[Study of nervous control of blood circulation in the nasal mucous membrane by cross thermocouple method].
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Biomedical subjects
Publications and source records attributed to J Naito.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
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Recently, we and other groups showed that analysis of transthoracic pulmonary venous flow velocity patterns is useful in the estimation of left ventricular diastolic function and left atrial pressure; however, it is unclear whether transthoracic tracings, in contrast to transesophageal tracings, provide reliable quantitation of the abnormal pulmonary venous flow characteristics in patients with and without cardiac disorders. This study was attempted to validate transthoracic pulmonary venous flow measurements by comparing them with transesophageal measurements in eight normal volunteers and 17 patients with a variety of cardiac disorders. Transesophageal and transthoracic measurements of peak diastolic forward flow velocity, the ratio of peak systolic/diastolic forward flow velocities, and the peak reversal flow velocity at atrial contraction sampled in the right upper pulmonary vein showed good correspondence to each other. The flow velocities were higher in the right upper pulmonary vein than in the left upper pulmonary vein. Narrower spectral flow velocity patterns with higher velocities were obtained 1 to 2 cm distal to the orifice in the pulmonary vein than at the orifice. Thus transthoracic measurements of the pulmonary venous flow velocity pattern are feasible and accurate in patients and may be used to assess left ventricular function and hemodynamics as a substitute for transesophageal measurements.
Left ventricular (LV) diastolic function in the early diastolic phase includes both active and passive processes, but in the atrial contraction phase it includes only passive processes. To elucidate the relation between the intraventricular dispersion of the flow velocity in diastole and LV diastolic process, 31 normal volunteers and 12 patients with hypertensive heart disease were studied. In these subjects the flow velocity pattern at the mitral tip was recorded simultaneously with regional flow velocity patterns 1, 2, or 3 cm from the mitral tip toward the apex, respectively, with multigate pulsed Doppler echocardiography from the apical long-axis view with the guidance of Doppler color-flow imaging. Although the ratio of regional peak flow velocity/mitral peak flow velocity in the atrial contraction phase decreased from the mitral tip to the apex to the same degree in the normal volunteers and patients with hypertensive heart disease, there was a significant difference in the intraventricular dispersion of the early diastolic flow velocity between the two groups. These results suggest that the progressive intraventricular drop of the flow velocity in the early diastolic phase in patients with hypertensive heart disease may reflect the impairment of active rather than passive LV diastolic function.
Although mitral flow velocity pattern changes with the progression of left ventricular (LV) diastolic dysfunction, it lacks predictive value in individual patients because of pseudonormalization in the presence of congestive heart failure and many physiologic and pathologic contributors to the mitral flow velocity pattern. To determine whether analysis of pulmonary venous flow velocity patterns complements the information obtainable from the mitral flow velocity patterns in the evaluation of patterns of LV dysfunction of hypertensive heart disease in individual patients, the ratio of the peak early diastolic filling velocity/peak filling velocity at atrial contraction (E/A ratio) in the mitral flow velocity pattern and the ratio of the peak systolic forward flow velocity (S)/peak diastolic forward flow velocity (D) (S/D ratio) in the pulmonary venous flow velocity pattern by the transthoracic approach were determined in 107 hypertensive patients with and without congestive heart failure. Age-related normal values of the E/A and S/D ratios were determined in 61 normal subjects and used to judge the normality or abnormality of the patterns. Results of the study indicate that (1) although an increased mitral E/A ratio is strongly indicative of heart failure with normal LV systolic function, the mitral E/A ratio is frequently within the normal range in hypertensive patients with heart failure; (2) association of decreased pulmonary venous S/D ratios with a normal mitral flow velocity pattern indicates the presence of heart failure as a result of LV systolic dysfunction that is usually observed at the most advanced pattern of LV dysfunction; (3) mild LV diastolic dysfunction is likely to exist in patients with normal E/A ratios if the pulmonary venous S/D ratio is higher than normal value; (4) predictive accuracy in the detection of LV systolic and diastolic dysfunction would be improved if both mitral and pulmonary venous flow velocity patterns rather than the mitral flow velocity pattern alone were analyzed. In conclusion, analysis of pulmonary venous flow velocity recordings improves accuracy and reliability of the Doppler assessment of LV systolic and diastolic dysfunction, particularly in individual hypertensive patients with normal mitral flow velocity patterns.
Pericardial constraining force is minimal in normal hearts; however, it is considered to be prominent in moderate to severe heart failure. Thus, effects of the pericardium on pulsed Doppler transmitral flow velocity pattern were examined in 17 dogs with acute left ventricular dysfunction. Left ventricular dysfunction with left ventricular end-diastolic pressure > or = 15 mm Hg was produced by injection of microspheres into the left coronary artery. Transmitral flow velocity pattern, left atrial and left ventricular diameters, and high-fidelity left atrial and left ventricular pressures were recorded before and after pericardiectomy. In five of the 17 dogs, mitral regurgitation with giant "v" wave of left atrial pressure occurred with reductions of left ventricular systolic pressure and peak rate of the left ventricular pressure fall (dP/dt) after pericardiectomy. In the other 12 dogs, peak early and late diastolic filling velocities increased with a decrease in left ventricular minimal pressure and increases in left arterial and left ventricular diameters and left atrial and left ventricular compliance after pericardiectomy. In these 12 dogs, left atrial to left ventricular crossover pressure, left ventricular end-diastolic pressure, and references for left ventricular relaxation did not change after pericardiectomy. Thus the release from pericardial constraining force in severe heart failure may increase chamber compliance of the left ventricle and left atrium and, in turn, increase peak early and late diastolic filling velocities through an increment in forward transmitral pressure gradient. Increased pericardial constraining force is a possible cause limiting left ventricular filling and hence cardiac output in heart failure.
Although acoustic properties of the myocardium are different between patients with cardiomyopathy and normal subjects, the frequency of the abnormal properties in patients with cardiomyopathy is unknown. We assessed the frequency of abnormal acoustic properties of the myocardium detectable with integrated backscatter in patients with cardiomyopathy and attempted more sensitive ultrasonic tissue characterization by combining dobutamine stress testing in patients with cardiomyopathy with apparently normal acoustic properties of the myocardium at rest. The magnitude of cyclic variation of integrated backscatter and calibrated myocardial integrated backscatter at end diastole were measured in 36 normal subjects and 40 patients with dilated cardiomyopathy. Either one of the integrated backscatter parameters was abnormal in 30 of 40 patients with cardiomyopathy. Dobutamine stress ultrasonic tissue characterization was performed in 10 patients with cardiomyopathy with normal values of both integrated backscatter parameters and 10 normal subjects. Calibrated myocardial integrated backscatter did not change during dobutamine infusion in any subject. The magnitude of cyclic variation in integrated backscatter increased in normal subjects but did not change in patients with cardiomyopathy despite a comparative associated increase in the systolic wall thickening during dobutamine infusion. Abnormal acoustic properties are detectable at rest with myocardial integrated backscatter about in three quarters of patients with cardiomyopathy. A combination of dobutamine stress testing would provide more sensitive ultrasonic myocardial tissue characterization and may make it possible to detect subtle changes in the acoustic properties of the myocardium in patients with dilated cardiomyopathy. Therefore dobutamine stress ultrasonic tissue characterization may detect mild dilated cardiomyopathy.
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