Pioglitazone improves endothelial function in non-diabetic patients with coronary artery disease.

OBJECTIVE: To test the hypothesis that pioglitazone, a peroxisome proliferator-activated receptor-gamma agonist, will improve endothelial function in non-diabetic subjects with coronary artery disease, we conducted a prospective study to evaluate the effect of this medication on the brachial artery vasomotor function and circulating markers of endothelial activation. METHODS: Baseline characteristics were collected. After initial endothelial function assessment, patients were treated with pioglitazone hydrochloride 30 mg daily. The medication was continued for 12 weeks and endothelial function was reassessed as well as the inflammatory markers. The study medication then was stopped, and all the tests were repeated 12 weeks later. RESULTS: Seventeen subjects completed all three-study phases. Mean age was 58 (range: 36-77 years). Compared with the baseline, the endothelium-dependent vasodilation improved significantly with the treatment (p < 0.001) from 4.4 +/- 3.9 to 8.4 +/- 4.1%, a relative increase of 91%. After withdrawal of treatment, the endothelium-dependent vasodilation returned towards baseline values. There was no change in endothelium-independent vasodilatation (12.27 +/- 6.35 to 13.9 +/- 9.23%, to 12.42 +/- 5.35%, p = 0.177). The urine asymmetric dimethlyarginine levels decreased significantly with the treatment, but also returned to the initial values after the wash-out period (1.27 +/- 0.5 micromol/ml to 0.97 +/- 0.3 micromol/ml to 1.34 +/- 0.5 micromol/ml, p = 0.017). No difference in the lipid profile, C-reactive protein, erythrocyte sedimentation rate, or fibrinogen levels was seen. CONCLUSION: Pioglitazone rapidly improves endothelial function in non-diabetic patients with coronary artery disease. This improvement is associated with a change in mean urinary asymmetric dimethylarginine levels, although a cause and effect cannot be determined from this investigation.

Pulmonary nodules and masses after lung and heart-lung transplantation.

The authors assess clinical and radiographic findings of pulmonary nodules and masses after lung and heart-lung transplantation. One hundred and fifty nine patients who survived at least 3 months after lung and heart-lung transplantation were followed by serial chest radiographs for a median of 27 months. Single or multiple lung nodules or masses were noted at chest radiography in 15 (9.4%) of 159 patients. Imaging findings and causes of these nodules and masses were reviewed retrospectively. Infection was found in 10 (6%) of 159 patients. Specific pathogens (11 pathogens in 10 patients) were Aspergillus (n = 4), Mycobacteria (n = 4), and other bacteria (n = 3). Noninfectious causes were found in 5 (3%) of patients and included B-cell lymphoma (n = 2), bronchogenic carcinoma (n = 2), and pulmonary infarcts (n = 1). Nodules and masses appeared a median of 11 months after transplantation (range: 0.2 to 36 months). Five patients (33%) had single lesions; the other 10 (67%) patients had multiple lesions (range 2 to 50). Aspergillus lesions were most commonly located in the upper lobes, were cavitary in three of four patients, and all were fatal. Nodules and masses arose in the transplanted lung in 12 (80%) of the patients, and in the native lung in 3 (20%) of the patients (2 bronchogenic carcinoma, 1 M. tuberculosis simulating bronchogenic carcinoma). Nodules and masses detected by chest radiography are not uncommon (9.4%) after lung and heart-lung transplantation. Infections are more common than noninfectious causes of posttransplant nodules and masses. Specific clinical and imaging characteristics may provide clues to etiology.