[Effectiveness of pharmacological prevention after the first attack of ventricular tachycardia].
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Biomedical subjects
Publications and source records attributed to M Uguccioni.
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The case of an eight-year old child suffering from sick sinus syndrome (SSS) is reported. The patient showed S-A conduction disturbances (Mobitz 1 sinoatrial exit block) as noted in two sequential 24-hour recording periods, and a pathologic response to atropine test. An involvement of the A-V node was also present, made clear by a first and a second degree Mobitz 1 block. The clinical, laboratory and noninvasive data excluded an organic cardiopathy. Idiopathic SSS was, therefore, diagnosed. The rare occurrence of this syndrome in the childhood, and the usefulness of Holter monitoring in its detection is emphasized.
An Ambulatory ECG monitoring (AM) was carried out over a 24 hr. period on 90 healthy children divided into 3 age groups (lst week of life, 1 year of age and 5 years of age). There was a high number (about 50%) of unusable registrations because of detached electrodes, broken leads, and artifacts. The AM on children is characterised by: a) high values of the maximum frequencies (mean maximum absolute frequency 178 at birth, 164 at one year, 154 at 5 years); b) a great difference between the maximums and minimums; c) hourly variations related, above all, to feedings in the new-born babies and of a circadian type in the 5 years old children; d) almost constant marked sinus arrhythmias (80%); extremely rare extrasystolia (7.5 atrial, 2.5 ventricular) and always isolated; e) presence of upward (27%) and downward deflection (10%) of the J point sometimes accompanied by modifications of the T wave (22%).
The aim of this single blind, placebo controlled study is to evaluate the efficacy and safety of quinapril in mild to moderate hypertension. Thirty-six patients (from 32 to 64 years old, mean 54.8 +/- 8.84) with diastolic blood pressure (DP) greater than or equal to 96 mmHg and less than or equal to 114 mmHg were enrolled. After a two week wash-out, a placebo was administered for two weeks and than for 12 weeks 20 mg of quinapril u.i.d. At the eighth week if DP was not less than less than or equal to 94 mmHg 40 mg of quinapril was administered. Blood pressure was evaluated at the onset of the study, at the beginning of every step and every 4 weeks. Mean DP and systolic pressure were respectively 159.17 +/- 11.43 and 101.14 +/- 4.39 at the enrolling time, 159.72 +/- 9.41 and 101.86 +/- 3.45 after the wash-out period, 152.78 +/- 9.22 and 98.33 +/- 2.9 after the placebo period, 150 +/- 9.34 and 95.28 +/- 3.52, 144.72 +/- 8.89 and 92.22 +/- 4.32, 140.25 +/- 8.21 and 88.24 +/- 5.27 after 4, 8, 12 weeks of treatment.
OBJECTIVE: Felty's syndrome (FS) is defined as rheumatoid arthritis (RA) with neutropenia and, in some cases, splenomegaly; the outcome is primarily determined by the risk of infection, which is related to the degree of neutropenia. We analysed whether the clinical manifestations of FS, especially neutropenia, could be explained by abnormalities in cytokine production. METHODS: We examined the production in FS of five cytokines involved in the maturation and activation of polymorphonuclear cells (PMNs): IL-1 beta, TNF alpha, IL-8, G-CSF and GM-CSF. Because of the role of systemic IL-8 in neutrophil migration, serum IL-8 levels were also evaluated. RESULTS: Spontaneous and anti-CD16 stimulated cytokine production was similar in FS, RA and healthy controls (NC). However, anti-CD3 stimulated IL-8 production was significantly increased compared to NC in both RA and FS. FS patients who spontaneously produced G-CSF in culture were protected from bacterial infections. Serum IL-8 levels were elevated in FS and RA compared to NC (p < 0.001 for both groups). In FS, serum IL-8 was higher in patients with a history of bacterial infections compared to those without (p < 0.01) and there was a weak inverse correlation between neutropenia and serum IL-8 levels (Kendal's tau B = -0.31, p = 0.05). CONCLUSION: The neutropenia of FS cannot be explained by changes in peripheral blood cytokine production, although changes in the bone marrow microenvironment cannot be excluded. Our data do suggest a possible role for G-CSF and IL-8 in the development of certain FS complications.