Väinö Turjanmaa

Lower respiratory tract inflammation can be detected by measuring exhaled nitric oxide (NO) concentration at a single exhalation flow rate, but this does not differentiate between alveolar and bronchial NO production. We assessed alveolar NO concentration and bronchial NO flux with an extended method of measuring exhaled NO at several exhalation flow rates in 40 patients with asthma, 17 patients with alveolitis, and 57 healthy control subjects. Bronchial NO flux was higher in asthma (2.5 +/- 0.3 nl/s, p < 0.001) than in alveolitis (0.7 +/- 0.1 nl/s) and healthy control subjects (0.7 +/- 0.1 nl/s). Alveolar NO concentration was higher in alveolitis (4.1 +/- 0.3 ppb, p < 0.001) than in asthma (1.1 +/- 0.2 ppb) and healthy control subjects (1.1 +/- 0.1 ppb). In asthma, bronchial NO flux correlated with serum level of eosinophil protein X (EPX) (r = 0.60, p < 0.001) and bronchial hyperresponsiveness (r = 0.55, p < 0.001). In alveolitis, alveolar NO concentration correlated inversely with pulmonary diffusing capacity (r = -0.55, p = 0.022) and pulmonary restriction. Glucocorticoid treatment or allergen avoidance normalized bronchial NO flux in asthma and decreased alveolar NO concentration toward normal in alveolitis. In conclusion, extended exhaled NO measurement can be used to separately assess alveolar and bronchial inflammation and to assess disease activity/severity in asthma and alveolitis.

AIMS: As a part of the Finnish Cardiovascular Study, we tested the hypothesis that T-wave alternans (TWA) predicts mortality in a general population of patients referred for a clinical exercise test. METHODS AND RESULTS: A total of 1037 consecutive patients (mean age+/-SD of 58+/-13 years, 673 men and 364 women) with a clinically indicated exercise test and with technically successful electrocardiographic (ECG) data during a bicycle ergometer test were included in the study. Digital ECGs were recorded and TWA was analysed continuously with the time-domain modified moving average method. The maximum TWA value at heart rate (HR)<125 b.p.m. was derived and its capacity to stratify risk for all-cause death, cardiovascular death, and sudden cardiac death (SCD) was tested. During a follow-up of 44+/-7 months (mean+/-SD), 59 patients died; 34 were due to cardiovascular causes and 20 were due to SCD. In multivariate analysis after adjustment for age, sex, use of beta-blockers, functional class, maximal HR during exercise, previous myocardial infarction, and other common coronary risk factors, the relative risk of TWA>or=65 microV for SCD was 7.4 (95% CI, 2.8-19.4; P<0.001), for cardiovascular mortality 6.0 (95% CI, 2.8-12.8; P<0.001), and for all-cause mortality 3.3 (95% CI, 1.8-6.3; P=0.001). CONCLUSION: Time-domain TWA analysis powerfully predicts mortality in a general population undergoing a clinical exercise test.

The purpose of the study was to estimate the reliability of whole-body impedance cardiography (ICGWB)-derived pulse wave velocity (PWV) and stroke volume index to pulse pressure (SI/PP) measurements. The repeatability and reproducibility of ICGWB parameters were also determined. Agreement between the impedance and Doppler ultrasound-based PWV measurements was estimated in 25 healthy subjects in two consecutive measurements. Impedance-derived SI/PP (SIICG/PP) estimates were compared with simultaneously measured SI/PP based on thermodilution (SITD/PP) and direct Fick (SIFICK/PP) methods in 30 surgical patients. PWV measured between the aortic arch and popliteal artery using the impedance technique with selective electrode configuration (PWVIS) agreed well with the Doppler ultrasound method (PWVDOPP), the bias (PWVDOPP - PWVIS) and precision (+/- SD of differences) being 0.00 and 0.79 m s-1, respectively. PWV derived from the whole-body and popliteal impedance plethysmograms (PWVICG) overestimated slightly PWVDOPP values. The repeatability value for PWVIS was excellent, being 0.54 m s-1. The reproducibility values for PWVDOPP and PWVIS were very similar (2.17 and 2.42 m s-1, respectively). Changes in PWVIS correlated strongly with changes in PWVDOPP (r=0.74; P<0.0001), indicating that both methods reflected the true physiological variation in PWV. The agreement between SIICG/PP and SITD/PP or SIFICK was almost identical to the agreement between the SITD/PP and SIFICK/PP. In conclusion,whole-body impedance cardiography provides handy and reliable means of evaluating arterial stiffness on the basis of PWV and SI/PP simultaneously with conventional haemodynamic parameters. The method is highly repeatable and reproducible.

Nocturnal asthma symptoms and impaired lung function at night are related to inflammatory activity in the peripheral lung compartment. Exhaled nitric oxide (NO) measurement at multiple exhalation flow rates can be used to separately assess alveolar and bronchial NO production and inflammation. The authors hypothesised that asthmatic patients with nocturnal symptoms have a higher alveolar NO concentration than those with only daytime symptoms. The authors asked 40 patients with newly-diagnosed steroid-naïve asthma about their nocturnal asthma symptoms through the use of a written questionnaire. Alveolar NO concentration and bronchial NO flux were assessed in the 40 asthmatics and 40 healthy controls. Nineteen of the 40 patients reported nocturnal symptoms. Patients with nocturnal symptoms had a higher alveolar NO concentration (1.7±0.3 (mean±sem) parts per billion (ppb)) than patients without nocturnal symptoms (0.8±0.3 ppb, p=0.012) or healthy controls (1.0±0.1 ppb, p=0.032). Bronchial NO flux was higher both in patients with (2.4±0.4 nL·s −1 , p&lt;0.001) and without (2.6±0.4 nL·s −1 , p&lt;0.001) nocturnal symptoms, compared to controls (0.7±0.1 nL·s −1 ). Nocturnal symptoms in asthmatic patients are related to a higher alveolar nitric oxide concentration. The results suggest that assessment of alveolar nitric oxide concentration can be used to detect the parenchymal inflammation in asthmatic patients with nocturnal symptoms.