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Background: Intra-arterial Doppler is a novel technique which enables accurate assessment of blood flow haemodynamics. We evaluated the feasibility of using intra-arterial Doppler for insights into the pulmonary artery flow velocity profile in patients with pulmonary arterial hypertension (PAH), and determined the changes in the flow velocity profile following pulmonary vasodilator therapy.Methods: Intra-arterial Doppler was performed in the pulmonary arteries of seven subjects with PAH before and after six months of Bosentan therapy. The following Doppler derived parameters were measured: acceleration time (AcT), systolic ejection time (ET), ratio of acceleration time to systolic ejection time (AcT/ET), systolic velocity time integral (sVTI), diastolic velocity time integral (dVTI) and total velocity time integral (tVTI). Relationships between Doppler parameters and clinical response to Bosentan therapy were analysed.Results: At baseline, all PAH patients displayed a Doppler flow velocity profile consisting of a sharp rise to peak velocity followed by mid-to-late systolic notching. In one patient, systolic notching disappeared following Bosentan therapy. Only clinical responders (n = 3) demonstrated a significant increase in tVTI (583 ± 132 versus 897 ± 138, p = 0.023), and an increase in dVTI (62 ± 28 versus 195 ± 40, p = 0.044). No significant change was observed in VTI amongst non-responders.Conclusion: Intra-arterial Doppler is feasible in the quantitative characterisation of pulmonary artery flow velocity profile. An increase in pulmonary blood flow, particularly diastolic flow, was associated with a clinical response to Bosentan therapy. This technique may provide additional insights into the haemodynamics of the pulmonary circulation in pathophysiological states.

Cardiovascular diseases (CVDs) and diabetes are two of the most important public health problems. Outcomes for patients with these disorders vary considerably, likely due to the added influence of a range of interacting clinical, metabolic, environmental, lifestyle, genetic and psychosocial risk factors associated with these diseases. The Baker Biobank study was designed to characterise these factors to inform better risk prediction, earlier diagnosis and better treatment of CVDs and diabetes. Methods This paper describes the detailed methods for the establishment of the Baker Biobank. The study collected extensive phenotypic detail about the participants recruited from Victoria, Australia. Data and samples were collected at the Departments of Cardiology and Respiratory Medicine at the Alfred Hospital and Healthy Hearts Program at the Baker Institute. Results A total of 6,530 adults with age 18-69 years were recruited into the Biobank. The majority of these participants (63%) were male. The mean (standard deviation [SD]) age of the Biobank Cohort at the time of data collection was 57(15) years. The study collected data on socio-demographic characteristics, behavioural and lifestyle factors, anthropometric measurements, medical and medication history, and blood levels of various biomarkers. The study also collected and stored Guthrie cards, serum, plasma, buffy coat, whole blood collected in Tempus tubes (for RNA extraction). For some samples extracted DNA and RNA is stored. The Biobank data is also linked to echocardiogram, hospital admission, pathology and mortality datasets. The Baker Biobank data and samples are available for health researchers with approval of Biobank Steering Group and Human Research Ethics Committee. Conclusion The Baker Biobank provides valuable data and samples into the study of the interplay among cardiovascular diseases risk factors and their impact on morbidity and mortality in Australia.

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IntroductionIt is now well documented that DL propranolol produces a decrease in plasma concentrations of L-triiodothyronine (T 3 ) and a rise in serum reverse T 3 (rT 3 ) in euthyroid, hyperthyroid and hypothyroid subjects on thyroxine (T 4 ) supplements (Harrower, Fyffe, Horn and Strong 1977; Lumholtz, Siersbaek-Nielsen, Faber, Kirkegaard and Frits 1978;Jung, Shetty and James 1980). DL propranolol inhibits T 4 deiodination to T 3 at peripheral sites by a reduction of the T 3 production rate, the clearance of T 3 remaining unaltered (Lumholtz et al. 1978). The mechanism by which propranolol exerts this effect is unclear and may not be due solely to its (3-receptor blocking activity for L propranolol, which has no j3 blocking action but is a potent membrane stabiliser, and also reduces serum T 3 levels in hypothyroid subjects receiving T 4 replacement (Jones, Jones and Birtwell 1980).