, 47.1 to 63.5 %) higher for chronic CHD compared to metropolitan Victoria from 2005 to 2012. Conclusion Annual decreases in acute CHD age-standardised event rates might reflect improvements in primary prevention, while annual increases in chronic CHD age-standardised event rates suggest a need to improve secondary prevention strategies. Consistently higher acute and chronic CHD age-standardised event rates were evident in regional/remote Victoria compared to metropolitan Victoria from 2005 to 2012

Lipemic serum in hyperlipidemic pancreatitis

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Metabolomics improves the histopathological diagnosis of asphyxial deaths: an animal proof-of-concept model

The diagnosis of mechanical asphyxia remains one of the most difficult issues in forensic pathology. Asphyxia ultimately results in cardiac arrest (CA) and, as there are no specific markers, the differential diagnosis of primitive CA and CA secondary to asphyxiation relies on circumstantial details and on the pathologist experience, lacking objective evidence. Histological examination is currently considered the gold standard for CA post-mortem diagnosis. Here we present the comparative results of histopathology versus those previously obtained by 1H nuclear magnetic resonance (NMR) metabolomics in a swine model, originally designed for clinical purposes, exposed to two different CA causes, namely ventricular fibrillation and asphyxia. While heart and brain microscopical analysis could identify the damage induced by CA without providing any additional information on the CA cause, metabolomics allowed the identification of clearly different profiles between the two groups and showed major differences between asphyxiated animals with good and poor outcomes. Minute-by-minute plasma sampling allowed to associate these modifications to the pre-arrest asphyxial phase showing a clear correlation to the cellular effect of mechanical asphyxia reproduced in the experiment. The results suggest that metabolomics provides additional evidence beyond that obtained by histology and immunohistochemistry in the differential diagnosis of CA

Mood and transient cardiac dysfunction in everyday life

Emotion in daily life may be associated with transient myocardial ischemia, ventricular tachycardia and impaired autonomic function in cardiac patients, but the precise temporal sequence is unclear. Eighty-eight patients with suspected coronary artery disease underwent 24-h electrocardiographic monitoring, and affect was measured with the Day Reconstruction Method. Thirteen patients (15%) experienced one or more episodes of ST depression or ventricular tachycardia, nine of whom provided concurrent mood data. Mood and heart rate variability were analyzed for the 15 min before, during, and 15 min after each ST depression/ventricular tachycardia episode, and were compared with control periods not associated with cardiac dysfunction. Patients reported more negative mood in the 15 min preceding cardiac dysfunction compared with control periods (P = 0.02). Heart rate increased in the 5 min before cardiac dysfunction (P = 0.005), whereas low frequency heart rate variability was reduced at onset but not before cardiac dysfunction (P = 0.007). There were not changes in high frequency heart rate variability. This small study indicates that emotional state may contribute to vulnerability of cardiac dysfunction in everyday life