Fumio Ohmori

Rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves

The rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves, and its relation to aging and valve anatomy are not well known. To elucidate these aspects, 75 patients aged 15 to 76 years were examined by echocardiography. Aortic valve sclerosis began from the second decade, the sclerotic index progressing with age (r = 0.72; p < 0.0001). Aortic valve calcium was noted from the fourth decade. Aortic valve pressure gradient increased approximately 18 mm Hg each decade, concomitant with progression of valve sclerosis (r = 0.78; p < 0.0001). Progression of cusp sclerosis was faster in patients with anteroposteriorly located cusps than in those with right-left-located cusps (p < 0.005), and was faster in those with eccentric cusps (width ratio of major and minor cusps > or = 1.2) than in those with symmetric cusps (p < 0.05). In patients with eccentric and anteroposteriorly located cusps, aortic valve pressure gradient increased 27 mm Hg per decade. In patients with congenital bicuspid aortic valves, the progression of aortic stenosis is rapid, and the rapidity depends to some extent on the position and eccentricity of the cusps.

Involvement of cyclo-oxygenase-generated vasodilating eicosanoid(s) in addition to nitric oxide in endothelin-1-induced endothelium-dependent vasorelaxation in guinea pig aorta

SummaryThis study investigates the vasodilatory effects of endothelin-1 (ET-1) in isolated guinea pig aortic rings in vitro. Cumulative dose-response curves to ET-1 were constructed and ET-1 actions on prostaglandin F2α (PGF2α)-precontraction were studied in both endothelium-intact and endothelium-denuded preparations, in the presence or absence of a cyclooxygenase inhibitor (indomethacin) and/or nitric oxide inhibitors (NG-nitro-L-arginine methyl ester and hemoglobin). In endothelium-intact preparations, pretreatment with indomethacin (10−5M, 30 min), alone or in combination with NG-nitro-L-arginine methyl ester (L-NAME, 10−4M), significantly augmented the constrictive responses to ET-1, whereas indomethacin, L-NAME, and hemoglobin (10−5M) had no significant effects in the endothelium-denuded preparations. Furthermore, in PGF2α-precontracted, endothelium-intact preparations, ET-1, at a dose of 10−9M, induced initial relaxation followed by subsequent contraction, while it only contracted the endothelium-denuded preparations. The initial relaxation was abolished by indomethacin, but not by L-NAME or hemoglobin. In addition, this relaxation was not inhibited by a specific ETA receptor antagonist, BQ-123 (6 × 10−6M). In addition to the involvement of nitric oxide, these results show the involvement of cyclo-oxygenase-generated vasodilating eicosanoid(s) derived from endothelium in ET-1-induced vasorelaxation in guinea pig aorta in vitro. The results also indicate that this vasorelaxation is mediated by ETB receptor activation.

Acute reduction of mitral valve area after percutaneous balloon mitral valvuloplasty : assessment with Doppler continuity equation method

Mitral valve areas before and after balloon mitral valvuloplasty were serially determined by the Doppler continuity equation method in 16 patients. Ultrasound examinations were performed before and immediately after balloon inflation and 24 hours, 1 week, and 1 month after valvuloplasty. Mitral valve area determined by the Doppler continuity equation method correlated well with that determined at catheterization by the Gorlin formula, not only before but also immediately after balloon inflation (y = 0.87 x + 0.05, standard error of estimate = 0.22 cm2, r = 0.90). Serial calculation of mitral valve area by the Doppler continuity equation method showed a slight but significant decrease in the valve area at 24 hours after balloon mitral valvuloplasty but no change after that. We conclude that the Doppler continuity equation method provides an accurate estimation of mitral valve area before and even after balloon valvuloplasty. Mitral valve area dilated by balloon inflation is decreased slightly within 24 hours after the procedure, which corroborates valve stretch as one mechanism for increasing mitral valve area with balloon valvuloplasty. Estimation of mitral valve area immediately after balloon mitral valvuloplasty may overestimate the long-term efficacy of the procedure.

Serial Doppler echocardiographic evaluation of bioprosthetic valves in the tricuspid position

OBJECTIVES This study sought to evaluate bioprosthetic valve dysfunction in the tricuspid position by serial Doppler echocardiography. BACKGROUND Few reports on the long-term results of tricuspid valve replacement with bioprosthetic valves are evaluated by serial Doppler echocardiography. METHODS Between September 1979 and December 1993, 95 patients underwent tricuspid valve replacement with bioprosthetic valves at our facility. Sixty patients who underwent serial Doppler echocardiographic examination at intervals of at least 2 years after operation were included in the final analysis. These patients were followed up from 1.5 to 13.0 years (mean 5.8 +/- 2.5). RESULTS The actuarial rates of freedom from bioprosthetic valve stenosis and regurgitation at 10 years were 46% and 51%, respectively. The prevalence of bioprosthetic valve stenosis and regurgitation increased progressively in a linear manner beginning 1 or 2 years after tricuspid valve replacement. Right heart failure developed during follow-up in 20 of the 25 patients with bioprosthetic valve dysfunction. CONCLUSIONS The long-term durability of bioprosthetic valves in the tricuspid position was substantially lower in our study than that reported in previous studies. Tricuspid bioprosthetic valve dysfunction increased progressively in a linear manner beginning 1 to 2 years after tricuspid valve replacement.

Diastolic suction in the human ventricle: Observation during balloon mitral valvuloplasty with a single balloon

Diastolic suction has been demonstrated experimentally as a ventricular negative pressure when the ventricle is allowed to relax completely in the absence of filling, but it has not been extensively studied in the in vivo human heart. In balloon mitral valvuloplasty with a single balloon, the mitral orifice is occluded and inflow is considered to be completely obstructed during a balloon inflation. To demonstrate diastolic suction in the human ventricle, we measured left ventricular pressure during valvuloplasty with a high-fidelity catheter tip manometer in 17 patients. Left ventricular pressure fell below zero during a balloon inflation in all patients (-2 to -12 mm Hg). The peak negative diastolic pressure showed significant correlations with end-systolic volume index (r = 0.53, p = 0.03) and with the ejection fraction (r = 0.80, p = 0.0001). Thus diastolic suction was demonstrated in the human beating heart, and the sucking effect was potent in the heart with small end-systolic volume and high-ejection fraction.

Different modes of sensory neuropeptides and nitric oxide involvement in relaxation of guinea-pig vessels

This study investigated involvement of calcitonin-gene-related peptide (CGRP), substance P (SP) and nitric oxide (NO) in transmural nerve stimulation (TNS)-induced non-adrenergic, non-cholinergic (NANC) relaxation in isolated guinea pig anterior mesenteric artery (AMA) and posterior caval vein (PCV). Effects of cyclo-oxygenase-generated eicosanoids were blocked with indomethacin (10(-5) M) and so were adrenergic and cholinergic responses with phentolamine (3 x 10(-6) M), propranolol (10(-6) M) and atropine (10(-6) M). In both vessels precontracted by U-46619, TNS induced relaxation, which was almost completely abolished by capsaicin pretreatment (10(-6) M, 15 minutes). In AMA, a CGRP1 receptor antagonist (human CGRP8-37, 10(-5) M) significantly attenuated the relaxation, while did both human CGRP8-37 (10(-5) M) and neurokinin-1 receptor antagonists (spantide, 2 x 10(-5) M and FK888, 3 x 10(-6) M) in PCV. NG-nitro-L-arginine methyl ester (10(-4) M) did not significantly attenuate either the NANC-or CGRP-induced relaxation in AMA. However, it significantly did attenuate both the NANC-and SP-induced relaxation, and it also considerably attenuated CGRP-induced relaxation although insignificantly, in PCV. Thus, CGRP could be significantly responsible for the NO-independent NANC relaxation in AMA, whereas both CGRP and SP could additionally relax PCV in a NO-dependent manner.

A Comparative Study on the Sites of Nitric Oxide Release on Perivascular Nerve Stimulation in Different Arteries from Guinea Pig

This study investigates the sites of nitric oxide (NO) release on perivascular nerve stimulation (PNS) in organ bath experiments with isolated guinea pig pulmonary (PA) and iliac artery (IA). All the preparations were pretreated with indomethacin (10−5M), to exclude the effects of cyclo-oxygenase-generated eicosanoids. NG-nitro-L-arginine methyl ester (L-NAME, 10 −6 M) significantly augmented the PNS-induced adrenergic contraction and subsequently administered L-arginine (3 × 10 −4 M) reversed this augmentation in both arteries. In PA, endothelial denudation did not abolish but significantly attenuated this L-NAME-induced augmentation, while it abolished the augmentation in IA. In prostaglandin F2α -precontracted PA after blockade of both adrenergic and cholinergic effector responses, PNS induced tetrodotoxin (3 × 10−7M)-sensitive relaxation. This relaxation was attenuated by L-NAME (10−6 M) and reversed by L-arginine (3 × 10−4 M). But it was not abolished by endothelial denudation. On the other hand, PNS...

Hemodynamic effect of amrinone depends on pretreatment vascular resistance in patients with evolving congestive heart failure: correlation between vascular resistance and neurohormonal activity.

We investigated the hemodynamic effects of amrinone and assessed its effects on neurohormonal factors in 15 patients with evolving congestive heart failure with various origins. We serially determined the pulmonary and systemic vascular-resistance indices after amrinone infusion and examined the relation between changes in hemodynamic parameters and changes in concentrations of norepinephrine, atrial natriuretic peptide, angiotensin II, and endothelin-1 in the pulmonary capillary wedge region (PCWR) and in the peripheral veins. Amrinone significantly reduced pulmonary vascular-resistance index (PVRI; Wood x m2) in patients with high PVRI (> or =15) before the infusion, significantly reduced systemic vascular-resistance index (SVRI; Wood x m2) in patients with high SVRI (> or =50) before the infusion, and had little effect on vascular resistances in patients with low PVRI (<15) and low SVRI (<50). The reduction in PVRI was correlated with the reduction in the endothelin-1 level (r = 0.75) in the PCWR, and the reduction in SVRI with norepinephrine level (r = 0.70) in the peripheral veins. The angiotensin II level did not change throughout the study. These findings suggest that amrinone had selective hemodynamic effects on pulmonary and systemic circulations with neurohormonal effects, according to PVRI and SVRI before infusion.