Biomedical subjects
Takashi Oki
Publications and source records attributed to Takashi Oki.
Calcium-promoted catalytic degradation of PCDDs, PCDFs, and coplanar PCBs under a mild wet process.
The authors achieved highly efficient degradation of polychlorinated aromatic compounds, including polychlorinated dibenzo-p-dioxins, dibenzofurans, and dioxin-like compounds such as coplanar polychlorinated biphenyls (co-PCBs), which are known as persistent organic pollutants. Degradation was accomplished in 24 h through a simple stirring operation using safe and high workability metallic calcium, which acts as both a scavenger and a reducing agent, and Rh/C catalyst in an alcohol solution under mild conditions in a sealed tube at 25 degrees C without a temperature increase within 0.15 MPa of increasing internal pressure during the reaction. In this system, reductive dechlorination by metallic calcium and catalytic reduction by Rh/C and generated hydrogen gas, without any external addition of hydrogen, exert a synergistic effect on the degradation of chlorinated compounds. Alcohol was used as a proton source and hydrogen, which was generated by a side reaction, causes an increase in the activity of Rh/C catalyst. Through the degradation of 4-chloroanisole in ethyl alcohol, anisole and cyclohexyl methyl ether were obtained in good conversions. Using ethyl alcohol as a solvent, treatment of dioxins and co-PCBs in a solution was markedly effective for degradation to reduce 2806 pg TEQ/ml of initial concentration to 31.8 pg TEQ/ml; its yield was 98.5%. Moreover, degradation in methyl alcohol took place in a 99.3% yield. That concentration ultimately reached 20.3 pg TEQ/ml under a mild wet process. All congeners of dioxins and co-PCBs were degraded in high conversions. In this degradation, lower aliphatic alcohol, such as methyl alcohol, is effective for making a new calcium surface as compared to alcohol with more methylene chains. In addition, it seemed that a higher pressure of hydrogen was easily generated in methyl alcohol, and then catalytic degradation was effectivley influenced.
Rationale and design of a randomized trial to assess the effects of beta-blocker in diastolic heart failure; Japanese Diastolic Heart Failure Study (J-DHF).
BACKGROUND: Heart failure consists of two phenotypes: systolic heart failure and diastolic heart failure (DHF). A growing body of evidence demonstrated benefits of beta-blocker, angiotensin-converting enzyme inhibitor, and angiotensin II receptor blocker in systolic heart failure; however, evidence leading to therapeutic strategy of DHF is lacking. METHODS AND RESULTS: The Japanese Diastolic Heart Failure Study (J-DHF) is a multicenter, prospective, randomized trial designed to assess effects of beta-blocker in patients with DHF. A total of 800 patients (400 patients in each group) will be enrolled. The primary outcome is a composite of cardiovascular death and unplanned admission to hospital for congestive heart failure. Other outcomes include all-cause mortality, worsening of the symptoms of heart failure, or a need for modification of the treatment for heart failure. Serial assessment of echocardiographic and neurohumoral parameters and cost analysis of the treatment regimen will be conducted. The follow-up period is a minimum of 2 years. CONCLUSION: This study will provide important evidences for the treatment of DHF.
Left ventricular geometry and myocardial contractility in patients with essential hypertension evaluated by myocardial velocity profile.
BACKGROUND: Left ventricular (LV) systolic function in the hypertensive heart has been evaluated considering geometric differences. The maximal systolic myocardial velocity gradient (Gmax) obtained from myocardial velocity profile can evaluate regional myocardial contractility. The purpose of this study was to assess LV myocardial contractility in the hypertensive heart using Gmax regarding geometric differences. METHODS: The study included 93 patients with essential hypertension. Gmax was correlated with relative wall thickness and LV mass index. LV myocardial contractility was assessed by classifying patients into normal geometry, concentric remodeling (CR), eccentric hypertrophy, and concentric hypertrophy (CH). RESULTS: Gmax has shown significant negative relationship with LV end-diastolic dimension. LV end-diastolic dimension in CH and eccentric hypertrophy groups was significantly greater than that in normal geometry and CR groups (CH vs CR, 4.9 vs 4.2 cm, P < .001). LV mass index was significantly greater in CH and eccentric hypertrophy groups than in the other groups (CH vs CR, 196 vs 122 g/m2, P < .001). Although there was no difference in relative wall thickness between CH and CR groups, Gmax was significantly smaller in CH than in CR group (1.8 vs 2.8 s(-1), P < .05). CONCLUSIONS: In patients with essential hypertension, LV myocardial contractility worsened corresponding to increase in LV dimension with similar wall thickness. Gmax obtained from myocardial velocity profile detected depressed myocardial contractility in patients with increased LV dimension.
Diagnosis of cardiac amyloidosis based on the myocardial velocity profile in the hypertrophied left ventricular wall.
The myocardial velocity profile (MVP), derived from color-coded tissue Doppler imaging (TDI), can identify transmural heterogeneity based on the physiology and pathology of the myocardium. This study sought to clarify whether the MVP can differentiate cardiac amyloidosis from other causes of left ventricular hypertrophy. We recorded the MVP and determined its myocardial velocity gradient (MVG) in the ventricular septum and left ventricular posterior wall using color-coded TDI in 10 patients with cardiac amyloidosis, in 25 patients with hypertensive hypertrophied left ventricular wall, in 25 patients with asymmetric septal hypertrophy of hypertrophic cardiomyopathy, and in 20 clinically normal controls. End-diastolic ventricular septal thickness was similar among the cardiac amyloidosis, hypertension, and hypertrophic cardiomyopathy groups. Percent systolic thickening of the ventricular septum and left ventricular posterior wall calculated from M-mode left ventricular echocardiograms was lower in the cardiac amyloidosis group than in the hypertension, hypertrophic cardiomyopathy, or control group. Peak MVGs during systole and early diastole were lowest in the cardiac amyloidosis group, followed, in order, by the control, hypertension, and hypertrophic cardiomyopathy groups. The systolic and early diastolic MVPs in the ventricular septum and left ventricular posterior wall showed a characteristic serrated pattern in all patients with cardiac amyloidosis, but not in any other patient groups. In conclusion, MVPs in the ventricular septum and left ventricular posterior wall show a distinctive serrated pattern that may be related to amyloid deposition in the myocardium. Myocardial tissue characterization using color-coded TDI provides diagnostic information in patients with cardiac amyloidosis.
Potential application of tissue Doppler imaging to assess regional left ventricular diastolic function in patients with hypertrophic cardiomyopathy: comparison with 123I-beta-methyl iodophenyl pentadecanoic acid myocardial scintigraphy.
BACKGROUND: Tissue Doppler imaging (TDI) has been utilized to evaluate left ventricular myocardial dysfunction in patients with hypertrophic cardiomyopathy (HCM); however, no clear explanation for the abnormality of TDI variables has been forthcoming. HYPOTHESIS: Peak negative myocardial velocity gradient (MVG) derived from TDI may correlate with a disorder of fatty acid metabolism in patients with HCM. METHODS: Tissue Doppler imaging and 123I-beta-methyl iodophenyl pentadecanoic acid (123I-BMIPP) myocardial scintigraphy were performed in 15 patients with asymmetric septal hypertrophy (mean age 47 +/- 18 years) and in 12 healthy controls (mean age 43 +/- 10 years). RESULTS: In early 123I-BMIPP images, accumulation defects were observed in the ventricular septum in 12 patients and in the posterior wall in 8 patients with HCM. Peak negative MVG in the ventricular septum (1.1 +/- 0.5 vs. 2.8 +/- 0.5, p < 0.0001) and posterior wall (5.2 +/- 1.4 vs. 6.7 +/- 0.8, p < 0.01 ) was significantly lower in the HCM group than in the controls; also, these parameters were significantly lower in patients with than in those without a defect in the region in question. The peak negative MVG in the ventricular septum and posterior wall correlated inversely with the washout rate in all subjects. CONCLUSIONS: Peak negative MVG according to TDI is related to disorder of fatty acid metabolism in the regional left ventricular myocardium of patients with HCM.
Atrial electrophysiologic abnormalities in patients with Wolff-Parkinson-White syndrome but without paroxysmal atrial fibrillation.
BACKGROUND: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff-Parkinson-White (WPW) syndrome. HYPOTHESIS: The purpose of this study was to analyze the atrial electrophysiologic abnormalities and vulnerability to develop atrial fibrillation (AF) in patients with WPW syndrome but with no previous history of PAF. METHODS: We investigated atrial electrophysiologic abnormalities and vulnerability to AF in patients with WPW syndrome but without PAF. An electrophysiologic study was performed in 28 patients with WPW syndrome, 23 with atrioventricular nodal reentrant tachycardia (AVNRT) and 25 with other arrhythmias (control), all of whom had no history of PAF. The following atrial excitability parameters were assessed: effective refractory period (ERP), spontaneous or paced (A1) and extrastimulated (A2) atrial electrogram widths, percent maximum atrial fragmentation (%MAF; A2/A1 x 100), wavelength index (WLI; ERP/A2), and inducibility of AF. RESULTS: The ERP tended to be shorter in patients with WPW syndrome and in those with AVNRT than in the control group. The %MAF increased (154 +/- 33 vs. 137 +/- 23%, p < 0.05) and WLI decreased (2.7 +/- 0.8 vs. 3.4 +/- 1.0, p < 0.05) significantly in patients with WPW syndrome compared with the control group; however, these parameters in patients with AVNRT showed intermediate values. Atrial fibrillation was more inducible in patients with WPW syndrome (4/28 [14.3%]) than in those with AVNRT (4.3% [1/23]) and the control group (0/25 [0%]). With respect to patients with WPW syndrome and with and without inducible AF, the %MAF increased (195 +/- 23 vs. 148 +/- 30%, p < 0.01) and the WLI decreased (2.2 +/- 0.3 vs. 2.9 +/- 0.9, p < 0.05) in subjects with inducible AF. CONCLUSIONS: Atrial electrophysiologic abnormalities, especially atrial conduction delays, are more prominent in patients with WPW syndrome, even if they had no previous history of PAF. These abnormalities may play an important role in determining the vulnerability to AF.
A patient responding to combined therapy with pirmenol and midodrine for refractory neurally mediated syncope complicated by prostatic hypertrophy.
A 67-year-old man with neurally mediated syncope (NMS) complicated by prostatic hypertrophy responded well to combined therapy with pirmenol and midodrine. In 2003, syncope occurred while the patient was driving a car. Results of head-up tilt-table testing (HUT) suggested a mixed type of NMS. Oral administration of disopyramide provided severe urinary obstruction. Pirmenol treatment was not associated with syncope during ordinary HUT, but nausea, sweating, and syncope occurred during HUT with provocative administration of isosorbide dinitrate. Combined therapy with pirmenol and midodrine avoided syncope during HUT, and has prevented attacks since discharge from the hospital.
Losartan improves regional left ventricular systolic and diastolic function in patients with hypertension: accurate evaluation using a newly developed color-coded tissue doppler imaging technique.
BACKGROUND: Angiotensin II receptor antagonists have recently been accepted as antihypertensive therapy. Tissue Doppler imaging (TDI) has been developed as a noninvasive tool to assess quantitatively regional myocardial motion abnormalities. This study was designed to determine whether our newly developed technique of color-coded TDI may be a useful means of quantifying the improvement in regional left ventricular (LV) myocardial contractility and relaxation after treatment with losartan in patients with hypertension. METHODS AND RESULTS: Losartan (50 to 100 mg) was administered for 6 months to 37 previously untreated patients with essential hypertension. Averaged myocardial velocity profiles (MVPs) for color-coded TDI were recorded in the ventricular septum and LV posterior wall before and after treatment. Peak myocardial velocities and peak myocardial velocity gradients (MVGs) in the LV walls were determined during systole and early diastole. The plasma concentration of transforming growth factor (TGF)-beta1 also was measured in all patients. Blood pressure and plasma TGF-beta1 level decreased after initiation of losartan therapy. The LV mass index and LV meridional end-systolic wall stress also decreased after treatment with losartan. LV geometry changed from a pattern consistent with concentric hypertrophy to normal geometry in 10 patients and to a pattern consistent with concentric remodeling in 5 patients, and from concentric remodeling to normal geometry in 5 patients after treatment with losartan. The ratio of early to late diastolic filling for the transmitral flow velocity increased after losartan treatment. The peak systolic and early diastolic myocardial velocities and MVGs in the ventricular septum and LV posterior wall increased after treatment with losartan, although the values 6 months after treatment with losartan were still lower than those in normal individuals. There were good correlations between changes in plasma TGF-beta1 level and changes in systolic and early diastolic MVGs 6 months after losartan. However, there were no significant correlations between changes in the systolic blood pressure and LV end-systolic wall stress and changes in the TDI parameters. CONCLUSION: Losartan improves regional LV function in patients with hypertension. Our newly developed averaged MVP and MVG measurements may be useful for accurately evaluating regional LV myocardial contractility and relaxation in these patients.
Syncope upon swallowing caused by an esophageal hiatal hernia compressing the left atrium: a case report.
We describe a patient with syncope associated with swallowing. This syncope was caused by transient compression of the left atrium (LA) by an esophageal hiatal hernia. Two-dimensional echocardiography demonstrated a hyperechoic mass compressing the LA from the posterior. With air insufflation of the esophagus, compression of the LA by this hernia sac was seen to increase. Pulsed and color Doppler echocardiography revealed greatly decreased velocity of blood flowing into the LA and left ventricle (LV). Thus, marked compression of the LA by an esophageal hiatal hernia can cause syncope by impeding blood flow from the LA to the LV. Echocardiography proved highly useful in diagnosis.
Prognostic value of the atrial systolic mitral annular motion velocity in patients with left ventricular systolic dysfunction.
BACKGROUND: Transmitral flow velocity variables are powerful predictors of poor prognosis in patients with left ventricular (LV) systolic dysfunction. However, these variables may not accurately reflect the severity of pulmonary congestion. This study was designed to determine whether the peak atrial systolic mitral annular motion velocity (MA-Aw) measured by pulsed Doppler tissue imaging can predict cardiac death or hospitalization for worsening heart failure in patients with LV systolic dysfunction. METHODS: MA-Aw was recorded in 96 patients with LV systolic dysfunction who were followed up for 29 +/- 10 months. All patients underwent Doppler echocardiography on entry into the study, and cardiac catheterization was performed in 45 patients. Patients were divided into 3 groups on the basis of the ratio of early (E) to late (A) diastolic filling (E/A) of the transmitral flow velocity: group 1 (n=31; E/A < 1); group 2 (n=37; 1 < or = E/A < 2); and group 3 (n=28; E/A > or = 2). RESULTS: During follow-up, 36 patients (38%) died of cardiac causes and 34 (35%) were hospitalized for worsening heart failure. There were 2 cardiac deaths (6%) in group 1, 14 (39%) in group 2, and 20 (56%) in group 3. The MA-Aw correlated closely with the mean pulmonary capillary wedge pressure. Univariate Cox model analysis showed that MA-Aw < or = 5 cm/s was the most powerful predictor of cardiac death or hospitalization for worsening heart failure compared with clinical, hemodynamic, and the other echocardiographic variables. Furthermore, MA-Aw < or = 5 cm/s was clearly discernible as a good predictor of cardiac mortality on multivariate Cox model and as assessed by Kaplan-Meier method. CONCLUSION: The MA-Aw obtained by pulsed Doppler tissue imaging is a sensitive index of pulmonary congestion in patients with LV systolic dysfunction. It is a simple and noninvasive outcome measure and can be used to monitor treatment.
Relation of age and sex to atrial electrophysiological properties in patients with no history of atrial fibrillation.
Although atrial fibrillation is a common arrhythmia, especially in elderly men, little is known about age related changes in atrial electrophysiological properties or gender differences. The aim of this study was to analyze the effects of aging on vulnerability to atrial fibrillation and assessed gender differences in those age related changes. An electrophysiological study was performed on 73 patients with no history of atrial fibrillation, structural heart disease, or conditions with potential effects on cardiac hemodynamic or electrophysiological function, including 25 women (mean age 49 +/- 18 years; range 12-84 years). The following atrial excitability parameters were assessed: spontaneous or paced (A1) and extrastimulated (A2) atrial electrogram widths, percent maximum atrial fragmentation (A2/A1 x 100), effective refractory period, wavelength index (effective refractory period/A2), and inducibility of atrial fibrillation. There were no significant differences in percent maximum atrial fragmentation (143 +/- 28 vs 142 +/- 35%), effective refractory period (241 +/- 39 vs 238 +/- 50 ms), wavelength index (2.9 +/- 0.8 vs 3.1 +/- 0.9), induction of atrial fibrillation (10 [21%] vs 7 [28%]), or age (50 +/- 17 vs 49 +/- 20 years) between men and women. Age was not statistically different between those patients with and without induction of atrial fibrillation in men (48 +/- 14 vs 50 +/- 18 years) and women (48 +/- 18 vs 49 +/- 21 years). Percent maximum atrial fragmentation and effective refractory period were directly correlated with age in men (r = 0.35, P = 0.01; r = 0.46, P < 0.001, respectively) and women (r = 0.42, P = 0.04; r = 0.45, P = 0.02, respectively), though wavelength index did not correlate with age in men (r = -0.04) or women (r = -0.04) with no history of atrial fibrillation. Considering these findings, the authors conclude that the mechanism triggering atrial fibrillation may be different between older and younger patients with atrial fibrillation, because younger patients who have no marked substrate for atrial fibrillation may need many trigger beats to induce atrial fibrillation.
Novel approach to the quantitation of regional left ventricular systolic and diastolic function using tissue Doppler imaging to create a myocardial velocity profile and gradient.
The myocardial velocity profile (MVP) and gradient (MVG) between the endocardium and epicardium of the left ventricular (LV) wall measured by color-coded tissue Doppler imaging (TDI) are new indices for evaluating regional LV myocardial function. However, accurate recording and measurement of the MVP is difficult using conventional methodology because of the stochastic nature of the ultrasound signal; that is, the effect of speckled noise. The aim of this study was to validate the accuracy and establish the validity of a newly developed method for measuring the MVP and MVG using 10 clinically normal controls and 10 patients with a hypertensive hypertrophied LV posterior wall. A non-isotropic, averaging algorithm was developed that was capable of obtaining a stable MVP (averaged MVP). Averaged MVP was recorded using parasternal, LV short-axis, color-coded TDI, placing regions of interest along the LV posterior wall with the reference point for angle-correction being at the center of LV contraction. The velocity from epicardium to endocardium within the region of interest was automatically angle-corrected to calculate the velocity component radially relative to the LV cavity and was spatially averaged along the circumference within the region of interest. Inter- and intraobserber variabilities of measurements were lower in the averaged MVP and MVG than in the conventional MVP and MVG. The correlation coefficients of the linear regression lines of systolic and early diastolic MVPs in the LV posterior wall were higher in all controls and hypertensive patients with the averaged method than with the conventional TDI procedures. The mean peak systolic and early diastolic MVGs were lower in the hypertensive group than in the controls. In conclusion, the newly developed averaged MVP provides a stable and reproducible index for the quantitative assessment of regional LV myocardial function.
Age-related changes in the electrophysiologic properties of the atrium in patients with no history of atrial fibrillation.
Although atrial fibrillation is a common arrhythmia, especially in the elderly, little is known about age-related changes in the electrophysiologic properties of the atrium. The aim of this study was to analyze the effect of aging on atrial vulnerability to atrial fibrillation. An electrophysiologic study was performed in 45 patients with no history of atrial fibrillation, Wolff-Parkinson-White syndrome, structural heart disease, or conditions with potential effects on cardiac hemodynamic or electrophysiologic function (15 females; mean age, 52 +/- 18 years; range, 14 to 84 years). The following atrial excitability parameters were assessed: spontaneous or paced (A1) and extrastimulated (A2) atrial electrogram widths, percent maximum atrial fragmentation (A2/A1 x 100), effective refractory period, wavelength index (ERP/A2), and inducibility of atrial fibrillation. Atrial fibrillation was induced in 9 patients. Percent maximum atrial fragmentation was greater (176 +/- 36 vs 137 +/- 26%, P < 0.001) and wavelength index was shorter (2.4 +/- 0.4 vs 3.2 +/- 0.9, P < 0.01) in the patients with than without inducible atrial fibrillation. However, age was similar in patients with and without inducible atrial fibrillation (47 +/- 11 vs 53 +/- 19 years, P = 0.36). Percent maximum atrial fragmentation and effective refractory period directly correlated with age (r = 0.32, P < 0.05 and r = 0.45, P < 0.001, respectively). On the other hand, wavelength index (3.1 +/- 0.9) did not correlate with age (r = -0.05, P = 0.77). This study suggests that the mechanism triggering atrial fibrillation may be very well different between older and younger patients with atrial fibrillation, because younger patients have no marked substrate for atrial fibrillation.
Early systolic mitral annular motion velocities responses to dobutamine infusion predict myocardial viability in patients with previous myocardial infarction.
OBJECTIVE: This study was undertaken for the determination of the correlation between myocardial viability and regional systolic mitral annular motion velocity (MAV) response to dobutamine stress in patients with previous myocardial infarction (MI) with pulsed tissue Doppler scan imaging. METHODS: The study included 45 patients (mean age, 65 +/- 12 years) with previous MI with 1 major coronary lesion and 30 healthy individuals (mean age, 61 +/- 14 years). 99mTc-methoxyisobutylisonitrile scintigraphy was performed to divide the patients into 2 groups: the viability (+) group (n = 25) and the viability (-) group (n = 20). Dobutamine was infused (at 2, 5, 10, and 20 microg/kg/min), and the peak first and second systolic MAVs (Sw1 and Sw2, respectively) were measured at the level of the mitral annulus corresponding to the infarct regions in the MI group and to the 6 mitral annular sites in the control group. In addition, the left ventricular wall motion score index (WMSI) was determined with 2-dimensional echocardiography. RESULTS: At baseline, the WMSI was significantly greater and the mean Sw1 and Sw2 were significantly lower in both the viability (+) and (-) groups than in the control group, but there were no significant differences between the viability (+) and (-) groups. After dobutamine infusion, the WMSI improved only in the viability (+) group. The mean Sw1 and Sw2 increased significantly with 2 microg/kg/min and 5 microg/kg/min of dobutamine, respectively, in the viability (+) group. With an increase in Sw1 of 2.0 cm/s or more with 5 microg/kg/min of dobutamine, viable myocardium was detected, with a sensitivity of 92% and a specificity of 90%. There were no significant increases in Sw1 or Sw2 in the viability (-) group with dobutamine infusion. CONCLUSION: Viable left ventricular myocardium is identified with peak early systolic MAV during dobutamine infusion.
The role of short- and long-axis function in determining late diastolic left ventricular filling in patients with hypertension: assessment by pulsed Doppler tissue imaging.
Left ventricular (LV) wall motion velocity during atrial systole is mediated by both transmitral flow and LV myocardial compliance at end-diastole. LV wall distensibility along the long- and short-axis during atrial systole and late diastolic LV filling may vary according to the remodeling of LV morphology. We measured LV wall motion velocities along the long and short axes using pulsed Doppler tissue imaging in 127 patients with hypertension to evaluate the relationship between the hemodynamic changes and LV morphology and to determine the role of both long- and short-axis function in late diastolic LV filling. Participants were classified into 3 groups according to LV dimension and end-diastolic wall thickness determined by M-mode echocardiography: group A (n = 62) without LV dilation or hypertrophy, group B (n = 55) with LV hypertrophy, and group C (n = 10) with LV dilation and systolic dysfunction. The time constant of the LV pressure decay during isovolumic diastole and the LV end-diastolic pressure were longest and greatest, respectively, in group C, compared with groups B and A. There were no significant differences in active left atrial emptying volume during atrial contraction determined by computerized echocardiographic 3-dimensional reconstruction among patient and control groups. The peak atrial systolic motion velocity of the LV posterior wall along the long axis was significantly lower in groups B and C, particularly in the latter group, than in group A. The peak atrial systolic motion velocity of the LV posterior wall along the short axis was greatest in group B and was lowest in group C compared with the other groups, respectively. The peak atrial systolic motion velocity of the LV posterior wall was greater along the long axis than the short axis in group A, but was less than the short axis in group B. In conclusion, the long- and short-axis function of the LV wall during atrial systole varies in patients with hypertension according to the severity of hemodynamic and morphologic abnormalities. The degree of LV wall expansion along the short axis is an important factor resulting from the atrial kick, and a determinant of its effectiveness.
Assessment of the Systolic Left Ventricular Myocardial Velocity Profile and Gradient Using Tissue Doppler Imaging in Patients with Hypertrophic Cardiomyopathy.
To determine the systolic characteristics of the hypertrophied myocardium in patients with hypertrophic cardiomyopathy (HCM), we evaluated the left ventricular [left ventricle (LV)] myocardial velocity profile (MVP) and gradient obtained from tissue Doppler imaging (TDI). Transmural wall-motion velocities in the ventricular septum and LV posterior wall were recorded in 12 patients with asymmetric septal hypertrophy and 12 healthy volunteers, and their profiles and gradients were determined. The maximum systolic myocardial velocity gradient in the ventricular septum was significantly lower in the HCM group than in the control group (0.88 +/- 0.35 versus 2.24 +/- 0.41; P < 0.001), whereas the gradient in the LV posterior wall was only slightly lower in the HCM group than in the control group (2.69 +/- 0.82 versus 3.45 +/- 0.96). In the control group, the MVPs in the ventricular septum and LV posterior wall were closely linear, suggesting that the transmural velocity is uniform during systole. MVPs in the ventricular septum and LV posterior wall in the HCM group also were closely linear, whereas the distribution of velocities in the ventricular septum was fairly dispersed compared with the control group. The myocardial velocity gradient on the right ventricular side of the ventricular septum decreased or disappeared in the patients with HCM, suggesting a nonuniform distribution of velocities. In conclusion, the MVP and gradient obtained from TDI may represent new indices for evaluating regional LV contractile abnormality in patients with HCM.
Echocardiographic Detection of Occult Cor Pulmonale During Exercise in Patients with Chronic Obstructive Pulmonary Disease.
We tested the ability of cycle ergometer exercise echocardiography to detect cases of occult cor pulmonale among 25 patients with chronic obstructive pulmonary disease (COPD). The M-mode echocardiographic ventricular septal motion, left ventricular shape determined by short-axis two-dimensional (2-D) echocardiography, and right and left ventricular pressure curves were recorded at rest and during exercise and were compared between patients. The ventricular septal motion was normal at rest in all of the patients. In nine patients (dip group), there was marked downward ventricular septal motion in early diastole during exercise, indicating distortion of the left ventricular shape. There were no distinct changes in the remaining 16 patients (non-dip group). At rest, the cardiac index was significantly lower, and right ventricular systolic and mean pulmonary artery pressures were significantly higher in the dip group than in the non-dip group. However, no significant difference was noted in the right ventricular end-diastolic pressure between the two groups at rest. The right ventricular systolic and end-diastolic pressures were greater during exercise in the dip group than in the non-dip group. In all of the patients in the dip group, the right ventricular pressure exceeded the left ventricular pressure only in early diastole, coinciding with the early diastolic dip of the ventricular septum, during exercise. In conclusion, occult cor pulmonale can be diagnosed accurately by the appearance of an early diastolic dip of the ventricular septum and distorted left ventricular shape during exercise in patients with COPD.