Imported syphilis and other sexually transmitted infections among UK travellers to Russia and Poland.
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Biomedical subjects
Publications and source records attributed to G Luzzi.
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The results of studies on the effect of beta-adrenergic blockade on respiratory sinus arrhythmia (RSA) are discordant. In some studies in which an increased RSA was reported, central vagotonic activity has been proposed. The aim of this study was to verify whether chronic beta-adrenergic blockade is capable of increasing RSA, and therefore vagal outflow, and to analyze whether the mechanism of action is central or peripheral. Twenty normal subjects (mean age 28 +/- 2 years) were randomized to receive a hydrophilic (nadolol, N), a lipophilic (metoprolol, M) beta-blocker and placebo (PL). After 1 week of therapy a spectral analysis was made of the variability in heart rate and systolic blood pressure (SBP) while they controlled their breathing at 16 breaths/min for a period of 5 min. The high frequency component was calculated for the RR interval (HF-RR, RSA measure) and SBP (HF-SBP), and the squared coherence (K2) and phase functions (phi HF) were assessed between RR and SBP fluctuations in the respiratory band (RR-SBP); a negative phi HF means that RR changes follow SBP changes. The alpha HF (an index of the baroreflex gain) was also calculated. Both beta-blockers increased the mean RR interval (PL 808 +/- 21, N 1054 +/- 30, M 1031 +/- 27 ms; p < 0.0001), HF-RR (PL 6.3 +/- 0.3, N 7.1 +/- 0.3, M 7.2 +/- 0.3 ln-ms2; p = 0.002) and alpha HF (PL 13.6 +/- 1.5, N 21.9 +/- 2.8, M 24.5 +/- 3.6 ms/mmHg; p < 0.002), and both modified phi HF (PL -0.23 +/- 0.05, N -0.02 +/- 0.05, M -0.03 +/- 0.04 s; p < 0.0001). No difference was found between N and M. Chronic beta-adrenergic blockade enhanced RSA and baroreflex gain and reduced the phase between the RR interval and SBP oscillations. Since no difference was found between the hydrophilic and the lipophilic beta-blockers, these changes seem to be due to a peripheral effect.
To explore the role of heart rate in the genesis of ventricular premature complexes whose incidence increases when the length of the preceding cardiac cycle decreases, we analyzed the effect of nadolol alone and together with atrial pacing in 4 patients. Nadolol lengthened the RR cycle and suppressed ventricular premature complexes; atrial pacing, restoring the baseline RR cycle lengths, led to the reappearance of ventricular premature complexes, suggesting the major role of heart rate.
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From March 1992 to April 1996 a pectoral biphasic transvenous implantable cardioverter defibrillator without subcutaneous leads was implanted in 35 patients with life threatening ventricular tachyarrhythmias. Mean age was 58 +/- 9 years; 23 patients had coronary artery disease, 10 non ischemic dilated cardiomyopathy and 2 arrhythmogenic right ventricular dysplasia. All were in NYHA functional class I and II and 4 in class III: mean ejection fraction was 35 +/- 12%. The mean duration of the implantation procedure was 85 +/- 35 min. The mean defibrillation threshold, measured in 23 active-CAN devices was 8.8 +/- 5 J. There were no operative complications except in one case of transient ischemic electromechanical dissociation. The mean hospital stay from the time of implant to predischarge evaluation was 6.2 +/- 2 days. The average follow-up period was 18.5 +/- 11 months. Two patients had non sudden and non arrhythmic cardiac death in the third and sixth month, respectively. In 19 patients 171 implantable cardioverter defibrillator interventions were reported: in 5 patients five inappropriate interventions were reported and in the remaining 14 were reported: 35 ventricular fibrillation and 131 ventricular tachycardia. The short duration of the procedure, brief hospitalization with very low perioperative morbidity, high efficacy and low mid-term complications give a new image to this therapeutic option.
The aim of this study was to evaluate how heart rate variability changes during acute myocardial infarction (AMI) and whether this change is different in anterior and inferior AMI. For this purpose 10 patients with anterior (mean age 53 +/- 11 years) and 11 patients with inferior (mean age 55 +/- 11 years) AMI underwent 2 consecutive 24-hour Holter recordings (H1, H2) which started, at most, 6 hours after the onset of symptoms and a further two H at the 10th (H3), and 28th day (H4) of AMI. None of the patients suffered from diabetes or was taking beta-blockers. The standard deviation of the RR intervals (SDRR) for a 24-hour period was evaluated for each H in the group of patients with anterior and inferior AMI. In H1, SDRR was statistically lower in anterior compared to inferior AMI (64 +/- 20 versus 106 +/- 27; p < 0.0001). No statistically significant differences were found in H2 between the anterior and inferior AMI (72 +/- 19 versus 76 +/- 14), due to a reduction in SDRR in inferior AMI: from 106 +/- 27 in H1 to 76 +/- 14 in H2; p < 0.002. No statistically significant changes were present in anterior AMI patients between H1 and H2 (64 +/- 20 versus 72 +/- 19). SDRR recovers at H3 increasing in both groups (anterior: 101 +/- 28, p < 0.001; inferior: 108 +/- 29, p < 0.004). No further significant changes in SDRR were present at H4 for either group (anterior 117 +/- 30; inferior: 118 +/- 31).(ABSTRACT TRUNCATED AT 250 WORDS)