To evaluate pulmonary vasoreactivity in children and young adults with primary pulmonary hypertension, we performed cardiac catheterizations on nine patients with primary pulmonary hypertension (nine months to 23 years old) and made hemodynamic measurements: before and after infusing prostacyclin, and before and after administering sublingual nifedipine. Based upon the response to prostacyclin, patients were divided into responders and nonresponders using the following criteria: 20 percent or greater decrease in mean pulmonary arterial pressure; an increase in cardiac index; and no change, or a decrease in the pulmonary vascular resistance to systemic vascular resistance ratio. By these criteria, five of the nine patients had a reactive pulmonary vascular bed and responded to prostacyclin administration. In addition, they all responded to nifedipine. The remaining four did not respond to either drug. There was a close correlation (r = 0.85, p less than 0.01) between the magnitude of the pulmonary vasodilator response to treatment with prostacyclin and nifedipine. There was also a significant inverse correlation between the age of the patient at the time of the study and the pulmonary vasodilator response to administration of prostacyclin (r = 0.91, p less than 0.01) and nifedipine (r = 0.82, p less than 0.01); ie, both drugs produced a greater fall in pulmonary arterial pressure in younger patients with primary pulmonary hypertension than in older ones.

The study of animal models of IPF has demonstrated that there is a stereotyped response of the respiratory airspace walls to a wide variety of injuries. Inflammatory and immune effector cells play a major and complex role in the fibrosing process. They may contribute to the injury of the lung beyond the original insult. These cells secrete substances that play an important role in determining cell traffic in the lungs and in controlling the connective tissue-producing cells. Products derived from the inflammatory response may interfere with protection of normal lung matrix, although injury to lung matrix itself does not lead to fibrosis. Injury to endothelial cells and especially type I epithelial cells appears to play a major role in the fibrogenic response. Further understanding of the factors that injure these cells, the development of methods of protecting them from injury, and a clear understanding of their role in the fibrogenic process appear to be key to developing better methods of preventing and treating interstitial pulmonary fibrosis.

Few studies have compared the use of low-contrast dose digital subtraction ventriculography with conventional ventriculography for quantitative assessment of both global and regional left ventricular function. Accordingly, 34 patients underwent conventional ventriculography using 36 ml of ionic contrast material and digital ventriculography (mask-mode) using 10 ml of contrast diluted in 10 ml of saline and injected over two seconds. Data from two patients were excluded because of ectopy during cineventriculography and from one because of ectopy during both studies. End-diastolic and end-systolic volumes were calculated from both studies by an area-length method and used to calculate ejection fractions. Regional wall motion was quantitated by the centerline method. Results of linear regression analysis demonstrated high correlations for all parameters (end-diastolic volume, r = 0.85; end-systolic volume, r = 0.93; ejection fraction, r = 0.92; quantitative regional wall motion, r = 0.90). Thus, low-contrast dose digital subtraction ventriculography provides an accurate assessment of both global and regional ventricular function and minimizes the required dose and inherent risks of contrast media.

Asthma in children has many special features which deserve consideration. This disease is probably underdiagnosed and is often undertreated. Vague, persistent respiratory symptoms, especially chronic cough, may often be due to asthma. Chronic bronchitis is extremely rare in the pediatric patient and is a manifestation of reactive airway disease or cystic fibrosis. The absolute severity, the extent of the disease, responses to treatment, and long-term course should be evaluated by repeated pulmonary function tests. Fortunately, asthma responds well to pharmacologic and supportive therapy, and it is important to approach its management as that of a chronic rather than episodic illness. Therapy should include comprehensive, closely supervised drug therapy, health education, and a program of self-management. Asthma usually starts before youngsters enter school, and the majority get better as they get older. Nevertheless, many children with moderate or severe asthma will continue to be troubled by intermittent or chronic airway obstruction into adulthood, and they require long-term, anticipatory treatment programs. Comprehensive care will optimize the quality of life for the affected children and their families, and it will minimize the discomfort and restrictions to which some of them have been subjected unnecessarily. Asthma in childhood, especially when not well controlled, may constitute a risk factor for the development of chronic obstructive pulmonary disease in adulthood; however, this is as yet only suspected and not proved.

Leukocyte imaging with indium-111 is a relatively new technique which, to this point in time, has been discussed almost exclusively in the radiologic literature. Although this procedure has been used mainly to detect intra-abdominal infection, the thorax is routinely imaged along with the abdomen, and therefore detection of cardiac disease may be feasible. This case report is of a young woman after liver transplantation who developed occult purulent pericarditis initially detected by a leukocyte scan with indium-111. This case demonstrates that striking pericardial uptake on a whole-body indium-111 leukocyte scan can occur with purulent pericarditis, and it reemphasizes how insidiously purulent pericarditis may present in an immunosuppressed patient.

A patient with obstructive sleep apnea was monitored five times during three years while his weight fluctuated within a range of 26 kg. The number of apneas per hour of sleep varied from 59.6 at 111 kg of weight to 3.1 at 85 kg. The relation between apneas per hour of sleep and body weight was a logarithmic function. A modest decrease in weight was thus associated with a disproportionally larger decrease in the rate of apneas. Typical SaO2 levels during the apneic episodes also had a logarithmic relation with body weight. Apnea-related sinus bradycardia and sinus tachycardia were only present at the highest weight. The results suggested that dieting and weight loss lead to an improvement in sleep apnea and related sequelae.

Eighteen patients who survived an acute myocardial infarction were found to have a normal coronary arteriogram. Seven patients were younger than 35 years and six were female. The myocardial infarction was nontransmural in 11 cases. The mean follow-up was 21.6 months. Eleven patients developed residual chest pain at rest early after myocardial infarction. One, treated by beta-blockers, suffered a recurrent myocardial infarction. Eight became asymptomatic, and two improved under antispastic therapy. Another patient developed a severe form of variant angina three months after myocardial infarction; she died following plexectomy. Finally, two patients experienced rare episodes of angina at rest. The stress ECG was negative in all cases. Provocative test for spasm was positive in three out of nine patients. Diffuse narrowing associated with chest pain was demostrated in two patients at angiography. Thus, myocardial infarction and subsequent normal coronary angiogram are mainly found in young female patients, and infarction is often nontransmural. Clinical evidence of vasospastic phenomena and increased vasomotor tone are found in most patients. Whenever residual chest pain is controlled by antispastic therapy, the follow-up course seems benign.

Respiratory viral illness is a major cause of morbidity in both adults and children. This report focuses on both the acute and chronic effects on respiratory function of these ubiquitous infections. Infant airways are particularly vulnerable due to the relatively low conductance in immature peripheral airways. Bronchiolitis, caused predominantly by respiratory syncytial virus, is the most important of these viral illnesses and is emerging as a major risk factor for the subsequent development of obstructive airway diseases in adults, possibly by interference with normal alveolar proliferation. The basic pathogenic mechanism involved in adult respiratory viral infection is bronchial hyperreactivity, presumably secondary to epithelial damage and resultant sensitization of rapidly adapting airway receptors. In addition, there may be virus-related alterations in the autonomic and humoral regulation of airway tone. Viral infections may alter the effects of common air pollutants on respiratory function.

During a survey conducted for the cytodiagnosis of early bronchogenic carcinoma, cytoplasmic viral inclusion bodies were found sporadically in tracheobronchial smears of asymtomatic patients of both sexes (ages ranging from 18 to 80 years) undergoing general endotracheal anesthesia for surgery. A review of 3,049 cases performed to assess the frequency of occurrence of this phenomenon showed a 1.1 percent incidence in all smears studied. There was no relationship between smoking habit, age, or sex and the presence of inclusion bodies; however, there was a marked seasonal incidence, with 60 percent of inclusion-bearing smears being found during the months of January through March.