Toyoshi Yuasa

Spectral analysis of heart rate, arterial pressure, and muscle sympathetic nerve activity in normal humans

We investigated the frequency components of fluctuations in heart rate, arterial pressure, respiration, and muscle sympathetic nerve activity (MSNA) in 11 healthy women using an autoregressive model and examined the relation among variables using Akaikes relative power contribution analysis with multivariate autoregressive model fitting. Power spectral analysis of MSNA revealed two peaks, with low-frequency (LF) and high-frequency (HF) components. The LF component of MSNA was a major determinant of the LF component of arterial pressure and R-R interval variability (0.70 +/- 0.07 and 0.18 +/- 0.05, respectively). The effect of the LF component of MSNA on arterial pressure showed no change in response to propranolol but was diminished (0.35 +/- 0.08) by phentolamine (P < 0.02). The effect of the LF component of MSNA on R-R interval was not altered by pharmacological sympathetic nerve blockade. The HF component of MSNA did not influence other variables but was influenced by R-R interval, arterial pressure, and respiration. These findings indicate that the LF component of MSNA reflects autonomic oscillations, whereas the HF component is passive and influenced by other cardiovascular variables.

Detection of the Earliest Ventricular Contraction Site in Patients with Wolff-Parkinson-White Syndrome Using Two-Dimensional Guided M-Mode Tissue Doppler Echocardiography

Objective: The purpose of this study was to examine the feasibility of M-mode tissue Doppler imaging for localizing the accessory pathway in patients with Wolff-Parkinson-White (WPW) syndrome. Methods: Two-dimensional guided tissue Doppler M-mode was recorded at the mitral and tricuspid annular levels in 13 WPW patients. Time intervals were measured from the onset of the δ wave or the R wave to the beginning of the ventricular systolic motion. The earliest contraction site was defined as the site demonstrating the shortest time interval, and compared with the earliest activated site determined by body surface mapping and the successful ablation site. Results: In 6 patients with a left-sided pathway, tissue Doppler localization was identical to the ablation site. In 3 with a left-sided pathway and 3 with a right-sided pathway, localization was judged as an adjacent region of the ablation site. In 1 patient with a right lateral pathway, the pathway location was misdiagnosed. The tissue Doppler diagnosis for the left-sided pathways correlated well with the ablation site, in contrast to the right-sided pathways (p = 0.05). Prediction of the accessory pathway localization by tissue Doppler M-mode was equivalent to localization based on body surface mapping. Conclusions: In WPW syndrome, tissue Doppler M-mode can detect the earliest contraction sites and seems helpful in localizing the left-sided accessory pathways, but is of limited use for right-sided pathways.

Ultrasonic analysis of anthracycline-induced myocardial damage using cyclic variation of integrated backscatter ☆

To test the feasibility of integrated backscatter (IB) for detecting anthracycline cardiotoxicity, we performed conventional echocardiography and IB analysis. For interindividual comparison, 32 patients with non-Hodgkins lymphoma and 14 control subjects were selected. Of the patients, 10 had been treated with doxorubicin doses of </=200 mg/m(2) (low dose), 15 with </=400 mg/m(2) (moderate dose), and 7 with >400 mg/m(2) (high dose). In intraindividual comparison, 8 patients were examined before doxorubicin therapy and at a dose of 100 mg/m(2) and 8 were examined before and at a 300-mg/m(2) dose. Cyclic variation of IB (CV-IB) was obtained at the left ventricular posterior wall, using a modified, commercially available system in M-mode format. In interindividual comparison, CV-IB in high- and moderate-dose groups was smaller. In intraindividual comparison, CV-IB decreased after treatment with 300 mg/m(2) of doxorubicin. CV-IB was affected in some patients treated with a moderate dose of doxorubicin. IB analysis may be helpful for detecting early anthracycline cardiotoxicity.

Two-dimensional guided M-mode color tissue Doppler echocardiography in artificial preexcitation models.

The purpose of this study was to analyze the left ventricular contraction patterns in artificial preexcitation models by using 2-dimensional guided M-mode color tissue Doppler echocardiography. Three types of preexcitation models were produced in 12 patients by right atrio-mitral annular sequential pacing, carried out at the left ventricular lateral, posterior, and posteroseptal walls. Tissue Doppler M-mode was recorded at anteroseptal, posterior, lateral, and posteroseptal sites in the parasternal short-axis view. The time interval from the onset of the QRS complex during sinus rhythm or from the annular pacing spike during fusion beats to the beginning of systolic motion was measured. During sinus rhythm, the time interval at the anteroseptal wall was shortest. During fusion beats, the time intervals at the mitral annular pacing sites were shortest. In preexcitation models, tissue Doppler M-mode could clearly distinguish the difference of left ventricular contraction patterns and detect the earliest contraction site of the left ventricle.

Percutaneous transluminal mitral valvuloplasty improves cardiopulmonary baroreflex sensitivity in patients with mitral stenosis

Patients with heart failure frequently have increased sympathetic tone, which could result in part from impairment of the inhibitory influence of cardiopulmonary baroreflexes. Percutaneous transluminal mitral valvuloplasty (PTMV) provides a unique model for evaluating functional changes in cardiopulmonary baroreflexes without open-heart surgical manipulation. We examined the effects of PTMV on cardiopulmonary baroreflexes and sympathetic nerve activity in 10 patients with mitral stenosis. We measured muscle sympathetic nerve activity using microneurography. Cardiopulmonary baroreflex provocation was performed by applying a lower body negative pressure of -10 mm Hg, and its sensitivity was determined by dividing the percent change in muscle sympathetic nerve activity by the change in central venous pressure. Response to isometric exercise was assessed by handgrip at 30% of maximal voluntary contraction for 3 min. PTMV significantly increased mitral valve area and cardiac index and decreased mean left atrial pressure. PTMV significantly decreased burst rate from 25.1+/-2.5 to 15.6+/-2.6 bursts/min (p < 0.01) and burst incidence from 37.1+/-3.7 to 23.6+/-3.3 bursts/100 heart beats (p < 0.01). After PTMV, cardiopulmonary baroreflex sensitivities measured using burst rate and burst incidence were -39.9+/-4.9%/mm Hg and -38.7+/-6.2%/mm Hg, respectively, which were significantly steeper than those before PTMV (-9.2+/-1.1%/mm Hg and -8.4+/-1.1%/mm Hg; p < 0.01). There were significant correlations between muscle sympathetic nerve activity at rest and cardiopulmonary baroreflex sensitivity. PTMV did not affect muscle sympathetic responses to handgrip exercise. These results suggest that patients with mitral stenosis have baseline sympathetic nerve activation, which could result in part from impaired cardiopulmonary baroreflexes.

Effect of pimobendan on cardiopulmonary baroreflex control of sympathetic nerve activity in healthy young men.

In order to determine the effect of pimobendan on sympathetic nerve activity and cardiopulmonary baroreflex (CPB), electrocardiogram, direct arterial pressure, central venous pressure (CVP) and cardiac output were recorded along with muscle sympathetic nerve activity (MSNA) in 8 healthy young men. CPB function was evaluated before and 60 min after oral administration of 5 mg pimobendan using the response of MSNA to lower body negative pressure (LBNP) of -5 and -10 mm Hg. The same protocol also was performed during handgrip exercise. Cardiac index, MSNA increased and CVP decreased significantly (p<0.01, respectively), but arterial pressure and heart rate unchanged after pimobendan administration. During LBNP, CVP decreased and MSNA increased significantly. CPB sensitivity was augmented from 5.53+/-0.75 to 8.59+/-0.78 burst incidence/mm Hg after pimobendan administration (p<0.01). Pimobendan did not alter the percentage increase of MSNA during handgrip exercise. In conclusion, pimobendan induces an increase in basal sympathetic nerve activity by decreasing CVP and augmenting CPB sensitivity without changing arterial pressure in healthy young men.