Predicting mortality and hospital admission in patients with COPD: significance of NT pro-BNP, clinical and echocardiographic assessment.

AIMS: To quantify the ability of N-terminal pro-brain natriuretic peptide (NT pro-BNP) to predict mortality and hospitalization in patients with chronic obstructive airways disease (COPD). METHODS: Prospective single-centre observational study of 140 consecutive patients aged at least 18 years with COPD between 27 March 2004 and 28 February 2008 (median follow-up 3.9 years). RESULTS: Sixty-five (46%) men, 26 (19%) O2 therapy, 115 (82%) smokers, 38 (27%) patients receiving diuretics, 15 (11%) left-ventricular ejection fraction less than 45%. Median [interquartile range (IQR)] NT pro-BNP concentration 16.2 (25.4) pmol/l. NT pro-BNP was higher in those with a dilated left atrium (P<0.001), aortic stenosis (P=0.02), left-ventricular systolic dysfunction (P=0.027), right ventricular impairment (P=0.011), atrial fibrillation (P<0.001), patients receiving diuretics (P=0.010) and angiotensin-converting enzyme (ACE) inhibitors (P=0.006). One-year mortality and hospitalization rates were 2.9 and 25.4%. The median (IQR) time to hospitalization and length of first hospital stay: 383.5 (605) and 4.0 (7.0) days. NT pro-BNP was an excellent discriminator of right-ventricular impairment (C statistic=0.90) and predicted survival (highest quartile versus lowest quartile relative risk=3.02, P=0.001), but not hospital admission. After adjustment this association was not significant. CONCLUSION: NT pro-BNP predicts survival, but not hospital admission in patients with COPD. The ability of NT pro-BNP to independently predict death or hospitalization is superseded by the presence of a dilated left atrium, aortic stenosis and left-ventricular systolic dysfunction.

Atrial fibrillation associated with a thyroid stimulating hormone-secreting adenoma of the pituitary gland leading to a presentation of acute cardiac decompensation: a case report.

INTRODUCTION: Hyperthyroidism is a well established cause of atrial fibrillation (AF). Thyroid Stimulating Hormone-secreting pituitary tumours are rare causes of pituitary hyperthyroidism. Whilst pituitary causes of hyperthyroidism are much less common than primary thyroid pathology, establishing a clear aetiology is critical in minimising complications and providing appropriate treatment. Measuring Thyroid Stimulating Hormone (TSH) alone to screen for hyperthyroidism may be insufficient to appropriately evaluate the thyroid status in such cases. CASE PRESENTATION: A 63-year-old Caucasian man, previously fit and well, presented with a five-day history of shortness of breath associated with wheeze and dry cough. He denied symptoms of hyperthyroidism and his family, social and past history were unremarkable. Initial investigation was in keeping with a diagnosis of atrial fibrillation (AF) with fast ventricular response leading to cardiac decompensation.TSH 6.2 (Normal Range = 0.40 - 4.00 mU/L), Free T3 of 12.5 (4.00 - 6.8 pmol/L) and Free T4 51(10-30 pmol/L). Heterophilic antibodies were ruled out. Testosterone was elevated at 43.10 (Normal range: 10.00 - 31.00 nmol/L) with an elevated FSH, 18.1 (1.0-7.0 U/L) and elevated LH, 12.4 (1.0-8.0 U/L). Growth Hormone, IGF-1 and prolactin were normal. MRI showed a 2.4 cm pituitary macroadenoma. Visual field tests showed a right inferotemporal defect.While awaiting neurosurgical removal of the tumour, the patient was commenced on antithyroid medication (carbimazole) and maintained on this until successful trans-sphenoidal excision of the macroadenoma had been performed. AF persisted post-operatively, but was electrically cardioverted subsequently and he remains in sinus rhythm at twelve months follow-up off all treatment. CONCLUSION: This case reiterates the need to evaluate thyroid function in all patients presenting with atrial fibrillation. TSH-secreting pituitary adenomas must be considered when evaluating the cause of hyperthyroidism. Early diagnosis and treatment of such adenomas is critical in reducing neurological and endocrine complications.