Biomedical subjects
Publications and source records attributed to Kaoru Dohi.
Saphenous vein graft aneurysms are a rare complication of coronary artery bypass surgery. In this article, we present a 3-dimensional computed tomography image of two giant aneurysms of a single saphenous vein bypass graft.
BACKGROUND: Mechanical dyssynchrony is a potential means to predict response to cardiac resynchronization therapy (CRT). We hypothesized that novel echocardiographic image speckle tracking can quantify dyssynchrony and predict response to CRT. METHODS AND RESULTS: Seventy-four subjects were studied: 64 heart failure patients undergoing CRT (aged 64+/-12 years, ejection fraction 26+/-6%, QRS duration 157+/-28 ms) and 10 normal controls. Speckle tracking applied to routine midventricular short-axis images calculated radial strain from multiple circumferential points averaged to 6 standard segments. Dyssynchrony from timing of speckle-tracking peak radial strain was correlated with tissue Doppler measures in 47 subjects (r=0.94, P<0.001; 95% CI 0.90 to 0.96). The ability of baseline speckle-tracking radial dyssynchrony (time difference in peak septal wall-to-posterior wall strain > or =130 ms) to predict response to CRT was then tested. It predicted an immediate increase in stroke volume in 48 patients studied the day after CRT with 91% sensitivity and 75% specificity. In 50 patients with long-term follow-up 8+/-5 months after CRT, baseline speckle-tracking radial dyssynchrony predicted a significant increase in ejection fraction with 89% sensitivity and 83% specificity. Patients in whom left ventricular lead position was concordant with the site of latest mechanical activation by speckle-tracking radial strain had an increase in ejection fraction from baseline to a greater degree (10+/-5%) than patients with discordant lead position (6+/-5%; P<0.05). CONCLUSIONS: Speckle-tracking radial strain can quantify dyssynchrony and predict immediate and long-term response to CRT and has potential for clinical application.
BACKGROUND: Chronotropic effects on myocardial contractility (the positive force-frequency relation) and relaxation (the positive relaxation-frequency relation) are impaired in patients with congestive heart failure and depressed left ventricular (LV) ejection fraction (systolic heart failure [SHF]). However, the force- and relaxation-frequency relation and LV-arterial coupling in patients with diastolic heart failure (DHF) has not been fully investigated. METHODS AND RESULTS: To examine inotropic and lusitropic responsiveness to atrial pacing, LV pressure-volume relations were measured using a conductance catheter and microtip manometer in patients with DHF (n = 18) and SHF (n = 11). In patients with SHF, an increase in heart rate by 40 beat/min did not affect LV end-systolic elastance (Ees), which reflects LV contractility, or the time constant of LV relaxation. By contrast, in patients with DHF, an increase in heart rate by 40 beat/min significantly enhanced Ees (2.1 vs 2.9 mm Hg/mL, P < .05) but not the time constant. Furthermore, LV-arterial coupling, quantified as Ees/arterial elastance, was impaired during pacing in patients with DHF (1.1 vs 0.8, P < .05) as well as SHF. CONCLUSIONS: In patients with DHF, the force-frequency relation was preserved, but the relaxation-frequency relation was impaired. Furthermore, LV-arterial coupling was impaired as heart rate increased, which may be related to the impaired LV function. These results suggest that the impaired relaxation-frequency relation and exacerbated LV-arterial coupling during tachycardia may be an important therapeutic target in patients with DHF.
BACKGROUND: The development of right ventricular dysfunction is a poor prognostic sign in patients with heart failure (HF). Although left ventricular dyssynchrony has been well described, it is not known whether right ventricular dyssynchrony coexists in HF. We used tissue Doppler imaging to determine whether right ventricular dyssynchrony is also present in HF patients. METHODS AND RESULTS: In 34 HF patients (mean age 56 +/- 13 years), we measured longitudinal strain at the right ventricular free wall, interventricular septum, and left ventricular lateral wall. Right ventricular and left ventricular dyssynchrony were defined as the difference in time to peak strain between the right ventricular free wall and the septum and between the left ventricular lateral wall and septum, respectively. Mean right ventricular dyssynchrony was 59 +/- 45 ms and the mean left ventricular dyssynchrony was 80 +/- 62 ms. We found a strong correlation between right ventricular dyssynchrony and pulmonary artery systolic pressure (r = 0.73; P < .001) and a negative correlation between right ventricular dyssynchrony and right ventricular fractional area change (r = -0.43; P < .02). CONCLUSION: HF patients exhibit right ventricular dyssynchrony by strain imaging which correlates with pulmonary hypertension and right ventricular dysfunction.
Our objective was to test the hypothesis that novel angle-corrected radial strain imaging can quantify left ventricular dyssynchrony associated with contractile impairment and improved with biventricular pacing. Eight open-chest dogs were studied by novel angle-corrected color-coded radial strain imaging and high-fidelity pressure-conductance catheters recording pressure-volume loops. Heart rate was controlled by right atrial pacing and all timing intervals were corrected by R-R interval (corrected interval = measured interval/(R-R interval)(1/2)). Left bundle branch block, simulated by right ventricular free wall pacing, resulted in marked radial dyssynchrony, which we defined as maximal time difference between peak segmental strain, from 39 +/- 17 to 354 +/- 49 milliseconds and stroke work decreased from 157 +/- 40 to 60 +/- 37 mJ, (P < .005 vs baseline). Depression of contractility by high-dose esmolol (end-systolic pressure-volume relationship from 5.7 +/- 2.4 to 3.6 +/- 1.0 mm Hg/mL) was associated with augmented dyssynchrony to 388 +/- 53 milliseconds (P < .05 vs baseline right ventricular pacing). Biventricular pacing improved dyssynchrony to 55 +/- 19 milliseconds and stroke work to 143 +/- 33 mJ (P < .05 vs right ventricular pacing). Changes in radial dyssynchrony correlated significantly with 6-site average regional strain (r = -0.93 +/- 0.05 individually, r = 0.80 overall) and stroke work (r = -0.88 +/- 0.12 individually, r = -0.82 overall). Angle-corrected radial strain imaging has clinical potential to quantify mechanical dyssynchrony and effects of biventricular pacing.
Atrial fibrillation (AF) and congestive heart failure share several features and often coexist in the same patients; therefore, serial assessment of regional myocardial function is important for patients with AF. However, the clinical assessment of regional myocardial function in AF is unreliable and difficult because of beat-to-beat variation. Recent reports have shown that the ratio of the preceding to the prepreceding R-R interval (RR1/RR2) can be used to assess global left ventricular systolic function. Accordingly, we tested the hypothesis that regional wall motion can be estimated from a single beat based on RR1/RR2 in patients with AF. Peak systolic strain at basal, mid, and apical segments of the septal wall was measured by Doppler tissue imaging from an apical 4-chamber view for 30 seconds in 50 patients with AF (mean ejection fraction 52.1 +/- 15.3%; mean heart rate 76.4 +/- 16.0/min). There was a positive linear relationship between peak strain and RR1/RR2 and RR1, and a negative relationship with RR2, with the correlation of peak strain to RR1/RR2 was better than that in RR1 or RR2. Furthermore, peak strain at RR1/RR2 = 1 was calculated from the linear regression and compared with the average measured value of all recorded cardiac cycles in each patient. In all cases, average peak strain showed a significant positive correlation with RR1/RR2 at each segment (r = 0.99). In conclusion, regional myocardial strain at RR1/RR2 = 1 on the linear regression represents the average value of all recorded cardiac cycles in patients with AF.
The presence of right ventricular (RV) dysfunction is an adverse prognostic indicator but current echocardiographic methods have some limitations. RV apical angles in systole and diastole were correlated with known parameters of RV function in patients without pulmonary hypertension (Group 1) and in patients with pulmonary hypertension (Group 2). RV apical angles were significantly smaller in both systole (22 +/- 7 degrees) and diastole (33 +/- 6 degrees) in Group 1 patients when compared to Group 2 (54 +/- 18 degrees, p < 0.0001 and 59 +/- 17 degrees, p < 0.0001, respectively). RV apical angles, both in systole and diastole, were strongly correlated with RV end-systolic area (R = 0.89, p < 0.0001) and end-diastolic area (R = 0.81, p < 0.0001), respectively. Similarly, the apical systolic and diastolic angle correlated well with decreased tricuspid annular plane systolic excursion (TAPSE, R = -0.76 and R = -0.73, p < 0.001) as well as with decreased RV fractional area change (R = -0.81 and R = -0.77, p < 0.001). Therefore, we conclude that this new measurement of RV apical angle is simple and useful to quantify RV apical structural and functional abnormalities that are well correlated with global RV impairment in patients with chronic pulmonary hypertension.
Both atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) bind preferentially to the natriuretic peptide A receptor. Therefore, we hypothesized that the positive inotropic and lusitropic effects of ANP might be blunted in patients with moderate congestive heart failure and high BNP levels. Micromanometers and conductance catheters were used to obtain relatively load-insensitive left ventricular pressure-volume analysis in order to compare the myocardial and load-altering actions of ANP in 20 patients with low and high plasma BNP levels. In the low-BNP group (plasma BNP levels <230 pg/ml), ANP infusion significantly decreased end-systolic pressure and end-diastolic pressure and volume, increased end-systolic elastance, and shortened left ventricular relaxation. By contrast, in the high-BNP group (plasma BNP levels >230 pg/ml), the effect of ANP infusion on LV contractility was blunted but its beneficial effects on LV diastolic function and LV-arterial coupling remained. Thus, ANP infusion may improve LV diastolic function even in patients with moderate heart failure and high plasma BNP levels.
BACKGROUND: Abnormalities in right ventricular function are known to occur in patients with pulmonary arterial hypertension. OBJECTIVE: Test the hypothesis that chronic elevation in pulmonary artery systolic pressure delays mechanical activation of the right ventricle, termed dyssynchrony, and is associated with both symptoms and right ventricular dysfunction. METHODS: Fifty-two patients (mean age 46 +/- 15 years, 24 patients with chronic pulmonary hypertension) were prospectively evaluated using several echocardiographic parameters to assess right ventricular size and function. In addition, tissue Doppler imaging was also obtained to assess longitudinal strain of the right ventricular wall, interventricular septum, and lateral wall of the left ventricle and examined with regards to right ventricular size and function as well as clinical variables. RESULTS: In this study, patients with chronic pulmonary hypertension had statistically different right ventricular fractional area change (35 +/- 13 percent), right ventricular end-systolic area (21 +/- 10 cm2), right ventricular Myocardial Performance Index (0.72 +/- 0.34), and Eccentricity Index (1.34 +/- 0.37) than individuals without pulmonary hypertension (51 +/- 5 percent, 9 +/- 2 cm2, 0.27 +/- 0.09, and 0.97 +/- 0.06, p < 0.005, respectively). Furthermore, peak longitudinal right ventricular wall strain in chronic pulmonary hypertension was also different -20.8 +/- 9.0 percent versus -28.0 +/- 4.1 percent, p < 0.01). Right ventricular dyssynchrony correlated very well with right ventricular end-systolic area (r = 0.79, p < 0.001) and Eccentricity Index (r = 0.83, p < 0.001). Furthermore, right ventricular dyssynchrony correlates with pulmonary hypertension severity index (p < 0.0001), World Health Organization class (p < 0.0001), and number of hospitalizations (p < 0.0001). CONCLUSION: Lower peak longitudinal right ventricular wall strain and significantly delayed time-to-peak strain values, consistent with right ventricular dyssynchrony, were found in a small heterogeneous group of patients with chronic pulmonary hypertension when compared to individuals without pulmonary hypertension. Furthermore, right ventricular dyssynchrony was associated with disease severity and compromised functional class.
Several well-established echocardiographic parameters used in the assessment of right ventricular (RV) performance, as well as tissue Doppler imaging (TDI) to investigate RV free wall mechanical events, were prospectively obtained from a heterogenous group of 20 patients with varying degrees of pulmonary hypertension (mean age 51 +/- 13 years; World Health Organization class average 2.8, mean pulmonary systolic pressure 78 +/- 24 mm Hg) and compared with similar data retrospectively obtained from 20 healthy volunteers (mean age 45 +/- 15 years). Patients with varying degrees of pulmonary hypertension had worse RV performance parameters than healthy volunteers (RV fractional area change 37 +/- 13% vs 52 +/- 5%, p < 0.0001; RV myocardial performance index 0.76 +/- 0.31 vs 0.29 +/- 0.11, p < 0.0001; and eccentricity index 1.41 +/- 0.57 vs 0.98 +/- 0.06, p < 0.005). Similarly, in these patients with abnormal RV performance, TDI showed statistically significant smaller peak longitudinal RV free wall strain (-21.5 +/- 9.0% vs -28.0 +/- 4.1%, p < 0.01) and significantly delayed time to peak strain (459 +/- 76 vs 388 +/- 29 ms, p < 0.0005) values than in healthy volunteers; a very strong correlation between RV mechanical delay and RV fractional area change (r = -0.89) was noted.
Echocardiographic strain imaging was used to quantify radial mechanical dyssynchrony in 38 patients who underwent cardiac resynchronization therapy. Dyssynchrony, defined as the time difference of peak radial strain in the septum versus the posterior wall, was significantly greater in patients with acute hemodynamic responses, and changes in radial dyssynchrony correlated with changes in stroke volume. A > or =130-ms difference in septal versus posterior wall peak strain when combined with a favorable left ventricular lead position was strongly predictive of immediate improvement in stroke volume with resynchronization therapy (95% sensitivity, 88% specificity), regardless of electrocardiographic QRS duration.
The objective of this study was to determine the relation between left ventricular (LV) systolic function and the ratio of preceding (RR1) to prepreceding (RR2) R-R intervals in patients with chronic atrial fibrillation (AF) and dilated cardiomyopathy. LV systolic function (Emax) was examined using a conductance catheter with a micromanometer in 13 patients with chronic AF and dilated cardiomyopathy. We calculated Emax as a load-independent index of LV contractility and compared it with RR1, RR2, and the ratio of RR1/RR2. We analyzed 50+/-13 cardiac cycles (range 18-61) in each patient. Average heart rate was 80+/-13 beats/min, and ejection fraction over all cardiac cycle in each patient measured by conductance catheter was 31+/-8%. Emax was positively correlated with RR1 and RR1/RR2 in all patients, and negatively correlated with RR2 in all patients. In each patient, correlation coefficients of Emax with RR1/RR2 were greater than those with either RR1 or RR2. Furthermore, Emax at RR1/RR2=1 in the linear regression line reflected average Emax over all cardiac cycles in each patient. In conclusion, we have shown that LV contractility correlated positively with RR1/RR2 in patients with chronic AF and dilated cardiomyopathy, and LV contractility at RR1/RR2=1 represents the average value of contractility over all cardiac cycles.
This report described an 81-year-old woman with severe symptomatic heart failure, reduced ejection fraction, mitral regurgitation, and an electrocardiographic QRS width of 118 ms who had ventricular dyssynchrony identified by echocardiographic tissue synchronization imaging. Because of her severe heart failure symptoms on maximal medical therapy, referral to implant a defibrillator, and mechanical dyssynchrony, she underwent cardiac resynchronization-defibrillator therapy with lateral left ventricular lead placement. This resulted in an immediate 30% increase in stroke volume and 35% decrease in mitral regurgitation. Echocardiographic tissue synchronization imaging may play a role in identifying mechanical dyssynchrony in patients with narrow QRS duration who may potentially benefit from cardiac resynchronization therapy.
BACKGROUND: Ventricular assist devices (VADs) are approved for destination therapy because they improve survival in end-stage heart failure (HF). VADs are powered pneumatically or electrically. Pneumatic and electric left ventricular assist devices (LVADs) and biventricular assist devices (BiVADs) provide excellent hemodynamic support at rest, but differences in their effects on exercise tolerance are unclear. We sought to evaluate the effect of devices with varying operating parameters on exercise capacity. METHODS: Exercise physiology data obtained during maximal exercise with on-line gas-exchange analysis were collected for 38 consecutive VAD-implanted HF patients referred for exercise testing. RESULTS: Electric LVADs were implanted in 18 patients, and pneumatic LVADs in 10 patients. Percent of predicted peak exercise oxygen consumption (VO2%) was significantly greater in pneumatic LVAD patients (52.1 +/- 11.1% vs 38.2 +/- 11.3%, p < 0.05). The 10 patients implanted with a pneumatically powered LVAD were compared to 10 patients implanted with a pneumatically powered BiVAD. LVAD-supported patients had a higher VO2% (52.1 +/- 11.1% vs 36.5 +/- 17.7%, p < 0.05). CONCLUSIONS: HF patients supported with a pneumatic LVAD appear to have better exercise tolerance than those receiving an electric LVAD. Patients on LVAD support have better exercise tolerance than BiVAD-supported patients. This highlights the importance of right ventricular function to exercise tolerance in HF patients, and may have implications for future VAD design.
BACKGROUND: The early diastolic mitral valve pressure gradient and the rate of left ventricular filling are determined by the rate of left ventricular relaxation and left atrial pressure at the time of mitral valve opening. Accordingly, we hypothesized that the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved systolic function. METHODS: We evaluated the relationship between the logistic time constant of left ventricular relaxation and left ventricular filling pattern calculated from the time derivative of left ventricular volume using a microtipmanometer and a conductance catheter in 26 consecutive patients with preserved left ventricular ejection fraction (>45%). Left ventricular filling patterns were determined from the maximal rates of early diastolic left ventricular filling (E velocity) and atrial filling (A velocity) before and after preload reduction by inferior venal caval occlusion. RESULTS AND CONCLUSIONS: There was no significant relationship between the logistic time constant of left ventricular relaxation and the E/A velocity ratio at baseline. However, the time constant was correlated with the E/A velocity ratio after venal caval occlusion (r=-0.47, p=0.02). Furthermore, the time constant was correlated with %E/A velocity change, which was defined as the rate of change of E/A before and after caval occlusion divided by E/A after caval occlusion, more significantly (r=-0.67, p<0.01) than with the E/A velocity ratio after caval occlusion. Thus, the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved left ventricular ejection fraction.
Nitroglycerin abbreviates left ventricular (LV) relaxation through improved hemodynamics as well as by direct actions on the myocardium. The aim of this study was to examine whether the changing systolic loading sequence during nitroglycerin administration affects LV relaxation in patients with excessive arterial load. By use of a conductance catheter with microtip manometer, the effects of intravenous nitroglycerin (0.3-0.5 microg/kg/min) on LV function and hemodynamics were examined in 39 patients with various degrees of LV contractility. Patients were divided into two groups according to LV-arterial coupling, the ratio of end-systolic elastance (Ees) to effective arterial elastance (Ea). In patients with Ees/Ea ratio > 1, nitroglycerin had no effect on the time to peak force or on the time constant of LV relaxation (tau). On the other hand, in patients with Ees/Ea < 1, which represented excessive arterial load, nitroglycerin significantly shortened the time to peak force, shifted the peak of the loading sequence from late to early systole, and significantly decreased tau without any changes in Ees. Thus, nitroglycerin improved LV relaxation in patients with excessive arterial load partly by changing the systolic loading sequence.
An 80-year-old woman with severe symptomatic heart failure (ejection fraction of 13%), and left bundle branch block (QRS duration of 160 ms) underwent cardiac resynchronization therapy (CRT). She had significant baseline dyssynchrony with a septal to posterior wall delay of 160 ms by echocardiographic tissue synchronization imaging (TSI). Despite exhaustive efforts, a stable posterior-lateral coronary vein lead position could not be achieved with the standard percutaneous approach, resulting in anterior coronary vein lead placement. This resulted in no improvement in the patient's symptoms or ventricular function. Follow-up TSI revealed earlier activation of the anteroseptal site and worsened dyssynchrony with septal to posterior wall delay of now 290 ms. This information prompted surgical revision of the left ventricular (LV) lead position via limited thoracotomy and posterior-lateral epicardial lead implantation. Pacing at the new lead site resulted in a 30% increase in stroke volume and symptomatic improvement. TSI in this case redirected lead position in a clinical nonresponder, resulting in a favorable response to CRT.
OBJECTIVES: We tested the hypothesis that an immediate reduction in mitral regurgitation (MR) after cardiac resynchronization therapy (CRT) results from improved coordinated timing of the papillary muscle insertion sites, using the novel approach of mechanical activation strain mapping. BACKGROUND: Heart failure patients with left bundle branch block often benefit acutely from CRT; however, the role and mechanism of reduction of MR are unclear. METHODS: Twenty-six consecutive patients undergoing CRT with at least mild MR were studied (ejection fraction 24 +/- 6%; QRS duration 168 +/- 30 ms). Echocardiographic Doppler and strain imaging was performed immediately before and the day after CRT, as well as in 10 normal control subjects. Mechanical activation sequence maps were constructed using longitudinal strain from 12 basal and mid-LV sites, with color coding of time-to-peak strain. RESULTS: Mitral regurgitation by the volumetric method consistently decreased after CRT: regurgitant volume from 40 +/- 20 ml to 24 +/- 17 ml and regurgitant fraction from 40 +/- 12% to 25 +/- 14% (both: p < 0.001 vs. baseline). Normal controls had uniform segmental time-to-peak strain, with a difference of only 12 +/- 8 ms between all segments. In contrast, CRT patients at baseline had a 106 +/- 74 ms time delay between papillary muscle insertion sites (p < 0.001 vs. normal). This interpapillary muscle time delay shortened after CRT to 39 +/- 43 ms (p < 0.001 vs. baseline) and was significantly correlated with reductions in mitral regurgitant fraction (r = 0.77, p < 0.001). CONCLUSIONS: Cardiac resynchronization therapy significantly and immediately reduced MR. Improved coordinated timing of mechanical activation of papillary muscle insertion sites appears to be a mechanistic contributor to immediate MR reduction by CRT.