The effects of a new adrenergic blocking agent (K4423) on exercise tolerance in angina pectoris.
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Biomedical subjects
Publications and source records attributed to R Valentini.
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1. Cardiac performance in response to 30% maximal isometric handgrip exercise was studied in fourteen patients convalescing uneventfully from a first myocardial infarction. In each patient, heart rate, mean arterial blood pressure and cardiac index were measured, and total peripheral resistance was calculated. The covariance of changes in the mean arterial blood pressure and cardiac index in these patients was matched against tolerance limits calculated from published data for normal subjects. 2. All patients had normal haemodynamic values at rest, and showed the usual rise of heart rate and mean arterial pressure during handgrip exercise. However, in six patients (group 1) the rise in mean arterial pressure was, as in normal subjects, accounted for mainly by a rise in cardiac index, with no consistent change in peripheral resistance. In eight patients (group 2), the mean arterial pressure rose to the same level as in group 1, but with a consistent increase in peripheral resistance and a smaller rise in the cardiac index. 3. It is suggested that in a substantial proportion of patients who are making a seemingly uncomplicated recovery from myocardial infarction, it may be possible to unmask an impairment of left ventricular function by means of isometric handgrip exercise.
BACKGROUND: We evaluated the role of complications caused by Acinetobacter spp. in the setting of HIV infection. METHODS: Clinical records of 1,923 consecutive HIV-infected patients hospitalized in a 9-year period were retrospectively reviewed, in order to identify all cases of Acinetobacter spp. complications, and to assess their occurrence and outcome according to several epidemiological, clinical and laboratory parameters. RESULTS: Ten patients out of 1,923 (0.52%) developed Acinetobacter spp. infections: sepsis in four cases, urinary tract infection in three, pneumonia in two and septicaemic pneumonia in the remaining patient. All patients were severely immunocompromised, as shown by a mean CD4+ lymphocyte count of 122 cells/microl and a frequent prior diagnosis of AIDS. As opposed to other infections, septicaemia was associated with a significantly lower CD4+ cell count and a more frequent occurrence of neutropenia. Hospital-acquired Acinetobacter spp. infections were significantly more frequent than community-acquired ones, and prevailingly involved patients with AIDS and leucopenia, being responsible for frequent blood dissemination. Antimicrobial, corticosteroid and cotrimoxazole treatment were frequently carried out during the month preceding disease onset. Antibiotic susceptibility studies proved the complete resistance of microbial isolates to ampicillin and cephalothin and poor sensitivity to second-generation cephalosporins and gentamicin, while greater susceptibility was shown to ceftazidime, netilmicin and amikacin, followed by piperacillin, cotrimoxazole and quinolones. Appropriate antimicrobial treatment led to clinical and microbiological cure in all cases, with no related mortality or relapses. CONCLUSIONS: Since only 23 episodes of HIV-associated Acinetobacter spp. infections have been described to date in 11 different reports (nine cases of bacteraemia, eight of pneumonia, two of urinary tract involvement, one of intravenous access device infection, one of meningitis and two with unspecified localization), our series represents the largest one dealing with HIV-associated Acinetobacter spp. infections. According to our experience, Acinetobacter spp. may be responsible for appreciable morbidity among patients with HIV infection, above all when a low CD4+ cell count, neutropenia and hospitalization are present. Clinicians and microbiologists who work in the field of HIV infection should consider the potential pathogenic role of Acinetobacter spp. organisms even in the absence of some presumed risk factors, because of the relationship between these infections and immunodeficiency, hospitalization, other infectious complications, prior antibiotic and steroid treatment and extended antimicrobial resistance patterns.