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Biomedical subjects

Y Koiwaya

Publications and source records attributed to Y Koiwaya.

At least 19 recordsLinked to original sources
PubMed1996

Increased plasma adrenomedullin levels in chronic congestive heart failure.

Adrenomedullin is a potent vasodilator peptide and occurs in circulating blood of human beings and experimental animals. Because it is produced in intact aorta of rats and in cultured vascular endothelial cells, adrenomedullin seems to participate in regulation of local vascular tone. To determine the pathophysiological roles of adrenomedullin, we investigated its plasma concentrations in 49 patients with heart failure. Plasma adrenomedullin levels increased significantly with advancing severity of the disease (New York Heart Association functional class I, 4.1 +/- 1.0; II, 5.6 +/- 1.6; III, 6.4 +/- 0.8; IV, 13.2 +/- 6.8 (fmol/l). Plasma adrenomedullin was correlated with pulmonary artery pressure (r = 0.44, p = 0.0114) and pulmonary capillary wedge pressure (r = 0.53, p = 0.0002). These findings indicate that adrenomedullin may play some important role in the pathophysiologic makeup of heart failure by its vasodilating effects against the concomitant exaggeration of humor pressor agents such as catecholamine and the renin-angiotensin system. Hemodynamic changes in pulmonary circulation may have some influence on the increased synthesis and secretion of plasma adrenomedullin in chronic congestive heart failure.

Adrenomedullin↗
PubMed1996

Increased plasma adrenomedullin in acute myocardial infarction.

Adrenomedullin has a potent vasodilating effect comparable to that of calcitonin gene-related peptide. To investigate the pathophysiologic role of endogenous adrenomedullin, we determined sequentially the plasma adrenomedullin level in 15 consecutive patients with acute myocardial infarction (AMI). Plasma adrenomedullin was higher immediately after the onset of AMI and decreased gradually; plasma levels during the 3-week period after the AMI were higher than plasma levels in 15 healthy control subjects (p < 0.001), with higher levels in patients with congestive heart failure than in patients without congestive heart failure throughout the period of the study (p < 0.05). Plasma adrenomedullin was positively correlated with pulmonary capillary wedge pressure, pulmonary arterial pressure, right atrial pressure, and heart rate in the early stage of AMI. These findings suggest that the elevation of plasma adrenomedullin is related to the retention of body fluid volume, the enhancement of sympathetic activity, and/or the elevation of pressure in pulmonary vascular beds. Adrenomedullin may act against excessive vasoconstrictors increased in AMI.

Adrenomedullin↗
PubMed1996

Plasma adrenomedullin concentration in patients with heart failure.

We measured plasma concentrations of adrenomedullin (AM), a novel bioactive peptide with potent vasodilator activity, in 21 patients with chronic congestive heart failure due to various heart diseases and compared them to levels in age- and sex-matched healthy subjects to examine the pathophysiological role of plasma AM in heart failure. In addition, the relationship between plasma AM and other hormones known to control the cardiovascular system was examined in these patients. The plasma AM level in the patients with heart failure was significantly (P < 0.01) higher than that in the control subjects (mean +/- SEM, 2.94 +/- 0.15 fmol/mL; n = 16), with a significantly (P < 0.05) higher concentration in patients in class III or IV (11.82 +/- 1.81 fmol/mL; n = 5) of the New York Heart Association functional classification than in those in class I or II (8.74 +/- 0.44 fmol/mL; n = 16). There were no significant correlations between plasma AM and catecholamine levels, whereas the plasma AM level was significantly correlated with the concentrations of plasma atrial natriuretic peptide (r = 0.58; P < 0.01), brain natriuretic peptide (r = 0.47; P < 0.05), and PRA (r = 0.77; P < 0.01) in the patients. Thus, the plasma AM concentration increased in proportion to the severity of heart failure along with the hormones known to modulate the development of congestive heart failure. The present findings suggest a possible role for AM as a circulating hormone participating in the defense mechanism against further deterioration of congestive heart failure in patients with heart disease.

Adrenomedullin↗
PubMed1994

The severity of residual coronary stenosis immediately after thrombolytic therapy does not influence the size of later left ventricular asynergic area.

To determine whether the severity of residual coronary artery stenosis immediately after thrombolytic therapy influences the size of later left ventricular (LV) asynergic area, we reviewed coronary angiograms (CAGs) and left ventriculograms (LVGs) of 31 patients with acute myocardial infarction (AMI). All patients received intracoronary urokinase therapy within 6 h after onset of AMI due to total occlusion of the proximal left anterior descending coronary artery (LAD). A dose of 960,000 IU urokinase was infused into the ostium of the left coronary artery over 40 min. Patients in whom antegrade blood flow without delayed distal filling was restored received rigorous anticoagulation. The patients were divided into three groups according to the severity of the coronary lesion immediately after urokinase therapy: 9 patients with complete occlusion in Group 1, 15 with > 90% stenosis in Group 2, and 7 with < 90% stenosis in Group 3. There were no significant differences in the baseline clinical characteristics among the patients in the three groups. The LADs in Group 1 were also totally occluded 1 month after urokinase therapy, the treated vessels in both Groups 2 and 3 were still patent, and patients in Group 2 showed a further reduction in residual stenosis. When LV asynergic area, regional wall motion, and global ejection fraction (EF) were compared among the three groups, no significant differences were demonstrated. In comparison with the data immediately after urokinase therapy, all parameters 1 month after therapy were significantly improved in both Groups 2 and 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Coronary angiographic ruptured atheromatous plaque as a predictor of future progression of stenosis.

To determine whether or not angiographic coronary morphology can predict future development/progression of narrowing, we reviewed coronary angiograms (CAGs) from 29 patients who underwent CAG studies twice but who had no myocardial revascularization during the period of the studies. The mean age of the patients was 52.9 +/- 8.5 years, and the mean interval between the studies was 25.4 +/- 22.6 months. Mean luminal diameter stenosis of 77 lesions that reduced the diameter by 50% or more on either CAG, but were not totally occluded on the initial CAG, increased from 62% to 79% (p less than 0.01). Progression of stenosis developed in 35 lesions (45%); the progression in 13 lesions of the 35 (37%) was on sites associated with no stenosis or mild stenosis on the initial CAG. No relation was found between the development/progression of stenosis and either its initial severity or elapsed time; however, the prevalence of the development/progression of stenosis was more frequent on sites with possible or probable ruptured atheromatous plaque on the initial CAG than on sites without such plaque (p less than 0.05). The evidence suggests that there is no apparent relation between the future development/progression of coronary narrowing and either the severity of stenosis on the initial CAG or elapsed time but that some of the development/progression can be predicted on the basis of certain specific coronary morphology.

Adult↗
PubMed1990

[Left ventricular ejection fraction derived from resting 201Tl myocardial images].

To determine if resting 201Tl myocardial scintigraphy (rest-Tl) provides the information on left ventricular function, we compared preliminarily the parameters derived from rest-Tl with left ventricular ejection fraction (LVEF) derived from left ventriculography; while the parameters included Extent Score (ES), Severity Score (SS), Percent Uptake (PU), Area Index (AI). AI was derived from the averaging of [(A/B) x 100] in three or four central slices of short axis view on single photon emission computed tomography (A; area surrounded by inner edge of 201Tl myocardial image, B; area surrounded by outer edge of 201Tl myocardial image). The patients were comprised of 38 males and 16 females with a mean age of 53 years old (range 15-70) and classified into two groups; patients with myocardial infarction (n = 28, Group I), and patients with miscellaneous disease but without myocardial infarction (n = 26, Group II). In Group I, ES, SS and AI correlated with LVEF. If ES was less than 0.30, SS was less than 26.2, or AI was less than 19.8, LVEF was suggested more than 60% with an accuracy of 92%, 85% and 85%, respectively. In Group II, these did not correlate with LVEF. If there were area with PU less than 70% in the region perfused by left anterior descending artery or left circumflex artery, LVEF was less than 60% with an accuracy of 78%. In conclusion, rest-Tl images provide some informations on left ventricular function in some patients.

Adolescent↗
PubMed1989

Pacing failure due to markedly increased stimulation threshold 2 years after implantation: successful management with oral prednisolone: a case report.

In a 53-year-old male who had undergone transvenous permanent pacing, intracardiac potential reduced progressively over a 2-year period and exit block developed, while the stimulation threshold was markedly increased. After oral prednisolone for 5 months, the stimulation threshold reduced gradually along with an increase in intracardiac potential, culminating in no recurrence of exit block for the ensuing 2 years. The clinical course suggests that progressive reduction in intracardiac potential may have presaged the late development of exit block, and that oral prednisolone may be a therapeutic approach for the restoration of ventricular capture even 2 years after implantation.

Administration, Oral↗
PubMed1988

Aortic regurgitation secondary to diastolic prolapse of a tubular intimal flap into the left ventricle in a patient with anuloaortic ectasia.

A 32-year-old man with distal skeletal manifestations of Marfan's syndrome had experienced shortness of breath and orthopnea for one month. Physical examination showed the presence of severe aortic regurgitation. Both noninvasive and invasive studies revealed that the aortic regurgitation was induced by previously undescribed peculiar and unusual etiology: diastolic prolapse of a circumferentially dissected tubular intimal flap into the left ventricle. The patient underwent surgical repair with striking clinical improvement.

Adult↗
PubMed1988

Angiographic features in the infarct-related artery after intracoronary urokinase followed by prolonged anticoagulation. Role of ruptured atheromatous plaque and adherent thrombus in acute myocardial infarction in vivo.

To unravel sequential morphological features in infarct-related coronary arteries (IRCA), we performed coronary angiography (CAG) before, during, and immediately after intracoronary urokinase infusion in 43 consecutive patients. After 1 month of rigorous anticoagulation by intravenous heparin and subsequent oral warfarin or after the same period of treatment by antiplatelet agents, we repeated CAG in all patients except for one, who died 6 days after thrombolytic therapy. Thirty-two IRCAs were totally occluded, and 11 were severely occluded at baseline. With recanalization and/or reduction in luminal narrowing at the site of the occlusion by progressive removal of the overlying thrombus and plaque content, we recognized the development of extraluminal contrast pooling in an ellipsoid shape (type A), single or paired linear radiolucency(ies) with or without outpouching (type B), and definite outpouching (type C). The development of type A, B, and C lesions occurred in 4, 6, and 0 IRCAs immediately after thrombolytic therapy and in 0, 18, and 3 IRCAs 1 month later, respectively. Throughout the study, at least one of type A-C lesions developed in 23 of 43 (53.5%) IRCAs. Lesion development proceeded from total or severe occlusion to type A, then to type B or C, both accompanied by progressive reduction in luminal narrowing and frequent enlargement of outpouching. A postmortem study in one patient whose CAG immediately after thrombolytic therapy was interpreted as a type B lesion demonstrated a ruptured plaque with paired ridges. Serial observations in vivo indicate that many IRCAs are associated with a complex underlying spatial structure, probably composed of some part of ruptured atheromatous plaque with or without adherent thrombus. Recognition and identification of such complex structures beneath the accumulated thrombus are of great importance in both CAG interpretation and elucidation of the pathophysiological sequence of acute myocardial infarction in vivo and may enable prevention or more effective therapy of acute coronary events.

Aged↗
PubMed1987

A case of swallow syncope induced by vagotonic visceral reflex resulting in atrioventricular node suppression.

A 48-year-old man repeatedly experienced syncope associated with paroxysmal atrioventricular block (PAVB) while swallowing. PAVB ("Mobitz type II" AH block) occurred only when "balloon-like" deformity of the lower esophagus developed. Balloon inflation in the lower esophagus induced PAVB. However, inflation in the upper or mid portion, or other vagal maneuvers, caused only sinus slowing. PAVB was not induced after intravenous atropine. The PAVB in this patient was probably caused by a vagotonic reflex triggered by tensoreceptors in the lower esophagus, resulting in selective suppression of the atrioventricular node.

Deglutition↗