Biomedical subjects

Kaoru Dohi

Publications and source records attributed to Kaoru Dohi.

25 records · Page 2Linked to original sources

PubMed2004

Quantification of radial mechanical dyssynchrony in patients with left bundle branch block and idiopathic dilated cardiomyopathy without conduction delay by tissue displacement imaging.

Cardiac resynchronization therapy has made assessment of cardiac dyssynchrony clinically important. To test the hypothesis that echocardiographic displacement imaging can quantify dyssynchrony, 22 patients with left bundle branch block (LBBB), 14 with idiopathic dilated cardiomyopathy (IDC) without electrical conduction delay, and 22 normal controls were studied using radial angle-corrected displacement imaging. Control subjects had coordinated wall movement, whereas patients with LBBB had dyssynchrony characterized by early inward anteroseptal movement and markedly delayed posterior, lateral, or inferior regions (157 +/- 99 ms; p <0.001 vs normal). An interesting subset of patients with IDC without conduction delay (36%) had dyssynchrony with anteroseptal to posterior wall delays of 169 +/- 56 ms (p <0.001 vs normal), similar to patients with LBBB.

Adult↗

PubMed2004

Usefulness of echocardiographic tissue synchronization imaging to predict acute response to cardiac resynchronization therapy.

Echocardiographic tissue synchronization imaging (TSI) consists of color-coding time-to-peak tissue Doppler velocities. This study of 29 patients who underwent cardiac resynchronization therapy (CRT) demonstrated that differences in baseline time-to-speak velocities of opposing ventricular walls by TSI were greater in 15 patients, with an acute hemodynamic improvement. A >/=65 ms delay from the anterior septum to the posterior wall using the apical long-axis view had 87% sensitivity and 100% specificity for predicting an acute response. Although a subgroup without acute improvement had later decreases in end-systolic volume, suggesting that acute response underestimates long-term effects, TSI has potential to assist in guiding CRT.

Aged↗

PubMed2004

Candesartan prevents myocardial fibrosis during progression of congestive heart failure.

BACKGROUND: The goal of this study was to determine whether an Angiotensin II receptor antagonist, candesartan, prevents myocardial fibrosis more effectively than enalapril in animals with a non-ACE pathway during the progression of congestive heart failure (CHF). METHODS AND RESULTS: Dogs were randomly assigned to one of four groups: (1) rapid ventricular pacing (240 bpm); (2) concomitant candesartan cilexetil (1.5 mg/kg/d) and rapid pacing; (3) concomitant enalapril (1.9 mg/kg/d) and rapid pacing; (4) sham-operated control. The expression of collagen type I & III mRNA and the collagen volume fraction, which were significantly increased in the pacing-only group, were suppressed by both treatments; it was lower in the candesartan than the enalapril group. Although there were no differences in the LV stiffness coefficient (beta) among all pacing groups, the absolute changes in beta from the control values were smaller in the candesartan group, but not the enalapril group, compared with the rapid-pacing-only group. CONCLUSIONS: The present study demonstrates that in animals with a non-ACE pathway, candesartan suppressed myocardial fibrosis during the progression of CHF in comparison with enalapril. Furthermore, candesartan prevented an increase in LV stiffness. These findings imply potential clinical applications for candesartan in the management of CHF to prevent myocardial fibrosis. Further prospective evaluation and clinical study will be necessary before deciding on the net benefits of candesartan in comparison to enalapril.

Animals↗

PubMed2004

Combined angiotensin receptor blocker and ACE inhibitor on myocardial fibrosis and left ventricular stiffness in dogs with heart failure.

Angiotensin receptor blocker (ARB) and angiotensin-converting enzyme (ACE) inhibitor (ACEI) each act in a different manner to prevent myocardial fibrosis and left ventricular (LV) stiffness in animals with pathways in the heart for generating ANG II as well as ACE. A model of pacing-induced congestive heart failure (CHF) was used to test the central hypothesis that ARB + ACEI prevents myocardial fibrosis and decreases LV stiffness to a greater extent than ARB or ACEI alone. Thirty-five dogs were assigned to the following treatment protocols on the 8th day of a 4-wk pacing schedule: 1) rapid ventricular pacing, 2) ARB (candesartan cilexetil, 1.5 mg.kg(-1).day(-1)) with pacing, 3) ACEI (enalapril, 1.9 mg.kg(-1).day(-1)) with pacing, 4) ARB (candesartan cilexetil, 0.75 mg.kg(-1).day(-1)) + ACEI (enalapril, 0.95 mg.kg(-1).day(-1)) with pacing, and 5) sham operation. The LV stiffness coefficient was significantly increased after rapid pacing but was significantly lower with ARB + ACEI than with ARB or ACEI alone. The collagen volume fraction and mRNA levels of collagen I and III, which were increased by rapid pacing, were significantly lower with ARB + ACEI than with ARB or ACEI alone. Thus ARB + ACEI prevents myocardial fibrosis and decreases LV stiffness during the progression of CHF compared with ARB or ACEI alone.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2004

Alternans decay of postextrasystolic potentiation in human left ventricle.

An organ-level assessment of the total Ca2+ handled in the excitation-contraction coupling in a beating heart has been accomplished in canine left ventricles (LVs). This approach combines the intramyocardial Ca2+ recirculation fraction (RF) with the cardiac O2 consumption for the excitation-contraction coupling. The RF has conventionally been obtained from the exponential decay of the postextrasystolic (PES) potentiation of myocardial contractility. However, in canine LVs, the PES contractility in terms of Emax (end-systolic pressure-volume ratio) has been shown to decay generally in alternans under both physiological and pathological conditions. Nevertheless, the RF can be obtained from the exponential decay component in the PES Emax alternans decay. We expected that the same Ca2+ assessment could be applied to the human heart. As the first step, we investigated whether the PES Emax would decay in alternans or exponentially in patient LVs. We retrospectively analyzed 13 patient cases that had stable regular beats unexpectedly interrupted by a spontaneous extrasystole followed by a PES compensatory pause during their diagnostic examination. These patients had either mitral regurgitation, old myocardial infarction, or dilated cardiomyopathy. Their LV Emax decayed consistently in alternans within the first several PES beats. These Emax alternans decays resemble those reported in canine LVs. This finding suggests for the first time the applicability of the same organ-level RF assessment method developed for canine hearts to human hearts.

Animals↗

PubMed2003

Second-generation tissue Doppler with angle-corrected color-coded wall displacement for quantitative assessment of regional left ventricular function.

To test the hypothesis that a new tissue Doppler (TD) approach using angle-correction and transformation of velocity data to color-coded displacement data may objectively quantify regional left ventricular function, in vitro experiments were first performed with an oscillating echo target precisely controlled by a microstepping motor. Displacement varied from 1 to 15 mm (60 to 130 cycles/min) at angles of 0 degrees and 45 degrees to the echo transducer. Custom software transformed TD data to displacement data. Sixty-five subjects were then studied: 35 with wall motion abnormalities and 30 normal controls. Results were compared with independent visual assessment and caliper measurements of endocardial excursion from gray-scale images. In vitro displacement imaging strongly correlated with true displacement (r = 0.99, p <0.0001). In humans, peak transmural displacement discriminated normal results (6.3 +/- 3.2 mm) from hypokinesia (2.7 +/- 1.8 mm, p <0.05), akinesia (0.4 +/- 1.2 mm, p <0.05) from hypokinesia, and dyskinesia (-1.9 +/- 1.2 mm, p <0.05) from akinesia. Normal subendocardial displacement was 5.9 +/- 2.9 versus 4.0 +/- 3.9 mm in the epicardial layer (p <0.01). This displacement gradient was absent in abnormal segments. Displacement data correlated with endocardial excursion by calipers (parasternal views: r = 0.86, all views: r = 0.79, both p <0.0001). Overall accuracy of displacement imaging was 82% (kappa = 0.71) versus 66% (kappa = 0.43) for visual assessment with caliper data as the standard of reference. Angle-corrected displacement imaging was superior to routine visual assessment and is a promising new method to quantify regional left ventricular function.

Aged↗

PubMed2003

Addition of angiotensin II receptor antagonist to an ACE inhibitor in heart failure improves cardiovascular function by a bradykinin-mediated mechanism.

Whether cardiovascular responses to bradykinin are augmented by additional treatment with angiotensin II receptor antagonism (ATRA) to angiotensin-converting enzyme inhibition (ACEI) in congestive heart failure (CHF) is unknown. To clarify the level and functional effects of endogenous bradykinin in CHF with combined ATRA and ACEI, 35 dogs were assigned to the following treatment protocols: 1). rapid ventricular pacing (240 bpm), 2). concomitant ATRA (TCV116, 1.5 mg x kg-1.day-1) and rapid pacing, 3). concomitant ACEI (enalapril 1.9 mg x kg-1.day-1) and rapid pacing, 4). concomitant combined ATRA (TCV116, 0.75 mg x kg-1.day-1) and ACEI (enalapril 0.95 mg x kg-1.day-1) and rapid pacing, and 5). sham-operated control. Plasma bradykinin levels were increased and B(2) receptors were synergistically upregulated in CHF groups treated with combined ATRA and ACEI compared with those treated with ATRA or ACEI alone. HOE-140 (0.3 mg/kg), a bradykinin B(2) receptor antagonist, produced an increase in total systemic resistance and a decrease in left ventricular contractility in CHF with combined therapy compared with either monotherapy. Thus, endogenous bradykinin partially contributes to the synergistic improvement of cardiovascular function in CHF with additional treatment with ATRA to ACEI.

Angiotensin Receptor Antagonists↗