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Abstract-Recent evidence suggests that the prodownregulatory Gly16 allele of the ␤-2 adrenergic receptor (␤-2 AR) is associated with essential hypertension in African Caribbeans. To further investigate the effect of the glycine (Gly)16 and arginine (Arg)16 ␤-2 AR variants on hemodynamics, we investigated the agonist-mediated in vivo vasodilation in normotensive Austrian Caucasians and analyzed the results with respect to the Gly16/Arg16 polymorphism. Fifty-seven normotensive men, 20 to 32 years of age with body mass index of 18.7 to 29.9 kg/m 2 , were genotyped for the Arg16/Gly16 ␤-2 AR alleles. All 15 Gly16/Gly16 subjects, all 12 Arg16/Arg/16 subjects, and 27 of 30 heterozygous subjects underwent hemodynamic measurements while supine after an overnight fast. The observers were unaware of the subjects' genotypes. The subjects received a graded infusion of the selective ␤-2 AR agonist salbutamol (0.07, 0.14, and 0.21 g/kg per minute, respectively), each dose over 8 minutes. Stroke volume and blood pressure were determined continuously by means of impedance cardiography and oscillometry, respectively. The last 4 minutes of each infusion were evaluated statistically. Basal mean blood pressure was higher in the Gly16/Gly16 subjects compared with Arg16/Arg16 subjects (meanϮSD: 81.6Ϯ6.14 versus 75.2Ϯ4.93 mm Hg, PϽ0.01). Homozygous Gly16 subjects showed a significantly decreased vasodilation during the first dose of salbutamol infusion compared with Arg16/Arg16 subjects (⌬total peripheral resistance index Ϫ17.9Ϯ14.4 versus Ϫ30.6Ϯ8.3%, PϽ0.01) despite increased sympathetic counterregulation in the Arg16/Arg16 group (⌬heart rate ϩ16.9Ϯ7.0% versus ϩ8.6Ϯ7.0%, PϽ0.01; ⌬cardiac index ϩ39.5Ϯ18.5% versus 21.4Ϯ18.8%, PϽ0.05). Our results provide additional evidence that the Gly16/Arg16 alleles of the ␤-2 AR are intimately related to blood pressure regulation and deserve further studies in the pathogenesis of essential hypertension. (Hypertension. 1999;33:1425-1430.)

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Wearable sensors to continuously measure blood pressure and derived cardiovascular variables have the potential to revolutionize patient monitoring. Current wearable methods analyzing time components (e.g., pulse transit time) still lack clinical accuracy, whereas existing technologies for direct blood pressure measurement are too bulky. Here we present an innovative art of continuous noninvasive hemodynamic monitoring (CNAP2GO). It directly measures blood pressure by using a volume control technique and could be used for small wearable sensors integrated in a finger-ring. As a software prototype, CNAP2GO showed excellent blood pressure measurement performance in comparison with invasive reference measurements in 46 patients having surgery. The resulting pulsatile blood pressure signal carries information to derive cardiac output and other hemodynamic variables. We show that CNAP2GO can self-calibrate and be miniaturized for wearable approaches. CNAP2GO potentially constitutes the breakthrough for wearable sensors for blood pressure and flow monitoring in both ambulatory and in-hospital clinical settings.

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The CNAP system (CNSystems Medizintechnik AG, Graz, Austria) provides noninvasive continuous arterial pressure measurements by using the volume clamp method. Recently, an algorithm for the determination of cardiac output by pulse contour analysis of the arterial waveform recorded with the CNAP system became available. We evaluated the agreement of the continuous noninvasive cardiac output (CNCO) measurements by CNAP in comparison with cardiac output measurements invasively obtained using transpulmonary thermodilution (TDCO). In this proof-of-concept analysis we studied 38 intensive care unit patients from a previously set up database containing CNAP-derived arterial pressure data and TDCO values obtained with the PiCCO system (Pulsion Medical Systems SE, Feldkirchen, Germany). We applied the new CNCO algorithm retrospectively to the arterial pressure waveforms recorded with CNAP and compared CNCO with the corresponding TDCO values (criterion standard). Analyses were performed separately for (1) CNCO calibrated to the first TDCO (CNCO-cal) and (2) CNCO autocalibrated to biometric patient data (CNCO-auto). We did not perform an analysis of trending capabilities because the patients were hemodynamically stable. The median age and APACHE II score of the 22 male and 16 female patients was 63 years and 18 points, respectively. 18 % were mechanically ventilated and in 29 % vasopressors were administered. Mean ± standard deviation for CNCO-cal, CNCO-auto, and TDCO was 8.1 ± 2.7, 6.4 ± 1.9, and 7.8 ± 2.4 L/min, respectively. For CNCO-cal versus TDCO, Bland-Altman analysis demonstrated a mean difference of +0.2 L/min (standard deviation 1.0 L/min; 95 % limits of agreement -1.7 to +2.2 L/min, percentage error 25 %). For CNCO-auto versus TDCO, the mean difference was -1.4 L/min (standard deviation 1.8 L/min; 95 % limits of agreement -4.9 to +2.1 L/min, percentage error 45 %). This pilot analysis shows that CNCO determination is feasible in critically ill patients. A percentage error of 25 % indicates acceptable agreement between CNCO-cal and TDCO. The mean difference, the standard deviation, and the percentage error between CNCO-auto and TDCO were higher than between CNCO-cal and TDCO. A hyperdynamic cardiocirculatory state in a substantial number of patients and the hemodynamic stability making trending analysis impossible are main limitations of our study.

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