Takeshi Takamura

Reversible Right Ventricular Regional Non-Uniformity Quantified by Speckle-Tracking Strain Imaging in Patients With Acute Pulmonary Thromboembolism

BACKGROUND The aim of this study was to evaluate the effects of acute right ventricular (RV) pressure overload (RVPO) on RV systolic function and its regional uniformity using speckle-tracking strain analysis in patients with acute pulmonary thromboembolism (APTE). METHODS Twenty-three patients with APTE (mean age, 59 +/- 16 years) and 23 age-matched and gender-matched normal subjects (the control group) were examined using echocardiography. Global and segmental longitudinal RV peak systolic strain (PSS) was analyzed using speckle-tracking strain echocardiography. The heterogeneity of RV regional function was assessed by calculating the standard deviation from 6-segmental PSS divided by the absolute value of global PSS. The standard deviation of the heart rate-corrected intervals from QRS onset to PSS for the 6 segments was used to quantify RV dyssynchrony. RESULTS Patients with APTE had reduced regional PSS, resulting in reduced global PSS and augmented regional heterogeneity, and had delayed myocardial contraction in the basal and mid RV lateral walls, resulting in large dyssynchrony (global PSS, -14 +/- vs -25 +/- 3%; heterogeneity, 0.54 +/- 0.26 vs 0.24 +/- 0.09; dyssynchrony, 91 +/- 38 vs 25 +/- 10 ms; P < .05 vs controls for all comparisons). After the amelioration of acute RVPO by primary treatment, both RV heterogeneity and dyssynchrony returned to normal values. CONCLUSION Speckle-tracking strain echocardiography can effectively quantify reversible RV regional nonuniformity caused by acute RVPO and can characterize the pattern of RV regional impairment in patients with APTE.

Role of Radial Strain and Displacement Imaging to Quantify Wall Motion Dyssynchrony in Patients With Left Ventricular Mechanical Dyssynchrony and Chronic Right Ventricular Pressure Overload

Left ventricular (LV) deformation with ventricular septal shift is one of the most distinctive echocardiographic observations in patients with chronic right ventricular (RV) pressure overload (PO). However, little is known about the effects of RVPO on LV performance and regional synchrony. Accordingly, our objective was to test the hypothesis that chronic RVPO affects regional wall motion, synchronicity, and global LV function using a novel speckle-tracking approach to quantify and characterize regional LV wall motion dyssynchrony. Displacement and strain imaging echocardiographic studies were performed in 20 patients with RVPO from pulmonary arterial hypertension or pulmonic stenosis (mean age 53 +/- 16 years, New York Heart Association class 2.6 +/- 0.7, and peak RV systolic pressure 73 +/- 28 mm Hg) and 20 age-matched normal subjects (mean age 47 +/- 16 years). Segmental signals from 6 segments around the mid-LV short axis were defined as dyssynchronous if their changes were opposite to that of the global LV signal at each time frame, and overall LV dyssynchrony was calculated as the percentage of dyssynchrony in all 6 segments within the specified time interval from onset of QRS to the end of isovolumic relaxation. RVPO was associated with a large degree of regional dyssynchrony with paradoxical ventricular septal motion observed by displacement imaging (21 +/- 6%, p <0.05 vs control group), which was closely associated with LV eccentricity index (r = 0.79, p <0.05) and LV myocardial performance index with linear regression (r = 0.76, p <0.05). In contrast, strain imaging showed uniform segmental radial thickening in the RVPO group, which was similar to the control group, and suggests that there was no intrinsic LV contractile dyssynchrony. In conclusion, LV wall motion dyssynchrony assessed by displacement imaging, not intrinsic contractile dyssynchrony by strain imaging, coexists with LV chamber deformation with ventricular septal shift and is closely associated with impairment of LV performance.

Patients with a Hypertensive Response to Exercise Have Impaired Left Ventricular Diastolic Function

An exaggerated increase in systolic blood pressure prolongs myocardial relaxation and increases left ventricular (LV) chamber stiffness, resulting in an increase in LV filling pressure. We hypothesize that patients with a marked hypertensive response to exercise (HRE) have LV diastolic dysfunction leading to exercise intolerance, even in the absence of resting hypertension. We recruited 129 subjects (age 63±9 years, 64% male) with a preserved ejection fraction and a negative stress test. HRE was evaluated at the end of a 6-min exercise test using the modified Bruce protocol. Patients were categorized into three groups: a group without HRE and without resting hypertension (control group; n=30), a group with HRE but without resting hypertension (HRE group; n=25), and a group with both HRE and resting hypertension (HTN group; n=74). Conventional Doppler and tissue Doppler imaging were performed at rest. After 6-min exercise tests, systolic blood pressure increased in the HRE and HTN groups, compared with the control group (226±17 mmHg, 226±17 mmHg, and 180±15 mmHg, respectively, p<0.001). There were no significant differences in LV ejection fraction, LV end-diastolic diameter, and early mitral inflow velocity among the three groups. However, early diastolic mitral annular velocity (E′) was significantly lower and the ratio of early diastolic mitral inflow velocity (E) to E′ (E/E′) was significantly higher in patients of the HRE and HTN groups compared to controls (E′: 5.9±1.6 cm/s, 5.9±1.7 cm/s, 8.0±1.9 cm/s, respectively, p<0.05). In conclusion, irrespective of the presence of resting hypertension, patients with hypertensive response to exercise had impaired LV longitudinal diastolic function and exercise intolerance.

Left ventricular contraction-relaxation coupling in normal, hypertrophic, and failing myocardium quantified by speckle-tracking global strain and strain rate imaging.

OBJECTIVE The aim of this study was to noninvasively quantify global left ventricular (LV) contraction and relaxation, and to investigate their relationship in normal, hypertrophic, and failing myocardium. METHODS Fifty patients with hypertensive LV hypertrophy (LVH) (LVH group), 50 patients with dilated cardiomyopathy (DCM) (DCM group), and 50 normal subjects (control group) had echocardiographic evaluations. Global LV peak systolic strain (PSS) and peak relaxation rate (PRR) during early diastole were analyzed by speckle-tracking strain and strain rate imaging in the longitudinal and circumferential directions. RESULTS Both global PSS and PRR were reduced in the LVH group in the longitudinal direction. In the circumferential direction, global PSS was maintained and global PRR was reduced in the LVH group. The reductions in both global PSS and PRR were more pronounced in both directions in the DCM group compared with the other 2 groups. Global PSS correlated strongest with global PRR among the clinical and echocardiographic variables, which exhibited the best fit with exponential regressions in both the longitudinal and circumferential directions in all subjects (longitudinal: y=0.15e(-0.10x), r2=0.75; circumferential: y=0.21e(-0.09x), r2=0.76, P<.01, respectively). Multiple regression analysis indicated that global PSS was the most powerful determinant of global PRR in both longitudinal and circumferential directions. CONCLUSION Global LV function quantified using speckle-tracking echocardiography revealed strong coupling of LV contraction to relaxation sequentially from normal to failing myocardium, regardless of their heterogeneous pathophysiology. In addition, the extent of myocardial systolic shortening was the most powerful independent contributor of LV relaxation in both the longitudinal and circumferential directions. These results strongly indicate that LV myocardial systolic contraction directly regulates its relaxation.

Reversible left ventricular regional non-uniformity quantified by speckle-tracking displacement and strain imaging in patients with acute pulmonary embolism.

BACKGROUND The aim of this study was to investigate the impact of acute right ventricular pressure overload (RVPO) on left ventricular (LV) function and regional uniformity using speckle-tracking displacement and strain analyses in patients with acute pulmonary embolism (PE). METHODS Twenty-five patients with acute PE (mean age, 59 ± 16 years) and 25 normal subjects were enrolled. Radial, longitudinal, and circumferential LV wall motion and myocardial deformation were analyzed using speckle-tracking displacement and strain imaging echocardiography, respectively, from the mid-LV short-axis and apical four-chamber views. The standard deviation of the heart rate-corrected intervals from QRS onset to peak systolic displacement (PSD) and peak systolic strain for the six segments was used to quantify LV systolic dyssynchrony. The standard deviation of regional PSD and peak systolic strain divided by their global values was used to quantify LV systolic heterogeneity. Mechanical discoordination of LV regional wall motion and myocardial deformation was assessed by averaging the frame-by-frame percentage discordance between segmental and global signal changes in the six segments. RESULTS Patients with acute PE had reduced radial PSD and peak systolic strain and a large extent of displacement-derived nonuniformities (PSD dyssynchrony, 74 ± 32 vs 40 ± 20 m sec; PSD heterogeneity, 0.39 ± 0.13 vs 0.17 ± 0.08; and PSD discoordination, 23 ± 2% vs 15 ± 3%; P < .05 vs normal subjects for all comparisons) associated with a leftward shift of the interventricular septum. In contrast, all indices of strain-derived radial LV nonuniformities were not augmented by acute RVPO in patients with acute PE. Patients with acute PE also had impaired LV systolic function and regional uniformities in the longitudinal and circumferential directions. After the amelioration of acute RVPO by primary treatment, most of the indices of LV function and regional uniformity were restored to normal values. Multiple regression analysis indicated that only radial LV wall motion discoordination was a significant determinant of cardiac index. CONCLUSIONS Acute RVPO induces reversal LV regional uniformities, which are closely associated with reduced LV function and abnormal geometry of the left ventricle, and radial LV wall motion coordination plays a key role in the short-term regulation of cardiac output in patients with acute PE.

Ventricular function and dyssynchrony quantified by speckle-tracking echocardiography in patients with acute and chronic right ventricular pressure overload.

BACKGROUND The aim of this study was to noninvasively investigate right ventricular and left ventricular (LV) adaptation to right ventricular pressure overload in patients with acute pulmonary thromboembolism (APTE) and chronic pulmonary artery hypertension (CPAH). METHODS Thirty-seven patients with APTE, 36 patients with CPAH, and 33 controls were retrospectively enrolled. Myocardial deformation and wall motion were analyzed using speckle-tracking strain and displacement imaging echocardiography in the right and left ventricles. The standard deviation of the heart rate-corrected intervals from QRS onset to peak systolic strain and peak systolic displacement (PSD) for the six segments was used to quantify right ventricular and LV mechanical dyssynchrony (peak systolic strain dyssynchrony and PSD dyssynchrony). The myocardial performance index in both ventricles was also evaluated. RESULTS The APTE and CPAH groups had reduced ventricular performance (LV myocardial performance index, 0.40 ± 0.10, 0.66 ± 0.18 [P < .05 vs controls], and 0.58 ± 0.19 [P < .05 vs controls] in the control, APTE, and CPAH groups, respectively) and large mechanical dyssynchrony (LV longitudinal PSD dyssynchrony, 58 ± 41 msec, 119 ± 49 msec [P < .05 vs controls], and 83 ± 37 msec [P < .05 vs controls and the APTE group] in the control, APTE, and CPAH groups, respectively) in both ventricles. Multiple regression analysis indicated that LV longitudinal PSD dyssynchrony in the APTE group and the LV eccentricity index in the CPAH group were independent determinants of LV myocardial performance index. CONCLUSIONS Pathophysiologic mechanisms that regulate ventricular performance vary depending on whether the ventricles are exposed to acute or chronic right ventricular pressure overload.

Exaggerated hypertensive response to exercise in patients with diastolic heart failure.

Systolic load elevation during exercise prolongs left ventricular (LV) relaxation, compromises filling, and raises end-diastolic pressure, leading to reduced exercise tolerance. The aim of this study was to test the hypothesis that the hypertensive response to exercise is exaggerated in patients with diastolic heart failure (DHF). Echocardiograms and treadmill testing were performed in patients with DHF (n=20) and age-matched hypertension with LV hypertrophy (HTN; n=20). The Minnesota Living with Heart Failure Questionnaire was used to estimate quality of life (QOL). There were no differences in resting blood pressure or echocardiographic parameters between the groups. The maximum exercise time was significantly shorter in the DHF group than in the HTN group (6.0±3.0 vs. 12.5±2.5 min), and the peak systolic blood pressure during exercise was significantly higher in the DHF group (212±18 vs. 189±16 mmHg, p<0.05). After 4 weeks of treatment with candesartan, an angiotensin II receptor blocker (8 mg/d), peak systolic blood pressure during exercise decreased to 191±13 mmHg, maximum exercise time increased (10.4±3.0 min; p<0.05), and QOL improved in patients with DHF, while there was no change in patients with HTN, despite the similar resting blood pressure. In patients with DHF, systolic blood pressure markedly increased during exercise, and this was accompanied by impaired exercise tolerance and a decreased QOL, both of which were partly suppressed by blocking angiotensin II.

Biventricular pacing worsened dyssynchrony in heart failure patient with right-bundle branch block

The use of a biventricular pacing system for patients with complete right-bundle branch block (CRBBB) is still controversial. Although cardiac resynchronization therapy-defibrillator (CRT-D) was implanted in a heart failure patient with CRBBB, dyssynchrony worsened and stroke volume decreased, and this patient was re-admitted due to exacerbated heart failure. Therefore, evaluation of dyssynchrony and cardiac function after implantation of a biventricular pacing system may be needed in patients with atypical indications for CRT.

Conventional therapy with an ACE inhibitor diminishes left ventricular dyssynchrony during the progression of heart failure

PURPOSE Left ventricular (LV) mechanical dyssynchrony is an important codeterminant of cardiac dysfunction in heart failure (HF) patients exhibiting either a narrow or a wide QRS complex. We hypothesized that an angiotensin converting enzyme (ACE) inhibitor would prevent LV dyssynchrony during the progression of pacing-induced HF through its beneficial effects on hemodynamic change and myocardial fibrosis. METHODS Twenty-eight dogs were assigned to the following treatment groups; rapid ventricular pacing (HF group; n=10), concomitant ACE inhibitor and rapid pacing (enalapril 1.9 mg/kg/day: ACEI group; n=8), or sham-operated control (control group; n=10). After 4 weeks of pacing, cardiac function was evaluated using micromanometers and conductance catheters. We used indexes to quantify the temporal and spatial aspects of mechanical dyssynchrony derived from online segmental conductance catheter signals. At each time point, a segmental signal was defined as dyssynchronous if its change was opposite to the simultaneous change in the total LV volume. Mechanical dyssynchrony was calculated as the mean of the segmental dyssynchronies during systole, diastole, and throughout the cardiac cycle. RESULTS In the ACEI group, the LV ejection fraction was preserved, and total systemic resistance and end-diastolic volume were significantly decreased, while stroke volume was significantly increased compared to the HF group. The mechanical dyssynchrony index in the HF group was significantly higher compared to that of the control group, while it was significantly lower in the ACEI group. Thus, conventional therapy with an ACE inhibitor diminished LV dyssynchrony during the progression of pacing-induced HF.

Molecular diagnosis of prosthetic valve endocarditis with aorto-right atrial fistula

Definite diagnosis of infective endocarditis is impossible when all blood cultures are negative under antibiotic treatment. In this case, Streptococcus canis was identified using polymerase chain reaction from preoperative whole blood and excised valve tissue, and considered as the pathogen for infective endocarditis, despite negative blood cultures. This information was useful for diagnosis and selection of antibiotics.