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Background:\ud Databases for Congenital Heart Disease (CHD) are effective in delivering accessible datasets ready for statistical inference. Data collection hitherto has however been labour and time intensive and has required substantial financial support to ensure sustainability. We propose here creation and piloting of a semiautomated technique for data extraction from clinic letters to populate a clinical database.\ud \ud Methods: \ud PDF formatted clinic letters stored in a local folder, through a series of algorithms underwent data extraction, pre-processing and analysis. Specific patient information (diagnoses, diagnostic complexity, interventions, arrhythmia, medications, and demographic data) was processed into text files and structured data tables, used to populate a database. A specific data validation schema was pre-defined to verify and accommodate the information populating the database. Unsupervised learning in the form of a dimensionality reduction technique was used to project data into two dimensions and visualise their intrinsic structure in relation to the diagnosis, medication, intervention, and ESC classification lists of disease complexity. Nine-three randomly selected letters were manually reviewed for accuracy. \ud \ud Results: \ud 1409 consecutive outpatient clinic letters were used to populate the Scottish Adult Congenital Cardiac Database. Mean patient age was 35.4yrs, 47.6% female with 698, 49.5% having moderately complex, 369, 26.1% greatly complex, and 284, 20.1%, mildly complexity lesions. Individual diagnoses were successfully extracted in 96.95%, and demographic data was extracted in 100% of letters. Data extraction, database upload, data analysis and visualisation took 571 seconds (9.51 minutes). Manual data extraction in the categories of diagnoses, intervention and medications yielded accuracy of the computer algorithm in 94%, 93%, and 93% respectively. \ud \ud Conclusions: \ud Semi-automated data extraction from clinic letters into a database can be successfully achieved with a high degree of accuracy and efficiency.

Objective The study objective was to evaluate long-term trends in morbidity and mortality in a national cohort of adult patients with a systemic right ventricle due to the atrial switch for transposition of the great arteries or congenitally corrected transposition of the great arteries. Methods We performed a retrospective cohort study from a baseline of 18 years, including life table and Kaplan–Meier analysis for probability of death/transplant, arrhythmia, surgical or percutaneous intervention, and permanent pacemaker insertion. Results A total of 97 adults with transposition of the great arteries–atrial switch (Mustard procedure in 80/Senning procedure in 17) and 32 adults with congenitally corrected transposition of the great arteries survived. The median ages at latest follow-up were 29 and 34 years, respectively. At 40 years of follow-up, freedom from death or transplant was 0.90 for those with transposition of the great arteries–atrial switch and 0.84 for those with congenitally corrected transposition of the great arteries ( P = .833). Freedom from arrhythmia at 40 years of follow-up was 0.51 for those with transposition of the great arteries–atrial switch and 0.93 for those with congenitally corrected transposition of the great arteries ( P = .007). Freedom from intervention at 40 years of follow-up was 0.33 for those with transposition of the great arteries–atrial switch after initial repair and 0.53 for those with congenitally corrected transposition of the great arteries ( P = .938). Freedom from pacemaker insertion at 40 years of follow-up was 0.77 for those with transposition of the great arteries–atrial switch and 0.62 for those with congenitally corrected transposition of the great arteries ( P = .161). Conclusions Those patients who survive to adulthood with a systemic right ventricle experience low mortality and good functional status up to 40 years of age. However, there is a substantial burden of atrial tachyarrhythmia, and this occurs significantly earlier in those with transposition of the great arteries–atrial switch. Management of atrial tachyarrhythmia, along with systemic right ventricular dysfunction and systemic atrioventricular valve regurgitation, is likely to be the major challenge for this group of patients over the next decade.

OBJECTIVESThis study was designed to determine the effect of two weeks’ treatment with L-arginine on the ratio of plasma L-arginine to asymmetric dimethylarginine (ADMA), oxidative stress, endothelium-dependent vasodilatation to acetylcholine, exercise performance and heart rate variability in men with stable angina.BACKGROUNDThe ratio of plasma L-arginine:ADMA has been proposed as a determinant of endothelium-dependent dilation; dietary supplementation with L-arginine has been shown to improve endothelium-dependent vasodilation and symptoms in some conditions.METHODSMen (n = 40) with stable angina, at least one epicardial coronary artery with a stenosis >50% and a positive exercise test were randomized to receive L-arginine (15 g daily) or placebo for two weeks according to a double-blind parallel-group design. Plasma L-arginine, ADMA, 8-epi-prostaglandin F2α(a marker of oxidative stress) and forearm vasodilator responses to brachial artery infusion of nitroprusside and acetylcholine (±L-arginine) were measured. A standard Bruce protocol exercise test was performed before and at the end of the treatment period.RESULTSPlasma L-arginine increased after oral L-arginine, whereas ADMA remained unchanged, leading to an increase in the L-arginine/ADMA ratio of 62 ± 11% (mean ± SE, p < 0.01). Despite a significant enhancement in acetylcholine response by intra-arterial L-arginine at baseline, this response remained unchanged after oral L-arginine. Measures of oxidative stress and exercise performance after L-arginine/placebo were similar in placebo and active groups.CONCLUSIONSIn men with stable angina, an increase in plasma L-arginine/ADMA ratio after two weeks’ oral supplementation with L-arginine is not associated with an improvement in endothelium-dependent vasodilatation, oxidative stress or exercise performance.