Biomedical subjects
Publications and source records attributed to Fulvio Orzan.
Infection of devices for percutaneous transcatheter closure of atrial septal defects are exceedingly rare. Two cases of device-associated endocarditis have been reported, which were both operated on. We describe the successful treatment with antibiotics of a device-associated endocarditis.
BACKGROUND: Patients with myocardial infarction without angiographically significant coronary artery lesions are considered, as a whole, to have a better prognosis. Different degrees of coronary involvement, within this wide group, may portend different degrees of risk. The aim of this study was to assess which clinical and angiographic covariates are more useful in defining the individual prognosis. METHLODS: We prospectively followed 53 consecutive patients admitted to our coronary care unit between 1985-1990 with myocardial infarction and a culprit lesion causing < or = 50% angiographic luminal narrowing. RESULTS: Patients with normal angiograms (group A) were compared to those with minor parietal irregularities (group B) or discrete (< or = 50%) stenosis (group C). Group A patients were younger, had a lower peak creatine kinase release, and a higher ejection fraction. After a median follow up of 125 +/- 32 months, group A patients had a 100% 10-year survival compared to 77 and 58% for group B and group C patients respectively (p = 0.01). At univariate analysis, ischemic events correlated with the severity of coronary lesions (while group A patients had no ischemic events at follow-up, events occurred in 46 and 50% of group B and C patients respectively; p = 0.003) and with ejection fraction, that was lower in patients with events (56.0 +/- 17 vs 67 +/- 11%, p = 0.006). Cardiac death, too, correlated with the type of coronary lesions (p = 0.03) and with lower ejection fraction (p = 0.004). By means of multivariate analysis, on the contrary, only the vessel morphology was predictive of ischemic events at follow-up (p = 0.02), while the only significant predictor of death was ejection fraction (p = 0.0012). CONCLUSIONS: Patients with myocardial infarction and strictly normal vessels have very few ischemic events at follow-up, and may be distinguished from both patients with non-significant lesions as well as those with minor angiographic irregularities. On the other hand, cardiac mortality correlates strongly and independently with a depressed ventricular function.
Fever of unknown origin is one of the most intriguing issues in clinical practice. One of the most feared diagnoses, especially in patients with known valvular disease, is endocarditis. The differential diagnosis of fever is often complicated by the clinical-pathological overlap between the systemic inflammatory response in different types of pathologies such as infectious, autoimmune or neoplastic disorders. We report a case of a patient presenting with fever, cutaneous nodules and malaise, with a known mitral valve prolapse and moderate regurgitation, in which the diagnosis of Wegener's granulomatosis was finally made.
A large pulmonary arteriovenous fistula was discovered in a patient with long-standing cyanosis, clubbing and dyspnea, with no other cardiovascular signs or symptoms and a normal chest roentgenogram at the time of cardiac catheterization and pulmonary angiography. The fistula was overshadowed by the cardiac silhouette. Surgical resection was successful. Although rarely undetected on the chest roentgenogram, this potentially lethal malformation should be considered in the differential diagnosis of cyanosis unaccompanied by other cardiovascular signs or symptoms.
BACKGROUND/AIMS: 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. METHODOLOGY: 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. RESULTS: 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). CONCLUSIONS: 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.