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Biomedical subjects

K Komamura

Publications and source records attributed to K Komamura.

At least 37 records · Page 2Linked to original sources
PubMed1999

Clinical usefulness of 123I meta-iodobenzylguanidine imaging in predicting the effectiveness of beta blockers for patients with idiopathic dilated cardiomyopathy before and soon after treatment.

OBJECTIVE: To investigate the value of iodine-123 meta-iodobenzylguanidine (MIBG) myocardial imaging for defining high risk patients with idiopathic dilated cardiomyopathy from among candidates for beta blocker treatment, and for predicting functional improvement of the left ventricle in the early stages of treatment. METHODS: Echocardiographic indices, neurohormonal measurements, and myocardial MIBG distribution were assessed at baseline and after one month and three months of treatment in 27 patients with idiopathic dilated cardiomyopathy. Patients were classified into two groups, based on whether they reached a daily dose of > 20 mg of metoprolol without deterioration of heart failure at three months (group A, n = 20) or not (group B, n = 7). RESULTS: There were no significant differences in the echocardiographic indices or neurohormonal activity at baseline between the two groups, but MIBG uptake was higher, and the washout rate lower, in group A than in group B. After one month, though there were no significant changes in echocardiographic and neurohormonal variables, the heart to mediastinal (H/M) ratio on the delayed image was increased in group A but not in group B. In group A, the degree of increase in the H/M ratio on the delayed image after one month was also correlated with the degree of reduction in plasma concentrations of noradrenaline after three months. CONCLUSIONS: MIBG myocardial imaging may be useful for predicting the outcome of beta blocker treatment for heart failure patients with idiopathic dilated cardiomyopathy.

3-Iodobenzylguanidine↗
PubMed1999

Effects of long-term treatment with pimobendan on neurohumoral factors in patients with non-ischemic chronic moderate heart failure.

To evaluate the effects of the addition of pimobendan to an optimal basic regimen on plasma levels of neurohumoral factors in patients with non-ischemic, moderate heart failure during 2-year follow-up. This prospective, observational study involved 16 patients with non-ischemic, moderate heart failure [New York Heart Association (NYHA) functional class IIM-III] receiving an optimal basic regimen of digitalis, diuretics and angiotensin-converting enzyme inhibitor. Eight patients (Group P) were also administered pimobendan at a dose of 2.5 or 5 mg daily, while the other 8 served as controls (Group C). After 3 months of pimobendan administration, the plasma levels of norepinephrine and atrial natriuretic peptide and brain natriuretic peptide decreased and left ventricular ejection fraction improved. After 1 year, the cardiac symptoms, assessed using the Specific Activity Scale as well as the NYHA functional class, improved and the left ventricular end-diastolic diameter decreased. These improvements in Group P were maintained for 2 years. However, in Group C, the cardiac symptoms and the neurohumoral factor levels remained unchanged or deteriorated during this study, and one patient died of heart failure. Long-term combination therapy with the optimal basic regimen and pimobendan has potentially beneficial effects on neurohumoral factor levels and cardiac symptoms in patients with non-ischemic, chronic moderate heart failure.

Adult↗
PubMed1998

Nisoldipine selectively induces coronary vasodilation and improves mild myocardial ischemia in dogs: a potential role of cellular acidosis.

We examined whether nisoldipine, a calcium (Ca) channel blocker, increases coronary blood flow (CBF) without decreasing aortic blood pressure (AoP) with ischemic and nonischemic hearts, and whether the presence of cellular acidosis in ischemic myocardium contributes to the augmentation of coronary vasodilation due to nisoldipine. In 42 dogs, coronary perfusion pressure (CPP) was reduced so that CBF decreased to 60% of the baseline, and CPP was maintained constant thereafter. First, we administered nisoldipine into a systemic vein in the ischemic and nonischemic hearts. Second, nisoldipine was administered into the canine coronary artery of the ischemic myocardium, with and without administration of either sodium bicarbonate (NaHCO3), sodium hydroxide (NaOH), or amiloride. Nisoldipine (0.25-4.0 mg/kg, i.v.) increased CBF by 59% in the ischemic myocardium more than the nonischemic myocardium (by 34%) without reducing AoP. The infusion of nisoldipine (40 ng/kg/min, IC) increased CBF markedly by about 55% in the ischemic myocardium with increases in fractional shortening (FS; 11 +/- 2% to 21 +/- 2%) and lactate extraction ratio (LER; -19 +/- 4% to 15 +/- 2%). Increases in CBF, FS, and LER were markedly attenuated during administration of nisoldipine with concomitant administration of either NaHCO3 or NaOH. Furthermore, the extent of increases in CBF (54 +/- 2 mL/100 g/min), FS (13 +/- 2%), and LER (-17 +/- 4%) were also markedly attenuated due to the concomitant treatment with amiloride. We conclude that myocardial cellular acidosis plays an important role in mediating coronary vasodilation affected by nisoldipine in the ischemic myocardium. H+ may modulate the property of voltage-dependent Ca channels via Na(+)-H+ exchange.

Acidosis↗
PubMed1998

Elevation of plasma adenosine levels may attenuate the severity of chronic heart failure.

Adenosine is known to be an endogenous cardioprotective substance. Since we have reported that adenosine levels increase in patients with chronic heart failure, we tested whether further elevation of the adenosine levels due to dipyridamole or dilazep for 6 months modulates the pathophysiology of chronic heart failure. In patients with chronic heart failure, either dipyridamole (300 mg/d n = 17) or dilazep (300 mg/d n = 5) were administered for 6 months. Twenty-two patients (mean +/- SE age 58 +/- 4 years old) attending a specialized chronic heart failure (CHF) clinic over 6 months and judged as in New York Heart Association (NYHA) function class II or III were examined. The other drugs used for the treatment of CHF were not altered during the study. There were 5 patients with CHF caused by ischemic heart diseases, and 17 patients with either valvular heart diseases or dilated cardiomyopathy. We found that increases in the plasma adenosine levels (202 +/- 34 and 372 +/- 74) nmol/L before and after dipyridamole administration, P < 0.005 ameliorate the severity of CHF (NYHA: 2.1 +/- 0.5 to 1.7 +/- 0.2). Both ejection fraction and maximal oxygen consumption increased. These improvements in the severity of chronic heart failure returned to baseline levels 6 months after discontinuation of dipyridamole. Comparable results were obtained in the dilazep protocol. We suggest that the elevation of plasma adenosine levels improves the pathophysiology of CHF.

Adenosine↗
PubMed1998

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.

Aged↗
PubMed1998

[Experience of weaning from left ventricular assist system in an acutely-ill patient with dilated cardiomyopathy and severe left ventricular dysfunction: a case report].

A 21-year-old man with dilated cardiomyopathy recovered from terminal heart failure with the long-term use of the left ventricular assist system (LVAS). His heart failure was refractory to maximum medical therapy including beta-blockade and intravenous catecholamines. Application of LVAS restored renal and hepatic function and even cardiac function. Left ventricular size decreased from 79 to 57 mm, and cardiac index increased from 1.6 to 2.2 l/min/m2. After 6 weeks of LVAS application, he could walk in the ward and could start exercise on a bicycle ergometer 3 months after. Ninety-five days after implantation, the LVAS could be removed. His general condition remained good and stable for more than a year after the removal of the LVAS. Timely application of LVAS seems to be one of the most important factors for successful circulatory support. Detailed criteria for LVAS application are not established yet.

Adult↗
PubMed1998

Sympathetic reinnervation demonstrated on serial iodine-123-metaiodobenzylguanidine SPECT images after cardiac transplantation.

The transplanted heart is without autonomic nervous control in the early postsurgical period. We present here a case of cardiac transplantation in which 123I-metaiodobenzylguanidine (MIBG) SPECT and an exercise-loading test were used to monitor the sympathetic reinnervation. The distribution of myocardial 123I-MIBG uptake extended with time from 1 to 2 yr after surgery. However, functional improvement, estimated by the heart rate response to exercise, was not discernable during this period. The findings in this case suggest the feasibility of 123I-MIBG SPECT imaging in the serial monitoring of sympathetic reinnervation after transplantation and that scintigraphic evidence of reinnervation precedes functional recovery.

3-Iodobenzylguanidine↗
PubMed1998

[Effectiveness of surgical repair of mitral regurgitation concomitant with dilated cardiomyopathy].

Dilated cardiomyopathy (DCM) is often accompanied by severe mitral regurgitation (MR) which deteriorates the clinical course. Mitral reconstruction for severe MR may improve the symptoms and prognosis. Five patients with DCM and one patient with dilated phase of hypertrophic cardiomyopathy underwent mitral reconstruction for severe MR (4 males, 2 females, mean age 50 +/- 17 years) from 1983 to 1995. Their New York Heart Association (NYHA) functional class and findings of echocardiography and cardiac catheterization were compared before and after surgery. Five patients underwent annuloplasty and one patient underwent mechanical valve replacement. There was no operative or in-hospital death. NYHA class improved from 3.2 to 1.8 (p < 0.05). The degree of MR was reduced from 3.5 to 1.2 (p < 0.05), and left ventricular end-diastolic pressure decreased from 18 +/- 7 to 13 +/- 8 mmHg (p < 0.05). Left ventricular fractional shortening, ejection fraction and cardiac index (2.4 +/- 0.4 to 2.7 +/- 1.1 l/min/m2) did not change significantly. Two patients died within one year due to exacerbation of congestive heart failure (2.5 month later) or sudden death (6 months later). Three patients died at 21 months, 5 and 8 years after the operation (renal insufficiency, heart failure, sudden death, respectively). Mitral reconstruction improved the symptoms in patients with DCM and severe MR in the short term. However, 5 of 6 patients died in the intermediate or long-term. Mitral reconstruction may be a therapeutic option for early outcome in patients with refractory congestive heart failure due to DCM and severe MR.

Adult↗
PubMed1998

[Relationship between apoptosis-related markers and cardiomyopathy].

Increasing interest has been focused on the role of apoptosis in pathogenesis of idiopathic cardiomyopathy. Interactions between soluble Fas, tumor necrosis factor-alpha (TNF-alpha) and Fas ligand have been reported to play a pivotal part in signal transduction of apoptosis. Thus, we measured serum levels of apoptosis-related markers, namely sFas, TNF-alpha and two types of its receptor TNF-RI and TNF-RII in the patients with idiopathic cardiomyopathy. Serum level of TNF-alpha was higher in dilated cardiomyopathy (DCM) group as well as in hypertrophic cardiomyopathy (HCM) group than in the control group. There were significant correlation among TNF-alpha, TNF-RI and TNF-RII in DCM group. However, only slight tendencies among these parameters in HCM group, indicating different pathogenesis from DCM. No transcardiac production of TNF-alpha, TNF-RI and TNF-RII was found in cardiomyopathies in the present study. These data suggested that apoptosis-related markers could be used for the detailed classification of cardiomyopathy. Furthermore, the simultaneous measurement of receptors and their ligands of apoptosis-related markers might underscore clinical implications.

Apoptosis↗
PubMed1997

Role of intracellular Ca2+ in activation of protein kinase C during ischemic preconditioning.

BACKGROUND: Activation of protein kinase C plays an important role in ischemic preconditioning. Given that protein kinase C is activated by an increase in the intracellular Ca2+ concentration ([Ca2+]i) and that myocardial ischemia and reperfusion increase [Ca2+]i, the effect of transient exposures to Ca2+ on infarct size and the effect of administration of EGTA during ischemic and alpha1-adrenoceptor-mediated preconditioning on the limitation of infarct size were investigated in the canine heart. METHODS AND RESULTS: In open-chest dogs, 5 minutes after the completion of either three 5-minute infusions of CaCl2 or four 5-minute infusions of the alpha1-adrenoceptor agonist methoxamine into the coronary artery, the coronary arteries were occluded for 90 minutes; this occlusion was followed by a 6-hour reperfusion in both the Ca2+ preconditioning and methoxamine groups. Infarct sizes in the Ca2+ preconditioning (15.8+/-2.3%) and methoxamine (10.1+/-2.2%) groups were significantly (P<.01) smaller than in the control group (42.5+/-2.9%), and administration of either an inhibitor of protein kinase C (GF109203X) or an inhibitor of ecto-5'-nucleotidase (alpha,beta-methyleneadenosine 5'-diphosphate) reduced the infarct size-limiting effect of Ca2+ preconditioning. Administration of EGTA during ischemic or alpha1-adrenoceptor-mediated preconditioning inhibited both the infarct size-limiting effect and the activation of protein kinase C and ecto-5'-nucleotidase induced by these procedures. CONCLUSIONS: [Ca2+]i during ischemic and alpha1-adrenoceptor-mediated preconditioning plays an important role in the infarct size-limiting effect of these procedures by activating protein kinase C and ecto-5'-nucleotidase in the canine heart.

5'-Nucleotidase↗
PubMed1997

Plasma adenosine levels increase in patients with chronic heart failure.

BACKGROUND: Adenosine is believed to be cardioprotective; however, it has not been elucidated whether the plasma adenosine level is increased in chronic heart failure. METHODS AND RESULTS: Seventy-one patients attending a specialized heart failure clinic during a 6-month period were grouped according to the cause of chronic heart failure and the New York Heart Association function class. There were 40 patients with chronic heart failure due to ischemic heart diseases and 31 patients with valvular heart diseases and dilated cardiomyopathy. Control subjects consisted of 64 healthy laboratory staff members and patients without chronic heart failure. We found that the plasma adenosine levels were increased in patients with ischemic and nonischemic heart failure (218 +/- 23 and 211 +/- 21 nmol/L, respectively, versus 62 +/- 3 nmol/L for healthy subjects) and that the extent of increases in adenosine levels correlated well with the severity of chronic heart failure. CONCLUSIONS: We conclude that adenosine levels in the systemic blood increase in patients in ischemic and nonischemic chronic heart failure. Because adenosine counteracts catecholamine-, renin-angiotensin-, and cytokine-induced cellular injury, increased adenosine levels may be endogenous compensatory mechanisms for heart failure.

Adenosine↗
PubMed1997

Salutary effect of adjunctive intracoronary nicorandil administration on restoration of myocardial blood flow and functional improvement in patients with acute myocardial infarction.

Salutary effect of nicorandil, a K+ adenosine triphosphate channel opener, on restoration of myocardial blood flow and functional improvement after coronary revascularization was investigated in 20 patients with first anterior acute myocardial infarction. Ten patients received intracoronary administration of nicorandil (2 mg) after coronary revascularization; the other 10 patients received coronary revascularization only and served as control subjects. Myocardial contrast echocardiography and two-dimensional echocardiography were performed to assess microvascular integrity and regional function in the infarcted area. Nicorandil improved peak contrast intensity ratio (p < 0.001), calculated as the ratio of peak contrast intensity in the infarcted and noninfarcted areas, indicating the restoration of myocardial blood flow to the infarcted myocardium. Regional wall motion improved more significantly in 1 month in patients who received nicorandil (p < 0.01). Thus our results suggested the usefulness of intracoronary nicorandil administration after coronary revascularization for restoring blood flow and functional improvement in patients with acute myocardial infarction.

Angioplasty, Balloon, Coronary↗
PubMed1997

Ecto-5'-nucleotidase mediates infarct size-limiting effect by ischemic preconditioning in the rabbit heart.

We examined whether ecto-5'-nucleotidase mediates infarct limitation by ischemic preconditioning in the rabbit heart. Ecto-5'-nucleotidase activity in ischemic region after ischemic preconditioning was greater than that in nonischemic regions (23.6 +/- 2.5 vs. 13.6 +/- 1.0 nmol/mg protein/min; p < 0.01). With an inhibitor of 5'-nucleotidase, alpha,beta-methylene adenosine 5'-diphosphate (AMP-CP), ecto-5'-nucleotidase activity in the ischemic region was comparable to that in the nonischemic region. Mean blood pressure was reduced from 73 +/- 2 to 62 +/- 3 mm Hg with intravenous AMP, whereas it did not change with coperfusion of AMP and AMP-CP, suggesting effective inhibition of ecto-5'-nucleotidase. Separately, myocardial infarction was created by 30-min coronary occlusion and 3 h of reperfusion. Infarct size expressed as percentage volume in risk area was reduced by ischemic preconditioning compared with that in the control (7.8 +/- 2.5% vs. 38.1 +/- 4.0%; p < 0.01). However, infarct size in the group given AMP-CP plus ischemic preconditioning was similar to that in the control (36.2 +/- 2.8% vs. 38.1 +/- 4.0%; NS), suggesting that ecto-5'-nucleotidase mediates infarct limitation by ischemic preconditioning in the rabbit.

5'-Nucleotidase↗
PubMed1997

Disappearance of the 'no-reflow' phenomenon after adjunctive intracoronary administration of nicorandil in a patient with acute myocardial infarction.

Adjunctive intracoronary administration of nicorandil, an ATP-sensitive potassium channel opener, after successful coronary revascularization was performed in a 54-year-old patient with acute myocardial infarction. The 'no-reflow' phenomenon disappeared after nicorandil administration and significant functional recovery of the infarcted myocardium was achieved. This suggests that nicorandil could eliminate the 'no-reflow' phenomenon after successful coronary revascularization.

Coronary Circulation↗
PubMed1997

Intravascular ultrasound evidence for importance of plaque distribution in the determination of regional vessel wall compliance.

Regional vessel wall distensibility was determined by measuring luminal area and pressure, using intravascular ultrasound (Sonicath; Boston-Scientific, Watertown, MA, USA; 3.5 Fr, 30 MHz) in 45 left coronary sites from 40 patients. Luminal area in diastole (A) and in systole was measured at the diseased sites. With the ratio of luminal area changes (dA) to coronary pressure changes (dP) during a cardiac cycle, the total distensibility index was calculated by the formula: [(dA/A)/dP] x 10(3). At sites with non-circumferential disease, perimeters in diastole (L) and in systole were measured at the normal and diseased portions, and the changes in perimeters (dL) during a cardiac cycle were calculated. The regional distensibility index was obtained by the formula: [(dL/L)/dP] x 10(3). In 22 sites with circumferential disease, the total distensibility index was 1.03 +/- 0.61/mmHg, significantly lower than that for 23 sites with non-circumferential disease (1.45 +/- 0.89/mmHg; P < 0.05). In non-circumferential disease, the regional distensibility index at the diseased portion was significantly lower (0.33 +/- 0.47/mmHg) than that at the normal portion (1.11 +/- 0.75/mmHg; P < 0.01). Coronary sites with residual non-circumferential disease after angioplasty also exhibited heterogeneity of regional distensibility (0.73 +/- 0.76 at disease sites versus 1.58 +/- 0.95/mmHg at normal sites, n = 10, P < 0.05). These results indicate that heterogeneous regional wall distensibility exists at sites with non-circumferential disease where the total vessel distensibility is preserved by the presence of compliant normal portion. This heterogeneity of regional wall distensibility may represent a biomechanical factor that explains the mechanism of plaque rupture that occurs mainly at the shoulder of the non-circumferential disease.

Biomechanical Phenomena↗
PubMed1996

Elevation of the plasma histamine concentration in the coronary circulation in patients with variant angina.

In the present study plasma histamine was found to be elevated in the great cardiac vein in 8 of 11 patients with variant angina but in none of 8 control patients. Although further investigation is required to determine the exact cause-and-effect relation between histamine release and provocation of spontaneous variant anginal attacks, the present study presents clinical evidence that histamine may well be related to episodes of variant angina as suggested in animal studies.

Adult↗