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Background: We have developed a system to monitor, simultaneously and continuously, ambulatory SaO2 measured using a pulse-oximeter and ECG data for 24 hours. Methods: The ambulatory SaO2-ECG monitoring system consisted of a portable monitoring device (SM50) with two channels for ECG data and one channel for SaO2 data input; a sensor for SaO2 recording; and a pulse-oximeter. An ambulatory monitoring analyzer was used. The SaO2 report from the present analyzer included two types of data (i.e., a profile of heart rate [HR], pulse rate [PR], and SaO2 value per min), and a trend graph of HR, arrhythmia, ST level and slope, PR, and SaO2 per minute. We also designed and produced an analytical program to automatically remove noise errors relating to the SaO2 measurement. Results: Using this system, we performed a clinical study on ten healthy volunteers (Group N) and seven patients with chronic pulmonary diseases (Group CPD) to evaluate the usefulness of the system as a diagnostic means for respiratory failure and arrhythmia. Group N showed a stable value of 90% or over in SaO2 during the 24-hour monitoring while Group CPD showed values under 90% SaO2 in all patients at rest during the night or after a 15-minute walk. Transient atrial tachycardia (TAT) was observed in 3 of 7 CPD patients, and each episode was preceded by a decrease of SaO2. The occurrence of a single or double ventricular extrasystole was high in Group CPD compared with Group N (1.21 ± 0.89 vs 0.6%± 0.3%, P < 0.05), its occurrence was not associated with a decrease in SaO2. Conclusions: In outpatients, especially patients who are taken care of at home, the present system will certainly contribute greatly to the diagnosis of respiratory failure and arrhythmia as well as to evaluate the effects on these diseases of therapy. In addition it is suggested that in CPD, patients'hypoxemia may induce TAT. [ABSTRACT FROM AUTHOR]

Objective: The aim was to examine how regional variations in pericardial pressure affect the mechanical coupling between the ventricles. Methods: Canine hearts from 14 dogs (14.5-18 kg) were removed and placed in cold cardioplegia solution. Balloons were inserted into the left and right ventricles and the atria. Pericardial pressure over the left ventricle (Pclv) and the right ventricle (Pcrv) was measured with thin balloon catheters. Ventricular and pericardial pressures were measured, and ventricular and pericardial coupling was calculated, under control conditions and with increases in pericardial tension and fluid. Results: At baseline, regional differences in pericardial pressure occurred [Pclv>Pcrv, 4.0(SD 0.9) v 2.9(0.6) mm Hg, p < 0.05]. Ventricular coupling via the pericardium was defined as ΔPclv/ΔPcrv for right ventricular volume increases and ΔPcrv/ΔPclv for left ventricular volume increases. This ratio increased more after increasing right ventricular volume than after increasing left ventricular volume [ΔPclv/ΔPcrv>ΔPcrv/ΔPclv, 1.14(0.33) v 0.51(0.15), p < 0.05]. Increasing the pericardial tension by clamping the pericardium increased pericardial pressures, yet did not alter the regional variations in pressure [Pclv>Pcrv, 8.4(2.2) v 6.4(2.5) mm Hg, p < 0.05] or pericardial coupling [ΔPclv/ ΔPcrv>ΔPclv/ΔPcrv, 1.18(0.46) v 0.54(0.16), p < 0.05]. In contrast, creating a mild tamponade increased pericardial pressures, eliminated regional differences in pressure, and altered the coupling between ventricles [ΔPclv/ΔPcrv≈ΔPclv/ΔPcrv, 0.95(0.11) v 1.05(0.08), p=NS]. These regional differences in pericardial pressure might have a geometrical basis. In four in vivo canine experiments using cine magnetic resonance, the short axis radius of curvature for the right ventricle was greater than for the left ventricle [38.3(4.4) mm v 29.2(3.8) mm, p < 0.05]. Conclusions: The pericardium partially protects right ventricular filling: regional differences in pericardial pressure normally occurred with lower pericardial pressure over the right ventricle, and left to right ventricular coupling was less. This protection of right ventricular filling was lost with even a small pericardial effusion.Cardiovascular Research 1993; 27:1470-1476 [ABSTRACT FROM PUBLISHER]

Objective: The aim was to determine the slope (EES) of the left ventricular end systolic pressure-volume line (ESPVL) without altering preload or afterload in conscious dogs. Methods: Dogs (n=10) were instrumented to determine left ventricular volume from ultrasonic left ventricular internal dimensions, and to measure left ventricular pressure using a micromanometer. Studies were performed one to two weeks after instrumentation while the animals were conscious. ESPVL was determined from variably loaded left ventricular pressure-volume (P-V) loops generated by the vena caval occlusion. Contractile state was increased by intravenous dobutamine (8 μg·kg−1·min−1) and decreased by intravenous verapamil (10 mg) given after autonomic blockade. From a single normally ejecting beat, we calculated EES-single beat (mm Hg·ml−1) as peak isovolumetric pressure (Pmax) minus end systolic pressure divided by stroke volume. Sunagawa's technique was used to estimate Pmax by fitting the pressure during the isovolumetric contraction and relaxation as: P(t)=l/2 × Piso[1-cos(ωt+c)]+LVEDP, where Piso=peak isovolumetric developed pressure, LVEDP=left ventricular end diastolic pressure, c=constant accounting for variations in phase angle, and ω=2 π/T in which T is duration of contraction. Results: After dobutamine, EES increased, from 8.9(SEM 0.8) to 12.5(1.0) mm Hg·ml−1 (p < 0.05), and Epg-single beat increased from 9.1(0.9) to 12.0(1.4) mm Hg·ml−1 (p < 0.05). Conversely, after verapamil, EES decreased, from 11.1(1.2) to 6.3(1.1) mm Hg·ml−1, (p < 0.05), and EES-single beat also decreased, from 9.6(1.0) to 7.3(1.2) mm Hg·ml−1, (p < 0.05). Conclusions: EES calculated from one beat is similar to EES determined from variably loaded left ventricular loops and responds appropriately to inotropic stimulation. This technique provides a reasonable method to calculate EES from left ventricular pressure and stroke volume without altering preload or afterload.Cardiovascular Research 1993;27:868-873 [ABSTRACT FROM PUBLISHER]

Objective: The aim was to examine the hypothesis that an increased coupling occurs between the ventricles during tamponade via a ventricular-pericardial-ventricular interaction, but that ventricular coupling would be unaltered or reduced with positive end expiratory pressure (PEEP). Methods: An in situ arrested, canine heart preparation was used. Changes in left and right ventricular pressure (dP1, dPr) and volume (dV1, dVr) caused by increasing the volume of the other ventricle were measured at normal and at matched levels of raised pericardial pressures (PP) caused by 20 cm H2O PEEP and by tamponade. Results: With PEEP, the coupling between the ventricles was unaltered when compared to control. With tamponade, dP1/dPr, dV1/dPr, dPr/dP1, and dVr/dP1 increased significantly (p<0.05) by 0.21(SEM 0.03, unitless), 0.45(0.04) ml·mm Hg−1, 0.18(0.03), and 0.28(0.04) ml·mm Hg−1 respectively. Conclusions: Augmented ventricular interdependence occurs during tamponade but not with PEEP, which may help to explain the different haemodynamic patterns observed under these conditions. [ABSTRACT FROM PUBLISHER]

Study objective – The mechanical coupling between the ventricles occurs directly through the myocardium (ventricular-ventricular coupling) and indirectly through the pericardium (ventricular-pericardial-ventricular coupling). We postulated that the magnitude of ventricular-pericardial-ventricular coupling would increase at high pericardial pressures, while ventricular-ventricular coupling would be unaltered.Design – Canine hearts were removed and placed in cold cardioplegic solution. Balloons were inserted into each ventricle and the left and right ventricular pressure (dP1, dPr) and volume (dV1, dVr) changes caused by increasing the pressure and volume of the other ventricle and by increasing pericardial pressure (dPp) were measured.Experimental materials – Hearts from 10 random source dogs, weight 12.5-18 kg, were used.Measurement and main results – At control pericardial pressure levels, the magnitude of the pericardial ventricular interactions was greater than the ventricular-ventricular interactions: dP1/dPp, was significantly greater than dP1/dPr, at 0.71 (SEM 0.04), n = 6, v 0.18(0.03), p<0.01, and dVl/dPp, was significantly greater than dVl/dPr, at −0.83(0.09) v −0.24(0.06), p<0.05. Raising the pericardial pressure increased the mechanical coupling between the ventricles: dPl/dPr∼, dVl/dPr∼, dPr/dPl∼, and dVr/dPl∼ increased significantly (p<0.05) by 0.48(0.03), 0.67(0.13), 0.38(0.05), and 0.61(0.09) respectively. This increased coupling occurred through pericardial pressure changes. If pericardial pressure was maintained constant, the coupling between the ventricles was unaltered. This same pattern was observed in four in situ experiments. For these experiments, at the raised pericardial pressure levels, dPl/dPr increased, from 0.51(0.03) to 0.79(0.01), p<0.05, if pericardial pressure was allowed to vary, but was unaltered with a constant pericardial pressure, at 0.42(0.03) v 0.44(0.04), p>0.5.Conclusions – Ventricular interdependence was increased with raised pericardial pressure and this increased coupling was due primarily to an increased ventricular-pericardial-ventricular coupling. This increased coupling may help to explain the paradoxical pulse observed in cardiac tamponade. [ABSTRACT FROM PUBLISHER]

The authors discuss a study which compared the effects of glucagon-like peptide 1 receptor agonists (GLP-1RA) on heart rate and the autonomic nervous system. Researchers performed the study using Holter electrocardiography and power spectrum analysis of heart rate variability. They found the association between increases in heart rate and GLP-1RA. The administration of liraglutide by titration is mentioned.

Objective: We evaluated lung attenuation on inspiratory/expiratory computed tomography (CT) and spiral CT angiography (CTA) from patients with chronic pulmonary embolism and correlated the CT findings with pulmonary function test (PFT) results., Methods: We retrospectively reviewed 9 patients with chronic embolism (mean age, 62.3 years; 5 women and 4 men). Paired inspiratory, expiratory CT and matching CTA images were reviewed, and lung attenuation was evaluated in each segment. Lower attenuation on inspiratory images and air trapping on expiratory images were subjectively assessed and correlated with PFT results. The relationship between the presence of clot and lung attenuation was evaluated. Nine age-matched normal subjects served as controls., Results: Lower attenuation with mosaic perfusion and air trapping were identified in 6 and 9 patients, respectively (mean scores, 8.1 and 11.3, respectively). Air trapping was identified in 19 (42.2%) of 45 segments with lower attenuation on inspiratory images, but was also noted in 31 segments with normal inspiratory attenuation. Air trapping was associated with the presence of proximal arterial stenosis (P<0.01), and the area showed less contrast enhancement than the adjacent lung (P<0.05). Extent of air trapping correlated inversely with PFT parameters of peripheral airway obstruction such as maximum mid-expiratory flow rate (r=-0.86, P=0.003). On the other hand, extent of mosaic perfusion did not correlate with PFT., Conclusions: Air trapping is commonly seen in chronic embolism and is found in areas of relative hypoperfusion. The extent of air trapping correlates with parameters of peripheral airway obstruction.

RT-nested PCR has been introduced as a highly specific and sensitive assay method to detect the prostate-specific membrane antigen (PSM) mRNA in peripheral blood. However, appreciable percentages of false-positive cases have been reported. Additionally, primer sets reported previously could not discriminate between PSM and PSM', an alternatively spliced variant, mRNA. These isoforms can be produced from a single gene. Switches in alternative splicing patterns are often controlled with strict cell-type or developmental-stage specificity. Therefore, it is most important to discriminate between PSM mRNA and PSM' mRNA. Using our highly specific primer sets, PSM mRNA was detected in 3 of 24 peripheral blood samples of normal male volunteers (12.5%) and was not detected in peripheral blood of 11 normal female volunteers. PSM' mRNA was detected in 5 of 24 peripheral blood samples of normal male volunteers (20.8%) and in 4 of 11 of normal female volunteers (36.4%). PSM' mRNA induced false-positive results, it is important for genetic diagnosis of prostate cancer to discriminate between PSM and PSM' using our primer sets with high specificity. The advances in the uniquely designed primer sets may allow researchers to detect a real PSM mRNA without PSM' mRNA.

A 54-year-old man was admitted to our hospital complaining of sudden-onset dyspnea in shock. Chest computed tomography(CT) showed thrombi in the right main and left intermediate pulmonary arteries. The case was diagnosed as a massive acute pulmonary thromboembolism. Although his hemodynamic status was stable after catecholamine infusion, his dyspnea was still in progress. Emergency pulmonary embolectomy was performed and the life of patient was saved. It is thought that progressive dyspnea is an important sign of a deteriorating hemodynamic status and the predictive symptom indicating a surgical procedure in patients with massive acute pulmonary thromboembolism.