Objective: The objectives of this work is to develop and test the ability of a wearable physiological sensors system, based on ECG, EDA and EEG, to capture human stress and to assess whether the detected changes in physiological signals correlate with changes in salivary cortisol level, which is a reliable, objective biomarker of stress. Methods: 15 healthy participants, seven males and six females, mean age 40.8 $\pm$ 9.5 years, wore a set of three commercial sensors to record physiological signals during the Maastricht Acute Stress Test, an experimental protocol known to elicit robust physical and mental stress in humans. Salivary samples were collected throughout the different phases of the test. Statistical analysis was performed using a Support Vector Machine (SVM) classification algorithm. A correlation analysis between extracted physiological features and salivary cortisol levels was also performed. Results: 15 features extracted from heart rate variability, electrodermal and electroencephalography signals showed a high degree of significance in disentangling stress from a relaxed state. The classification algorithm, based on significant features, provided satisfactory outcomes with 86% accuracy. Furthermore, correlation analysis showed that the observed changes in physiological features were consistent with the trend of salivary cortisol levels (R2 = 0.714). Conclusion: The tested set of wearable sensors was able to successfully capture human stress and quantify stress level. Significance: The results of this pilot study may be useful in designing portable and remote control systems, such as medical devices used to turn on interventions and prevent stress consequences.
Background: Cardiac natriuretic hormones (CNHs) are a family of related peptides, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and other peptides derived from the N-terminal portion of the proANP and proBNP peptide chains. Assays for cardiac natriuretic peptides have been proposed to help assess clinical conditions associated with expanded fluid volume. In particular, the assays can be useful for distinguishing healthy subjects from patients in different stages of heart failure. Measurements of these hormones have also been considered for prognostic indicators of long-term survival in patients with heart failure and/or after acute myocardial infarction. The different CNHs differ in their production/secretion patterns and have different clearance rates. Furthermore, there are numerous proposed assay configurations for each of these hormones, and it is not clear which assay provides the best pathophysiological and/or clinical information. Approach: Here we review recent studies concerning the competitive (such as RIA, enzyme immunoassay, or luminescence immunoassay) and noncompetitive immunoassays (such as two-site IRMA, ELISA, or immunoluminometric assay) for the different cardiac natriuretic peptides to compare the analytical characteristics and clinical relevance of assays for the different CNHs and the different assay formats. Content: Developing sensitive, precise, and accurate immunoassays for cardiac natriuretic peptides has been difficult because of their low concentrations (on average, ∼3–6 pmol/L) in healthy subjects and because of their structural, metabolic, and physiological characteristics. Competitive assays have historically suffered from lack of sensitivity and specificity for the biologically active peptides. These usually require tedious extraction procedures prior to analysis. Recently, immunometric assays have been developed that have improved sensitivity and specificity; it appears these will be the methods of choice. Summary: To date, there is no consensus on the best assay procedure of cardiac natriuretic peptides. To facilitate widespread propagation of determination of these hormones in routine clinical practice, it will be necessary to study the new generation of noncompetitive immunometric methods that are less time-consuming and more sensitive and specific. Although several studies suggest that BNP exhibits better clinical utility than the other CNHs, more studies examining multiple CNHs in the same cohorts of patients will be necessary.
In order to study the relationships between sex hormones, aging, and circulating levels of cardiac natriuretic peptides and to define reference values for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) assays, we measured the plasma levels of cardiac natriuretic peptides in a large group of healthy adults divided according to age and sex. We studied 216 healthy subjects of both sexes (109 men and 107 women) with age ranging from 20 to 77 years (mean 43.2+/-14.8 years). All subjects were non-obese and had normal arterial blood pressure; they were free from acute diseases, including asymptomatic heart disease. Highly sensitive and specific IRMA methods were used to measure plasma ANP and BNP. The mean ANP value in healthy adult subjects of both sexes was 17.8+/-10.9 pg/ml with no significant difference between men (16.7+/-10.0 pg/ml) and women (18.8+/-11.7 pg/ml). The mean BNP value in healthy adult subjects of both sexes was 9.9+/-9.0 pg/ml with a significant difference (p<0.0001) between men (7.7+/-7.1 pg/ml) and women (12.2+/-10.2 pg/ml). There was a weak linear relationship between age and either ANP (r=0.350, p<0.0001) or BNP (r=0.254, p=0.0002) values. When the circulating levels of cardiac natriuretic hormones, and age and sex were analyzed by multiple stepwise regression analysis, both age and sex significantly and independently contributed to the regression. Our study indicates independent positive effects of aging and female sex hormones on ANP and BNP levels in healthy adult subjects. These effects should be taken into account in the calculation of appropriate reference values for cardiac natriuretic hormones.
1 December 2005 in European Journal of Heart Failure
Backgound: C-type natriuretic peptide (CNP), secreted by the endothelium and the heart, is structurally related to atrial and brain natriuretic peptides, but its clinical significance in chronic heart failure (CHF) is controversial. Aim: To investigate the role of CNP in CHF, plasma CNP levels were determined in a prospective series of 133 patients with CHF (age 64±1 years, left ventricular ejection fraction (EF), 31.5±0.7%, mean±S.E.M.) and in 21 age-matched healthy subjects. Methods and results: CNP was measured by a radioimmunoassay (sensitivity: 0.41±0.009 pg/tube) after a preliminary solid-phase extraction. Plasma level of CNP in healthy subjects was 2.7±0.2 pg/ml and significantly increased in CHF, as a function of clinical severity: 4.9±0.7 pg/ml in NYHA class I; 7.0±0.4 pg/ml in class II (p<0.001 vs. controls); 9.6±0.7 pg/ml in class III (p<0.001 vs. controls and class I and II), and 11.8±2.0 pg/ml in class IV (p<0.001 vs. controls, class I and II; Fisher’s test after ANOVA). A significant relation was also found between CNP plasma levels and EF (R=0.40, p<0.001). Conclusion: Plasma CNP elevation is related to clinical and functional disease severity. These findings suggest a pathophysiological role for this peptide that, for its vasorelaxing activity, could influence the endothelial vasomotor response in CHF.