Viruses exacerbating chronic pulmonary disease: the role of immune modulation

Chronic pulmonary diseases are a major cause of morbidity and mortality and their impact is expected to increase in the future. Respiratory viruses are the most common cause of acute respiratory infections and it is increasingly recognized that respiratory viruses are a major cause of acute exacerbations of chronic pulmonary diseases such as asthma, chronic obstructive pulmonary disease and cystic fibrosis. There is now increasing evidence that the host response to virus infection is dysregulated in these diseases and a better understanding of the mechanisms of abnormal immune responses has the potential to lead to the development of new therapies for virus-induced exacerbations. The aim of this article is to review the current knowledge regarding the role of viruses and immune modulation in chronic pulmonary diseases and discuss avenues for future research and therapeutic implications

AMBULATORY MONITORING OF PULMONARY-ARTERY PRESSURE - A PRELIMINARY CLINICAL-EVALUATION

Traditional measurement and recording methods are inadequate for continuous monitoring of ambulatory pulmonary artery pressure. Therefore a new miniaturised solid state system has been developed and assessed. A manometer tipped catheter, inserted via a subclavian or cephalic vein, was used together with an isolated amplifier and peak detectors to determine systolic and diastolic pressures. Pressures were averaged over 30 seconds and stored in digital memory. After a 24 hour recording period data were rapidly transferred to a microcomputer for numerical or graphical display. Thirteen patients had continuous ambulatory monitoring performed for between 24 and 96 hours, in seven to evaluate symptoms of dyspnoea in subjects with valvular or coronary disease (group 1), and in six to achieve optimal oral treatment for left heart failure (group 2). The catheter was calibrated before insertion and was rechecked after removal. There was less than 1% zero level drift and similar gain stability. Systolic pressures ranged from 10 to 97 (mean 39.5) mmHg, and diastolic from 1 to 46 (mean 15.3) mmHg. Four patients in group 1 had symptoms of dyspnoea associated with normal pressures, while three had raised pressures. Four of the six patients monitored in group 2 had major alterations in their treatment based on data obtained during monitoring. There were no complications. This system, which allows safe, reliable, and prolonged recording of ambulatory pulmonary artery pressure, represents a considerable advance in the ability to assess the cause of dyspnoea and to manage left heart failure