Progressive systemic sclerosis (PSS) is characterized in its first phases by vascular damage. Lungs are involved in two thirds of patients with initial progressive destruction of the capillary bed and consequent reduction of the functional reserve, which may lead to hypertension of the pulmonary circulation. For these reasons it is of great interest to have early information about the pressure of the pulmonary circulation, both at rest and during exercise, to follow the progression and the evolution of the illness independently from subjective symptoms. The aim of the study was to evaluate by a noninvasive method, saline-enhanced Doppler echocardiography, the behavior of the right ventricular systolic pressure in patients with PSS, at rest and during exercise, without clear instrumental or clinical signs of pulmonary involvement at rest. Nine patients (7 women and 2 men) with PSS, aged 55.7 +/- 8.7 years, and 9 control subjects were evaluated. All patients had normal pulmonary pressure at rest and negative history for effort dyspnea. Subjects underwent Doppler echocardiographic examination at rest and during exercise. Right ventricular systolic pressure was evaluated by saline-enhanced Doppler technique, at rest and throughout exercise. At rest the right ventricular systolic pressure was normal in all patients and controls. At the end of exercise, in 4 patients, values were still normal (40.7 +/- 2.2 mmHg); in the others pathologic values were recorded (59.8 +/- 3.9 mmHg). In the control group values were always normal (35.6 +/- 4.6 mmHg). In our study the saline-enhanced Doppler echocardiography has been demonstrated to be an important diagnostic tool for the noninvasive evaluation of right ventricular systolic pressure, both at rest and during exercise; it could be useful in monitoring the pulmonary vascular damage in patients with PSS.

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The effects of ischemia and reperfusion on QT interval dispersion (QTD: QTmax-QTmin in the 12-lead ECG) were analyzed in 15 patients (12 males, 57 +/- 13 years) undergoing coronary angioplasty (PTCA). All patients had single-vessel coronary artery disease (only one > or = 85% stenosis in a major coronary artery) and normal left ventricular function. All were in sinus rhythm with normal atrioventricular and intraventricular conduction on the surface ECG. No patient was on therapy that could affect the QT interval. The ECG was recorded (all 12 leads simultaneously) at 50 mm/s speed before the first balloon inflation, at the end of the first inflation during PTCA, and at 30" and 60" during reperfusion following the first inflation. In order to avoid ischemic preconditioning, only recordings of the first inflation were used. In each tracing QTmax and QTmin were evaluated. All values were rate corrected using a simple linear equation (QT linear corrected = QT + 0.154 [1-RR]). QTD increased significantly during both ischemia and reperfusion. QTmax was not changed by ischemia and was increased by reperfusion. QTmin was reduced by ischemia and increased by reperfusion. These results indicate that both ischemia and reperfusion alter ventricular repolarization, inducing a less homogeneous ventricular recovery pattern.

The aim of the present study was to define the different prevalence of hypertension when conventional office measurement and ambulatory monitoring are performed in a population of unselected workers. All the workers of a Florentine chemical company were invited to participate in the study. Enrolled subjects underwent blood pressure measurement using a conventional sphygmomanometer and ambulatory blood pressure monitoring. Of 191 workers, 145 agreed to participate in the study (76%). Six of the 145 were excluded from further analysis because they were undergoing antihypertensive therapy. Confidence limits for ambulatory monitoring were defined at 95% on normotensive workers. Thirty-five (25%) workers were found to be hypertensive according to World Health Organization parameters (diastolic pressure > 90 mmHg) but only 14 of the 35 had higher 24-h diastolic ambulatory blood pressure than the 95% confidence limits of controls.

A case of chronic intestinal infection due to adenovirus type 40 lasting for 13 months in a patient with AIDS is described. Adenovirus particles were detected by electron microscopy in biopsy samples taken from the duodenum 3 months after the onset of diarrhoea. The virus was identified as adenovirus type 40 in stool samples by ELISA monoclonal antibodies to adenovirus group antigen (MAd-g2) and types 40 and 41 (MA 40-1 and MA 41-1). No other enteropathogens were found. These data support a causal relationship between adenovirus 40 and the gastrointestinal symptoms of the patient. This is the first reported case of intestinal infection caused by adenovirus type 40 in a patient with AIDS.

This study evaluated: (1) if three orthogonal leads can provide the same information about QT dispersion (QT-D) as 12-lead ECG; (2) the circadian pattern of QT-D adopting 3-OL during 24hour Holter monitoring; (3) if the QT-D circadian pattern is influenced by therapy. In the first part of the study, we evidenced a significant direct correlation (r = 0.91; P < 0.0005) between QT-D values of 12 ECG leads and of 3-OL simultaneously recorded in 15 normal subjects and 11 patients with myocardial infarction. The second part of the study evaluated the circadian pattern of QT-D adopting 3-OL during Holter (ELA Medical, Mod. Synesis) monitoring in 15 patients with congestive heart failure (CHF: aged 73 t 8 yrs, Ill NYHA) in pharmacological washout and after 10 days of therapy (furosemide, digoxin, captopril) and in 15 age-matched normal subjects (N: aged 70 ? 3 yrs). Mean QT-D values of CHF before therapy were significantly higher at each hour than those of N (always P < 0.001). Mean hourly QT-D values after therapy were significantly lower than those before therapy (P < 0.03 up to P < O.OOl), except for the value at 9:00 A.M. Our results suggest that: (1) 3-OL can evaluate QT-D as much as the usual 12-lead ECG; (2) the use of 3-OL during Holter monitoring allows the evaluation of the QT dispersion circadian pattern both in N and in CHF; and (3) therapy is able to modify the circadian pattern of QT-D. A.N.E. 1998;3(1):32-37 QT dispersion; heart fa i I u re Address for reprints: Antonio Michelucci, M.D.al. Circadian Pattern of the QT Dispersion 33Holter monitoring; and (3) how the circadian pattern of QT-D could be useful in controlling the effects of therapy.

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