[Thyroid dysfunction and pulmonary hypertension]. / Distiroidismi e ipertensione polmonare.

Prior observational studies and several case reports have suggested an association between thyroid dysfunction and pulmonary hypertension. This review was designed to evaluate the prevalence and the pattern of pulmonary vasculature involvement in hyper- and hypothyroidism. We identified original research papers and reviews by going through leading journals that publish basic and clinical research in the fields of pulmonary hypertension, hyperthyroidism and hypothyroidism, by electronically searching the Medline database. We directed special attention to papers published from 1972 to 2003. Our findings indicate the presence of a frequent association between hyperthyroidism and pulmonary hypertension (35% in the largest series of cases) which decrease after achievement of a euthyroid state. A possible explanation includes an influence of thyroid hormones which affect growth and maturation of vascular cells and enhanced catecholamine sensitivity causing pulmonary vasoconstriction. Furthermore, several studies suggest a high prevalence of transient pulmonary hypertension in hypothyroidism (49% in the largest series of cases), in these cases autoimmunity play a key role.

Acute antiarrhythmic effects of bi-level positive airway pressure ventilation in patients with acute respiratory failure caused by chronic obstructive pulmonary disease: a randomized clinical trial.

BACKGROUND: Cardiac arrhythmias are common in patients with chronic obstructive pulmonary disease (COPD) and acute respiratory failure (ARF) and may be life threatening. Recently, non-invasive positive pressure ventilation has been advanced as a useful tool in COPD patients with ARF. This method can affect global cardiac performance through its effects on many determinants of cardiac function and may be helpful in reducing arrhythmias. OBJECTIVE: To assess the role of bi-level positive pressure ventilation (BiPAP) in the management of cardiac arrhythmias in patients with ARF caused by COPD. METHODS: We studied 30 consecutive patients with ARF related to COPD diagnosed according to American Thoracic Society criteria. All subjects were smokers; the mean age was 68 +/- 7 years. They were randomly assigned to receive BiPAP plus standard therapy (group 1) or standard therapy alone (group 2). Patients randomized to receive BiPAP were first fitted with a nasal mask, and BiPAP was administered after 12 h of standard therapy. All subjects were studied using a computerized 24-hour Holter ECG. Blood gases, plasma electrolytes, respiratory rate and blood pressure were measured at study entry, at 30, 60 and 120 min and then every 3 h. RESULTS: Heart rate decreased from 86.08 +/- 7.86 to 74.92 +/- 5.39 in group 1 (p < 0.001) versus 82.77 +/- 8.78 to 75.82 +/- 6.76 in group 2 (p = 0.033). Ventricular premature complexes decreased from 564.38 +/- 737.36 to 166.15 +/- 266.26 in group 1 (p < 0.001) versus 523.38 +/- 685.75 to 353.54 +/- 469.93 in group 2 (p = 0.021). Atrial premature complexes decreased from 570.00 +/- 630.36 to 152.31 +/- 168.88 in group 1 (p < 0.001) versus 513.77 +/- 553.81 to 328.62 +/- 400.81 in group 2 (p = 0.021). CONCLUSIONS: Cardiac arrhythmias decreased significantly in both groups after the start of both treatments, although data obtained from group 1 revealed a more important statistical significance. Our data seem to support the hypothesis that BiPAP may be a useful tool in managing COPD patients with ARF and mild arrhythmias.