Amiodarone induced pneumonitis and hyperthyroidism: case report.

Amiodarone is a highly effective antiarrhythmic agent used in life-threatening ventricular and supraventricular arrhythmias. Its long-term use may however lead to several adverse effects, including corneal deposits, liver and thyroid gland dysfunction, lung lesions, bone marrow injury, skin lesions, or neurological abnormalities. The article presents the case of a 56-year-old man with a history of a stroke, who after a few days of amiodarone therapy for an episode of atrial fibrillation was diagnosed with amiodarone-induced hyperthyroidism and interstitial pulmonary lesions. Clinical and laboratory symptoms of hyperthyroidism and radiographic signs of pulmonary involvement did not occur until several weeks after discontinuation of amiodarone therapy. Differential diagnosis of causes of hyperthyroidism and diseases causing nodular pulmonary lesions did not demonstrate any other pathologies. Empirical antibiotic therapy and administration of thiamazole and high doses of propranolol failed to improve the patient's clinical status. It was not until thiamazole was given in combination with glucocorticosteroids, when a slow relief of hyperthyroidism symptoms and resolution of radiographic pulmonary signs were observed. Based on the presented case, the risk of appearance of 2 serious concomitant adverse effects was demonstrated, even following a short-term amiodarone therapy. This paper also contains an overview of adverse effects which may be encountered during or after therapy with this effective antiarrhythmic agent. It was emphasized how important it is to select patients appropriately, and to monitor potential adverse effects during amiodarone therapy.

[Influence of nasal continuous positive airway pressure on response to exercise in patients with obstructive sleep apnea syndrome]. / Wplyw leczenia za pomoca ciaglego dodatniego cisnienia w drogach oddechowych na reakcje na wysilek fizyczny u chorych na obturacyjny bezdech podczas snu.

UNLABELLED: Obstructive sleep apnea syndrome (OSAS) patients are at risk of cardiovascular complications. The aim of this study was to assess the effect of treatment with continuous positive airway pressure (CPAP) on the response to symptom limited exercise test. METHODS: twenty nine OSAS patients (1 F, 28 M), mean age 50.7+/-9.7 yrs with body mass index of 32.6+/-4.5 kg/m2 participated in the study. OSAS was diagnosed by overnight polysomnography. Incremental cardiopulmonary exercise test (CPET) on a treadmill was performed twice: before and after 2-3 weeks of regular treatment with CPAP. RESULTS: mean apnea + hypopnea index (AHI) before therapy was 57.6+/-12 h(-1). CPAP treatment did not change peak oxygen consumption (VO2max) (38.3+/-9.0 vs. 38.9+/-6.9 mlO2/kg/min, p=ns) or peak heart rate (153.4+/-21 min- vs. 155.5+/-22 min(-1), p=ns). There were no significant changes in ventilation or gas exchange variables. However, a decrease in peak systolic blood pressure from 194.5+/-24 mmHg to 186.7+/-27.9 mmHg (p<0.05) with CPAP treatment was found. During recovery a decrease in heart rate (at 1st minute and minutes 3 - 6) and mean arterial pressure (MAP) (minutes 4-7) with CPAP treatment was observed. Significant correlations between VO2max and AHI (r=-0,38, p<0,05); MAP at peak exercise and: AHI, mean oxygen saturation (SaO2) during sleep, minutes of sleep with SaO2<90% (T90); MAP at recovery (minutes 3-8) and T90 before CPAP treatment were also noted. CONCLUSIONS: OSAS patients are not limited on exercise. Treatment with nasal CPAP attenuates circulatory response to incremental exercise on a treadmill.

[Maximal respiratory pressures and exercise tolerance in patients with COPD]. / Maksymalne cisnienia oddechowe i tolerancja wysilku u chorych na przewlekla obturacyjna chorobe pluc.

UNLABELLED: Many authors reported respiratory muscle function impairment in patients with chronic obstructive pulmonary disease (COPD). Impaired respiratory muscle function may contribute exercise intolerance which is frequently observed in this disease. AIM OF THE STUDY: was to determine the influence of respiratory muscle function on exercise capacity in patients with COPD. METHODS: 23 patients with stable COPD aged 62.7 +/- 9.3 years (6F, 17M; mean post-bronchodilator FEV1 = 47.9 +/-12.4% value predicted) participated in the study. Exercise capacity was assessed by the six-minute walk test and the incremental cardiopulmonary exercise test (CPET) on a treadmill. Maximal respiratory pressures (PImax, PEmax) were evaluated before and directly after CPET. RESULTS: The mean peak oxygen uptake (VO max) was 27.2 +/- 6.1 mlO2/min/kg and the mean distance walked during the 6MWT was 569.4 +/- 101.7 m. Both PIMax and PE max decreased significantly after maximal exercise (71.4 +/-23.0 vs 63.6 +/- 22.2 cmH2O, p = 0.001 and 124.9 +/- 46.5 vs 112.3 +/- 46.6 cm H2O, p = 0.02 respectively). No correlation between VO2max and the 6-minute walk distance and the maximal respiratory pressures was found. We observed a negative correlation between the 6-minute walk distance and the difference between the pre- and post CPET maximal inspiratory pressure. CONCLUSIONS: respiratory muscle function is impaired in patients with COPD but this does not affect exercise performance. Exercise causes a decrease of the respiratory muscle strength.