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Publications (3)3.25 Total impact

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    ABSTRACT: Non-cardiac chest pain is a frequent finding in patients admitted to emergency departments, and it has been shown that many of these patients may have an esophageal cause for their pain. However, little data are available on patients primarily referred to the cardiology unit, and especially those with coronary artery disease. The purpose of this study was to assess the role of esophageal dysfunction in chest pain patients with and without coronary artery disease. Eighty-one patients referred from a cardiology unit for chest pain and no myocardial infarction entered the study. Sixty-one patients had no evidence of coronary artery disease, whereas 20 had coronary artery disease with chest pain at rest. After the cardiological evaluation, the patients underwent esophageal function testing by means of upper endoscopy, manometry, and 24-hour pH-monitoring. Overall, 10% of patients (2.5% in the coronary artery disease group) had evidence of endoscopic esophagitis, 46% of esophageal motor disorders (12% in the coronary artery disease group), and 10% abnormal pH-monitoring (1% in the coronary artery disease group). We report that the esophagus might be responsible for non-cardiac chest pain in patients with and without coronary artery disease. In our experience, esophageal motor disorders, and not an increased acid reflux, are the abnormalities most commonly found in these patients.
    Hepato-gastroenterology 01/2005; 52(63):792-5. · 0.77 Impact Factor
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    ABSTRACT: In patients with mitral stenosis, symptoms do not always correlate with echocardiographic data. The aims of the study were to evaluate the role of cardiopulmonary exercise testing in the assessment of patients with mitral stenosis and to quantify nitric oxide production at rest and at the end of exercise. We evaluated 43 patients with moderate to severe mitral stenosis with a discrepancy between echocardiographic data and symptoms. Nitric oxide output was calculated by measuring nitric oxide concentration in the exhaled air at rest and at the end of exercise test. Patients were divided in 2 groups: group 1 with a functional capacity <75% at cardiopulmonary exercise test (VO2max in % of the predicted one) and group 2 with functional capacity >75%. Transvalvular gradient and pulmonary artery pressure were significantly higher in group 1 than in group 2 (respectively 9.07 +/- 2.11 mmHg vs 6.01 +/- 1.08 mmHg, p<0.001 and 42.8 +/- 7.2 mmHg vs 33.1 +/- 4.7 mmHg, p<0.001). Patients of group 1 had a lower nitric oxide output at the end of exercise compared to group 2 (231.4 +/- 96.6 nl/min vs 326.3 +/- 74.0 ml/min, p=0.01) and to normal subjects (511.15 +/- 180.1 nl/min, p<0.001). Cardiopulmonary exercise testing provides objective non invasive information in the evaluation of patients with discrepancy between symptoms and echocardiographic data. Different levels of nitric oxide output during exercise suggest the role of nitric oxide in regulating pulmonary vascular tone.
    Minerva cardioangiologica 03/2004; 52(1):29-35. · 0.43 Impact Factor
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    ABSTRACT: BACKGROUND: Pulmonary hypertension (PH) is an important limiting factor of exercise tolerance in patients with mitral stenosis (MS). We wished to investigate the relationship between respiratory nitric oxide (NO), a potent vasodilator, and exercise tolerance in patients with moderate MS. In the same patients, we wondered whether acute change in pulmonary hemodynamics could affect respiratory NO. METHODS: Ten patients with moderate MS (valve area 1.4+/-0.2 cm(2)) were studied at rest, during incremental cycle ergometry exercise, and during dobutamine stress echocardiography (DSE). The concentration of NO in exhaled air (FE(NO)) and NO output (V'(NO)) were measured at baseline, at the end of exercise, and at the end of DSE. Eight healthy subjects served as normal controls for NO output during exercise. RESULTS: During exercise, FE(NO) decreased both in patients and in controls, while V'(NO) increased in both. At the end of exercise, both VO(2) max and V'(NO) were significantly higher in controls than in patients. The increase in V'(NO) during exercise was significantly correlated with VO(2) max, both in patients and in controls. During DSE, cardiac output (CO), pulmonary artery pressure (PAP), and mitral valve gradient increased. No changes in mean FE(NO), V'(NO), or ventilation were observed during DSE. There was a significant inverse correlation between FE(NO) and mitral valve gradient at the end of DSE. CONCLUSIONS: In patients with moderate MS, exercise performance is correlated with respiratory NO output. In the same patients, during DSE, the increase in CO, which is not accompanied by an increase in ventilation, is not associated with an increase in respiratory V'(NO).
    European Journal of Internal Medicine 06/2003; 14(3):166-171. · 2.05 Impact Factor