Yukiko Onose

PULSED TISSUE DOPPLER IMAGING OF LEFT VENTRICULAR SYSTOLIC AND DIASTOLIC WALL MOTION VELOCITIES TO EVALUATE DIFFERENCES BETWEEN LONG AND SHORT AXES IN HEALTHY SUBJECTS

Our objective was to evaluate in healthy subjects the left ventricular (LV) wall motion velocities along the long and short axes by means of pulsed tissue Doppler imaging (TDI) to clarify the differences in the LV systolic and diastolic function between both axes. Wall motion velocities were recorded at the mid-wall portion of the middle site of the LV posterior wall in the parasternal long-axis view, and at the subendocardial portion of the middle site of the LV posterior wall in the apical long-axis view by pulsed TDI in 35 healthy subjects (mean age 26 +/- 10 years, mean heart rate 72 +/- 7 bpm). In all subjects, the LV pressure curve, its first derivative (dP/dt), the LV wall motion velocity, the phonocardiogram, and the electrocardiogram were simultaneously recorded. The systolic wave of the LV posterior wall motion velocity exhibited 2 peaks: the first and second systolic waves (Swl and Sw2, respectively). The diastolic wave also exhibited 2 peaks, the early diastolic and atrial systolic waves. The Swl along the long axis was greater than either the Sw1 and Sw2 along the short axis or the Sw2 along the long axis. The peak Sw1 along the long axis coincided with the peak dP/dt and was slightly earlier than the peak Swl along the short axis. The onset of Sw1 along the long axis coincided with the onset of the first heart sound. The Sw2 along the short axis was greater than that along the long axis. The early diastolic wave along the short axis was greater than that along the long axis, whereas the atrial systolic wave along the long axis was greater than that along the short axis. Thus, in healthy subjects, shortening of the longitudinal fibers predominated over that of the circumferential fibers during early systole, whereas shortening of the circumferential fibers predominated over the longitudinal fibers during the ejection phase. During diastole, the circumferential fibers predominated in the LV wall expansion at early diastole, whereas the longitudinal fibers predominated at atrial systole. In conclusion, pulsed TDI provided information that is useful in understanding the characteristics of LV wall motion along the long and short axes.

Effect of aging on diastolic left ventricular myocardial velocities measured by pulsed tissue Doppler imaging in healthy subjects.

We evaluated the effect of aging on diastolic left ventricular (LV) wall motion velocity in 80 healthy persons with the use of pulsed tissue Doppler imaging. The wall motion velocity patterns were recorded at the middle regions of the LV posterior wall and ventricular septum in the parasternal (along the short axis) and apical (along the long axis) LV long-axis views. In the posterior wall, the peak early diastolic wall motion velocities (Ews) along both axes correlated inversely with age (long axis: r = -0.61, P <. 0001; short axis: r = -0.55, P <.0001), and the peak atrial systolic wall motion velocities(Aws) along both axes correlated directly with age (long axis: r = 0.59, P <.0001; short axis: r = 0.65, P <.0001). In the ventricular septum, the Ew along the long axis correlated inversely with age (r = -0.51, P <.0001), and the Aws along both axes correlated directly with age (long axis: r = 0.57, P <.0001; short axis: r = 0.53, P <.0001). The Ews along both axes at the posterior wall correlated directly with the peak early diastolic transmitral flow velocity. The Aws along both axes at the ventricular septum and posterior wall correlated directly with the peak atrial systolic transmitral flow velocity. The times from the second heart sound to the peak of the early diastolic waves of the ventricular septum and posterior wall along both axes significantly increased with age. The times from the aortic component of the second heart sound to the peak of the early diastolic motion velocities along both axes were significantly longer at the ventricular septum than at the posterior wall. Pulsed tissue Doppler imaging may be useful for evaluating the effect of aging on diastolic LV function in healthy persons.

Left ventricular diastolic properties of hypertensive patients measured by pulsed tissue Doppler imaging.

Examination of left ventricular (LV) diastolic dysfunction in hypertensive patients has been based on parameters obtained from the transmitral flow velocity during pulsed Doppler echocardiography. However, these parameters are affected by loading conditions. We evaluated LV diastolic function along the longitudinal and transverse axes by pulsed tissue Doppler imaging (TDI) in 50 hypertensive (HT) patients and 36 age-matched healthy volunteers (N). Transmitral flow velocity was recorded by pulsed Doppler echocardiography. LV posterior wall motion velocity along the longitudinal and transverse axes also was recorded by pulsed TDI. In both groups, peak early diastolic velocity of the LV posterior wall (Ew) along the transverse axis (N: 15.8+/-5.2 cm/s, HT: 12.2+/-4.4 cm/s) was higher than that along the longitudinal axis (N: 12.7+/-3.1 cm/s, HT: 9.5+/-3.3 cm/s). Peak atrial systolic velocity of the LV posterior wall (Aw) along the longitudinal axis (N: 9.1+/-1.8 cm/s, HT: 9.7 +/-2.6 cm/s) significantly exceeded that along the transverse axis (N: 8.0+/-2.2 cm/s, HT: 8.4+/-2.4 cm/s) in both groups. The Ews were lower and the Aws were higher along both axes in the patient group than in the control group. The time intervals from the aortic component of the second heart sound to the peak of the early diastolic wave (IIA-Ews) along both the transverse (N: 142+/-18 ms, HT: 154+/-19 ms) and longitudinal (N: 151 16 ms, HT: 162+/-20 ms) axes were longer in the patient group. In 29 patients, Ews along both axes correlated negatively (transverse: r = -0.80, P < .0001; longitudinal: r = -0.71, P < .0001) and IIA-Ews correlated positively (transverse: r = 0.81, P < .0001; longitudinal: r = 0.74, P < .001) with the time constant of the LV pressure decay during isovolumic diastole. The Aws along both axes in the 24 patients without pseudonormalization in transmitral flow velocity correlated positively (transverse: r = 0.60, P < .001; longitudinal: r = 0.74, P < .0001) with the LV end-diastolic pressure. In conclusion, LV relaxation and filling along the longitudinal and transverse axes were impaired in many patients with hypertension. Pulsed TDI was useful for evaluating LV diastolic dynamics in this disease.

Influence of Aging on Systolic Left Ventricular Wall Motion Velocities Along the Long and Short Axes in Clinically Normal Patients Determined by Pulsed Tissue Doppler Imaging

Our objective was to evaluate the influence of aging on left ventricular (LV) regional systolic function along the long and short axes in clinically normal patients. We recorded LV wall motion velocity patterns at the mid-wall portion of the middle of the LV posterior wall in the parasternal long-axis view (short-axis direction) and at the endocardial portion of the middle of the LV posterior wall in the apical long-axis view (long-axis direction) with pulsed tissue Doppler imaging in 80 normal patients (age range 15 to 78 years). In all patients the LV pressure curve and its first derivative (dP/dt) were recorded. The systolic wave of the LV posterior wall motion velocity pattern exhibited 2 peaks, the first (Sw(1)) and second (Sw(2)) systolic waves. No significant changes were seen with aging in the percent LV fractional shortening determined by M-mode echocardiography, LV ejection fraction determined by left ventriculography, the peak Sw(1) and Sw(2) along the short axis, the peak Sw(2) along the long axis, and the peak dP/dt. The peak Sw(1) along the long axis correlated inversely with age (P <.0001) but did not correlate significantly with the peak dP/dt. These results suggest that shortening of the longitudinal fibers in early systole is impaired with increased age in healthy individuals. This impairment results in insufficient spherical change in the LV cavity, although global LV pump function and myocardial contractility are maintained.

Effect of an Acute Increase in Afterload on Left Ventricular Regional Wall Motion Velocity in Healthy Subjects

We recorded left ventricular (LV) wall motion velocities before and after angiotensin II infusion by pulsed tissue Doppler imaging in 20 healthy subjects, and evaluated the responses of systolic and diastolic LV function along the long and short axes during an acute increase in afterload. Angiotensin II was administered intravenously to obtain a 30% increase in mean blood pressure. After angiotensin II infusion, LV end-systolic dimension and end-systolic circumferential wall stress increased significantly, and the percentage of LV fractional shortening decreased significantly. Peak first systolic LV wall motion velocity (Sw1 ) along the long axis decreased markedly compared with that along the short axis, and peak second systolic LV wall motion velocity (Sw2 ) along the short axis decreased significantly compared with that along the long axis. Early diastolic LV wall motion velocities along both the long and short axes decreased significantly, whereas atrial systolic LV wall motion velocity did not change. In conclusion, an acute increase in afterload caused a significant decrease in longitudinal fiber shortening during the isovolumic contraction phase (Sw1 along the long axis), circumferential fiber shortening during the ejection phase (Sw2 along the short axis), and LV relaxation during early diastole (early diastolic LV wall motion velocities along both axes) in healthy subjects. Pulsed tissue Doppler imaging may be useful for detecting the effect of various loading conditions on LV wall motion velocities along the long and short axes.

Subendocardial Motion in Hypertrophic Cardiomyopathy: Assessment from Long- and Short-Axis Views by Pulsed Tissue Doppler Imaging * ** *

BACKGROUND Tissue Doppler imaging (TDI) is a recently developed technique that allows the instantaneous measurement of intrinsic regional myocardial motion velocity. Pulsed TDI is capable of separately assessing left ventricular (LV) regional motion velocity caused by circumferential and longitudinal fiber contraction. This particular feature of function is still controversial in patients with hypertrophic cardiomyopathy (HC). METHODS To better characterize intrinsic circumferential and longitudinal LV systolic myocardial function in HC, we used pulsed TDI to measure short- and long-axis LV motion velocities, respectively. The subendocardial motion velocity patterns at the middle of the LV posterior wall (PW) and ventricular septum (IVS) in LV parasternal and apical long-axis views were recorded by pulsed TDI in 19 patients with nonobstructive HC and in 21 normal controls (NC). RESULTS Peak short- and long-axis systolic subendocardial velocities in both the LV PW and IVS were significantly smaller in the HC group than in the NC group, and the time to peak velocity was significantly delayed. Furthermore, peak PW systolic velocity was significantly greater along the long axis than along the short axis in the NC group (8.8 +/- 1.5 cm/s vs 8.2 +/- 1.4 cm/s, P <.05), whereas the opposite was observed in the HC group (6.1 +/- 1.2 cm/s vs 7.5 +/- 1.0 cm/s, P <.0001). No significant differences were found in either group between the long- and short-axis IVS velocities (HC: 5.9 +/- 1.4 cm/s vs 5.5 +/- 1.3 cm/s; NC: 7.8 +/- 1.3 cm/s vs 7.9 +/- 1.6 cm/s). CONCLUSIONS By using the capability of pulsed TDI for the evaluation of intrinsic myocardial velocity instantaneously in a specific region and direction, we found impairment of LV myocardial systolic function in patients with HC not only in the hypertrophied IVS but also in the nonhypertrophied LV PW. We also found a greater decrease in LV PW velocities along the long axis than the short axis, suggesting greater impairment of long-axis contraction in patients with HC. Because our HC patients did not appear to have excessive intracavitary pressure, these results suggest that the relatively normal-appearing PW is directly affected by the HC pathologic process.

Increased soluble platelet/endothelial cell adhesion molecule-1 in the early stages of acute coronary syndromes.

Specific molecules including inflammatory cell adhesion molecules mediate attachment of blood leukocyte and platelets to the endothelium and mononuclear cell migration into the arterial intima. However, the clinical significance of soluble cell adhesion molecules very early in the course of acute coronary syndrome is not known. We assayed platelet/endothelial cell adhesion molecule-1 (PECAM-1, CD31), intercellular adhesion molecule-1 (ICAM-1, CD54), and P-selectin (CD62P) in plasma obtained from 20 patients within 3 h after the onset of acute myocardial infarction (AMI); 16 patients with unstable angina pectoris; 20 patients with stable angina pectoris, and 28 controls. Blood samples were obtained on hospital admission and again 1 week after onset of AMI and unstable angina, and on admission in patients with stable angina and controls. Plasma PECAM-1 concentration (ng/ml) on admission was higher in patients with AMI (25.6+/-4.7) and unstable angina (24.7+/-4.4) than in stable angina (20.5+/-4.4) and control (18.8+/-3.8) groups. In both AMI and unstable angina, plasma PECAM-1 had decreased significantly by 1 week (AMI, 20.8+/-4.0; unstable angina, 21.0+/-4.1). Plasma ICAM-1 concentration (ng/ml) on admission was higher in patients with AMI (254+/-70), unstable angina (264+/-78), and stable angina (245+/-68) than in controls (201+/-56), but did not differ between the three coronary syndromes. Plasma P-selectin concentration did not differ between the four groups, including controls. Therefore, soluble PECAM-1 concentration may be a sensitive markers providing early diagnostic aid in acute coronary syndromes.

Plasma concentrations of fibrinolytic factors in the subacute phase of myocardial infarction predict recurrent myocardial infarction or sudden cardiac death

BACKGROUND The prognostic value of plasma concentrations of tissue type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), and C-reactive protein has been reported in patients with coronary artery disease. However, the association between cardiac events and these factors during the acute and subacute phases of myocardial infarction (MI) is unknown. The purpose of this study was to determine whether elevated plasma concentrations of t-PA, PAI-1, and C-reactive protein in patients with MI are associated with future recurrent MI or sudden cardiac death. METHODS We studied 106 consecutive patients who survived a confirmed first MI between 1993 and 1998 in our hospital. The control group consisted of 50 patients who had no significant coronary artery stenosis. Blood samples were obtained at the time of admission for acute MI and on the 28th day after admission. Patients were followed for a mean of 50 months after these measurements. The primary end points were sudden cardiac death and fatal or nonfatal acute MI. RESULTS Of the 92 patients who were available for follow-up, 10 had cardiac events. Both the plasma t-PA and PAI-1 concentrations were elevated on day 1 of acute MI compared to the control group and decreased by day 28, but remained higher than those in the controls. Plasma C-reactive protein concentration was also elevated on day 1 and decreased by day 28. Using a stepwise variable choice model of Cox proportional hazards analysis including these fibrinolytic factors and C-reactive protein, only the t-PA concentration in the subacute phase was a significant predictor of cardiac events (relative risk per S.D. 3.20, P<0.01). We further found that independent of other risk factors, an elevated t-PA concentration was predictive of cardiac events. CONCLUSIONS This study reveals that a rise in endogenous t-PA concentration during the subacute phase of MI could predict recurrent MI or sudden cardiac death.

Transthoracic Doppler Echocardiographic Measurement of Left Atrial Appendage Blood Flow Velocity: Comparison with Transoesophageal Measurement

AIM We validated transthoracic echocardiographic measurements of left atrial appendage flow velocity by comparing them with transoesophageal echocardiographic measurements. METHODS AND RESULTS Eighty-four consecutive patients (mean age, 64.6 years) with various cardiac diseases, who underwent both transthoracic echocardiography and transoesophageal echocardiography were studied. Thirty-two patients were in sinus rhythm, and the remaining 52 patients were in atrial fibrillation. On transthoracic echocardiography, the transducer was placed somewhat superior and outside from the position viewing the conventional parasternal short-axis image of the aortic valve, so that the angle between left atrial appendage midline and Doppler beam could be narrowed. The left atrial appendage flow velocity pattern was recorded by pulsed Doppler mode with a sampling volume placed at the left atrial appendage orifice on both transthoracic echocardiography and transoesophageal echocardiography. In both approaches, the peak emptying velocity (LAA-E) and the peak filling velocity (LAA-F) of the left atrial appendage were measured. In sinus rhythm, the LAA-E was detectable in 25 of the 32 patients (78.1%) and the LAA-F in 20 of the 32 patients (62.5%). Both LAA-E and LAA-F were detectable in 46 of the 52 patients (88.5%) in atrial fibrillation. Good correlations of LAA-E and LAA-F were observed between transthoracic echocardiography and transoesophageal echocardiography measurements in sinus rhythm (r=0.94, r=0.95, respectively; both, P<0.0001) and in atrial fibrillation (r=0.89, r=0.95, respectively; both, P<0.0001). CONCLUSIONS The left atrial appendage flow velocities could be sufficiently recorded and assessed by transthoracic echocardiography in 84 Japanese unselected consecutive patients with sinus rhythm or atrial fibrillation.

Effects of angiotensin II receptor antagonists on [(123)I]metaiodobenzylguanidine myocardial imaging findings and neurohumoral factors in chronic heart failure.

Abstract Previous studies have not investigated the ef-ficacy of angiotensin II (AII) receptor antagonists against cardiac sympathetic overactivity in patients with chronic heart failure (CHF) using [123I]metaiodobenzylguanidine (MIBG) myocardial imaging. We studied 34 CHF patients with fractional shortening of the left ventricular (LV) diameter ≦25% or LV ejection fraction ≦45% in echocardiograms. An AII receptor antagonist (losartan or candesartan) was administered. Before and 6 months after the administration, MIBG myocardial imaging and echocardiography were performed, and neurohumoral factors were investigated. MIBG imaging revealed that the antagonist did not significantly change the heart-to-mediastinum ratio. However, the washout rate fell significantly (from 32.6% ± 7.6% to 28.2% ± 7.5%; P < 0.001). No significant changes occurred in LV diameter, fractional shortening, or LV ejection fraction. Circulating atrial (ANP) and brain natriuretic peptides (BNP), and aldosterone fell significantly. Changes in the MIBG washout rate correlated positively with changes in BNP (r = 0.35, P < 0.05). In 19 patients also being treated with angiotensin-converting enzyme (ACE) inhibitors, the MIBG washout rate also fell significantly with AII antagonists, as did BNP and aldosterone. The decreased MIBG washout and BNP in patients with CHF induced by the AII receptor antagonists suggests the efficacy of these agents in modifying cardiac sympathetic function and neurohumoral factors, even with ACE inhibition. Combination therapy with AII receptor antagonists and ACE inhibitors appears effective for CHF.