Increased circulating interleukin-18 in patients with congestive heart failure.
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Adult↗
Biomedical subjects
M Ohyanagi
Publications and source records attributed to M Ohyanagi.
Discordant iodine-123 metaiodobenzylguanidine uptake area reflects recovery time dispersion in acute myocardial infarction.
lodine-123 metaiodobenzylguanidine (MIBG) uptake was reported to be reduced compared to Tl-201 (Tl) in acute myocardial infarction (AMI). Within such an area, degrees of both sympathetic neural function and ischemic myocardial cell damage are considered to be greatly dispersed. These kinds of damage were reported to effect reporalization time in myocardial cells, and we evaluated our hypothesis that extension of the discordant MIBG uptake area correlates with recovery time (RT) dispersion and relate ventricular arrhythmias in AMI. MIBG and Tl images were obtained in AMI patients. Regional Tl or MIBG uptake was estimated in 9 segments of SPECT by using four-point scoring. The total score was the sum of scores in 9 SPECT segments. ATI-MIBG was calculated by subtracting the total MIBG score from the total Tl score. Corrected RT (RTc) was measured as a signal-averaged ECG. RTc dispersion was defined as the difference between maximal and minimal RTc. The patients were assigned to two groups (group A; < or = Lown 4a, group B; > or = Lown 4b) according to the results of 24-hour Holter monitoring. A positive correlation between RTc dispersion and ATI-MIBG was found. ATI-MIBG and RTc dispersion in group B were greater than those in group A. These results suggested that ATI-MIBG could be used to predict the development of malignant ventricular arrhythmias.
3-Iodobenzylguanidine↗
Usefulness of indium-111-oxine-labeled leukocyte scintigraphy in diagnosis of inflammation associated with chronic aortic dissection.
BACKGROUND: Patients with chronic aortic dissection require monitoring for indications of disease progression. In present study, inflammation adjacent to associated aortic wall was evaluated by indium-111-oxine-labeled leukocyte scintigraphy, scince inflammation of the blood vessel wall often associates with progression of chronic aortic dissection. METHODS AND RESULTS: Fifteen patients with aortic dissection underwent indium-111-oxine-labeled leukocyte scintigraphy. Seven showed positive images at sites corresponding to the actual sites of the dissociated aorta. Four patients with positive images underwent surgery. Histologic examination revealed inflammatory and necrotic changes of the aortic wall. During a mean follow-up period of 2.3 years, progression of aortic dissection was observed in two of the seven patients with positive intimal imaging. CONCLUSION: Indium-111-oxine-labeled leukocyte scintigraphy may be a useful noninvasive technique to assess the persistent inflammation in patients with chronic aortic dissection.
Adult↗
Detection of a coronary arterial thrombus by indium-111-oxine-labeled platelet scintigraphy.
Coronary arteriography revealed significant left anterior descending coronary artery stenosis in a 72-year-old man with a history of myocardial infarction. Stenting of the stenotic vessel was performed. Twelve hours after stenting the patient complained of chest pain but emergent coronary arteriography did not show sign of any coronary arterial stenosis. Under suspicion of coronary thrombus formation, indium-111-oxine-labeled platelet scintigraphy was performed 5 days after stenting, and revealed accumulation of indium-111-oxine in the area corresponding to the stent implantation site.
Aged↗
[Indium-111-oxine labeled platelet and leucocyte scintigraphy for diagnosis of thrombi and inflammation].
There were many studies for diagnosis of localization and activity of thrombi and inflammation using indium-111-oxine labeled platelet (In-plt) and leucocyte scintigraphy (In-WBC), respectively. The study using these techniques is decreasing recently, because other diagnostic modarities have been developed and the techniques of these scintigraphy are complicated. However, because these scintigraphy are noninvasive, it is expected that these are widely applied to the clinical diagnosis and follow up. 1. Platelet scintigraphy can visualized thrombi and distinguish the activation of platelet aggregation. There were many reports and reviews. I reviewed recent studies in cardiovascular diseases and our cases. 2. Leucocyte scintigraphy (In-WBC) is usually used for the detection of inflammation. Furthermore, it is possible that In-WBC can detect inflammation of the arteriosclerotic lesion of the aortic wall. I introduced our studies of In-WBC in aortic aneurysma and aortic dissection. The In-WBC maybe useful for detection of inflammation of the aortic aneurysma and evaluation of prognosis of aortic dissection.
Aortic Dissection↗
Transient increase in plasma brain (B-type) natriuretic peptide after percutaneous transluminal coronary angioplasty.
BACKGROUND: Brain (B-type) natriuretic peptide (BNP) is known to be secreted predominantly from the myocardium. Brain natriuretic peptide plasma concentrations have been shown to be markedly increased in patients with acute myocardial infarction; however, plasma BNP response during episodes of myocardial ischemia has not been established. HYPOTHESIS: This study was designed to examine plasma BNP in patients with transient myocardial ischemia induced by inflation of a percutaneous transluminal coronary angioplasty (PTCA) balloon. METHODS: Thirty consecutive patients (26 men and 4 women; mean age 61 years) who underwent PTCA, and another 49 patients (39 men and 10 women; mean age 63 years) who underwent diagnostic coronary angiography were enrolled in this study. Serum BNP concentrations were assayed in all patients. RESULTS: Plasma BNP was increased significantly with a peak concentration of 66.1 +/- 65.2 pg/ml 24 h after PTCA. Coronary angiography did not cause plasma BNP increase (immediately before 30.4 +/- 29.0 pg/ml, 24 h after 33.7 +/- 30.6 pg/ml). No significant differences were present in hemodynamic parameters measured immediately before and 24 h after PTCA. CONCLUSION: Plasma BNP is increased by transient myocardial ischemia induced by PTCA.
Adolescent↗
Relation between myocardial response to dobutamine stress and sympathetic nerve activation in patients with idiopathic dilated cardiomyopathy: a comparison of 123I-MIBG scintigraphic and echocardiographic data.
It is likely that a close association exists between findings obtained by two methods: dobutamine stress echocardiography and 123I-MIBG scintigraphy. Both of these methods are associated with beta-adrenergic receptor mechanisms. This study was conducted to demonstrate the relation between myocardial response to dobutamine stress and sympathetic nerve release of norepinephrine in the failing heart. In 12 patients with heart failure due to idiopathic dilated cardiomyopathy, the myocardial effects of dobutamine stress were evaluated by low-dose dobutamine stress echocardiography: and sympathetic nerve function was evaluated by scintigraphic imaging with iodine-123 [123I] meta-iodobenzylguanidine (MIBG), an analogue of norepinephrine. Echocardiography provided quantitative assessment of wall motion and left ventricular dilation; radiotracer studies with 123I-MIBG provided quantitative assessment of the heart-to-mediastinum (H/M) uptake ratio and washout rate. Results showed that H/M correlated with baseline wall motion (r = 0.682, p = 0.0146), wall motion after dobutamine stress (r = 0.758, p = 0.0043), the change in wall motion (r = 0.667, p = 0.0178), and with left ventricular diastolic diameter (r = 0.837, p = 0.0007). In addition, the 123I-MIBG washout rate correlated with baseline wall motion (r = 0.608, p = 0.0360), wall motion after dobutamine stress (r = 0.703, p = 0.0107), and with the change in wall motion (r = 0.664, p = 0.0185). Wall motion, especially in the myocardial response to dobutamine stress, is related to sympathetic nerve activity in heart failure.
3-Iodobenzylguanidine↗
Effect of angiotensin-converting enzyme inhibitors and nitroxy groups on human coronary resistance vessels in vitro.
We investigated the interaction between nitroxy groups and angiotensin-converting enzyme (ACE) inhibitors to assess the role of sulfhydryl groups and adenosine triphosphate (ATP)-sensitive potassium channels in vasodilation of human coronary resistance vessels in vitro. Coronary resistance vessels were resected from the right atrial appendage of 27 patients undergoing open heart surgery. The vessel ends were inserted into a microglass pipette with the internal pressure maintained at 40 mm Hg. Nitroglycerin did not change the vasoresponse, whereas nicorandil induced a concentration-dependent vasodilation that was not affected by methylene blue, but was markedly inhibited by glibenclamide. The ACE inhibitors, captopril, with a sulfhydryl group (1 x 10(-6) M), and enalaprilat, without a sulfhydryl group (1 x 10(-6) M), were added to either nitroglycerin or nicorandil to assess the incremental response of the sulfhydryl group to vasodilation. The addition of captopril or L-cysteine (1 x 10(-6) M) enhanced the activity of both nitroglycerin and nicorandil, whereas addition of enalaprilat did not. The responses of nicorandil and nitroglycerin to captopril and were similar. Cromakalim was not enhanced by L-cysteine or captopril. The response of nitroglycerin was not enhanced by captopril or L-cysteine after addition of N(G)-monomethyl-L-ARGININE (L-NMMA). Both nitroglycerin and nicorandil exhibited an increase in vasodilation in the presence of an ACE inhibitor containing a sulfhydryl group. The mechanism of the vasodilatory action in the coronary resistance vessels may involve the opening of an ATP-sensitive potassium channel and subsequent guanylate cyclase activation. These interactions have important clinical implications.
Angiotensin-Converting Enzyme Inhibitors↗
[Clinical characteristics of ventricular tachycardia and ventricular fibrillation in exercise stress testing].
OBJECTIVES: Ventricular tachycardia (VT) and ventricular fibrillation (Vf) induced in exercise stress testing should be treated urgently, although the occurrence of arrhythmia is rare. The conditions for the onset of arrhythmia and the clinical characteristics of VT and Vf patients in exercise stress testing were studied. METHODS: Fifty-nine patients (mean age 54 +/- 17 years, 41 males, 18 females) with VT (succession of 3 or more ventricular premature beats) or Vf induced in exercise stress testing were selected from 7,594 patients with consecutive treadmill stress testing in our hospital from January 1993 to February 1998. RESULTS: The incidence of exercise-induced VT or Vf was 0.8%, and there were no fatal accidents in all tests. Among the 59 patients with exercise-induced VT or Vf, 52 patients had non-sustained VT, 5 had sustained VT, and 2 had Vf. Of the 59 patients, 23 had rhythm or conduction disturbances, 14 had coronary artery disease, 13 had cardiomyopathy, and 9 had valvular heart disease. The VT or Vf incidence in coronary artery disease was 0.2%, and in valvular heart disease was 10.8%. VT or Vf occurred at over 80% of maximum heart rate exercise intensity in 40 patients, including 4 with sustained VT and 2 with Vf, of the 59 patients. Also, in 9 VT patients including the 4 sustained VT patients, VT occurred in the exercise recovery period within 2 min after the exercise. Although VT disappeared spontaneously in 52 non-sustained VT and 3 sustained VT patients, intravenous injection of lidocaine was needed in 2 sustained VT patients and direct current defibrillator was needed in 2 Vf patients. Furthermore, only one non-cardiac death was observed in the follow-up period of average 42 months. CONCLUSIONS: Our results showed clinical characteristics and incidence of VT or Vf similar to past reports. Furthermore, all sustained VT and Vf patients, who should be treated urgently, had a past history of ventricular premature beats or VT. Our data suggest that VT and Vf could occur during the recovery period, especially in patients with documented ventricular tachyarrhythmias when the stress intensity has reached the critical level in the exercise tolerance test.
Aged↗
Increased function of the voltage-dependent calcium channels, without increase of Ca2+ release from the sarcoplasmic reticulum in the arterioles of spontaneous hypertensive rats.
It has been reported that the increased function of the voltage-dependent calcium channels (VDCC) in the artery is involved in the increase of peripheral resistance in hypertension, and that the sarcoplasmic reticulum (SR) in the artery plays an important role in preventing the development of hypertension via a buffering effect. However, no reports have described the role of VDCC and SR in resistance arterioles in the development or maintenance of hypertension. We investigated the function of VDCC and of SR in the cremaster arterioles of spontaneous hypertensive rats (SHR) and age-matched Wistar Kyoto rats (WKY). The changes in diameter and the intracellular calcium ion concentration ([Ca2+]i) in the microdissected arterioles, using fluorescent dyes, were measured with videomicroscopy. The KCl concentration-response curves were analyzed in 4- to 5- and 7- to 8-week-old SHR and WKY. The changes in the vascular diameter and [Ca2+]i in response to ryanodine, an alpha-1 adrenoceptor, and angiotensin-II stimulation were compared between the 7- to 8-week-old SHR and WKY. We found an increase in the Ca2+ influx by VDCC in the early hypertensive stage, but not in prehypertensive SHR. However, after the onset of hypertension, there were no significant differences from WKY in the SR function mediated by Ca2+-induced Ca2+ release or inositol 1,4,5-trisphosphate-induced Ca2+ release. In conclusion, an increased influx of Ca2+ in the cell membrane, without a buffering effect of SR, was associated with progression of hypertension in the cremaster arterioles of SHR.
Animals↗
A simple, reliable method of assessing exercise capacity in patients with chronic heart failure.
OBJECTIVE: The accurate determination of limitations in physical activity is important in evaluating patients with heart failure and in assessing the efficacy of treatment. However, the conventional measures used to evaluate hemodynamics, functional class, and exercise capacity all have limitations. Our objective was to develop a simple method (The Master-Borg test) for evaluating the physical activity of patients with chronic heart failure using self-evaluation of the sensation of dyspnea at a constant workload. METHODS: Patients with NYHA class I (N = 20), class II (N = 20), and class III (N = 20) chronic heart failure performed a symptom-limited treadmill exercise test to determine peak VO2 and anaerobic threshold (AT). Patients subsequently performed Master's two-step test for 90 s and maximal dyspnea was self-rated using the visual analog Borg scale (the Master-Borg test). RESULTS: The mean workload in the Master-Borg test was 15.2+/-1.6 mL x min(-1) x kg(-1). A significant correlation was found between the Master-Borg score and peak VO2 (r = 0.87) or AT (r = 0.84). The reproducibility of the Master-Borg tests was represented by a correlation coefficient of 0.93. CONCLUSION: Although simple and inexpensive, the Master-Borg test accurately represents ordinary activity levels, relates the sensation of dyspnea to peak exercise tolerance, and can be completed by most patients with heart failure. Master-Borg scores correlated with peak VO2 and AT, and can differentiate among NYHA classes I, II, and III. The Master-Borg test appears to be clinically useful for evaluating the value of physical activity and exercise capacity of patients with chronic heart failure.
Aged↗
Clinical course of patients with coronary ectasia.
OBJECTIVE: To compare the clinical prognosis between patients with diffuse coronary ectasia and those with localized coronary ectasia. DESIGN: Patients with coronary ectasia were divided into two groups based on the Markis classification (group D: types I-III and group L: type IV), and the clinical manifestations and prognosis were compared between the two groups. RESULTS: Group D patients (52.1 +/- 4 years) were significantly younger than group L patients (62.5 +/- 7 years). During the study, 4 patients in group D died suddenly. Three of the patients had type I coronary ectasia, and 1 had left main coronary ectasia. CONCLUSION: The results of the present study indicate that patients with diffuse coronary ectasia and left main coronary ectasia should be followed carefully.
Aged↗
A decrease in the amount and function of inhibitory GTP-binding protein in the resistance small artery from spontaneously hypertensive rats.
The inhibitory GTP-binding protein (Gi protein) plays an important role in regulation of vascular tone. Many studies have implicated the role of Gi protein in conduit vessels. However, the physiological role of Gi protein in the control of peripheral microvascular tone in hypertension has not been established yet. Therefore, we investigated the concentration of Gi protein in the peripheral resistance arteries and aorta in the spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY) and renovascular hypertensive rats (RHR), using immunohistochemical methods semiquantitatively. Changes in the function of Gi protein in relation to alpha2-adrenoceptor were also investigated by microcannulation techniques. We have shown that the amount of alpha2 subunits of Gi protein in the cremaster small artery was significantly lower in SHR aged 4 weeks and older than in age-matched WKY and that there were no significant differences between RHR and WKY. We also demonstrated that the function of Gi protein in relation to alpha2-adrenoceptor was already lower in SHR before the onset of hypertension. The quantitative and functional decline in Gi protein in the smooth muscle cells of peripheral small arteries were observed in SHR even before the onset of hypertension, whereas rats with secondary hypertension did not exhibit this finding.
Aging↗
Acetylcholine-Induced response of coronary resistance arterioles in cholesterol-fed rabbits.
The extent to which reported abnormal responses of the human coronary circulation to acetylcholine in patients with hypercholesterolemia reflect endothelial injury is not clear. We used an in vitro rabbit model to determine whether these reactions involve endothelial or vascular smooth muscle dysfunction. Coronary resistance arterioles were isolated from hearts of rabbits fed 1% cholesterol to induce hypercholesterolemia or a control diet for 4 weeks. Arterioles were double cannulated with glass micropipettes and pressurized in a no-flow state. Acetylcholine contracted the arterioles in a concentration-dependent manner whether or not the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine was added. In control but not hypercholesterolemic preparations, contraction was significantly greater when endothelium was removed. In the hypercholesterolemic group, contraction significantly exceeded that in controls. In control but not high-cholesterol preparations, substance P dilated vessels with intact endothelium in a concentration-dependent manner. Addition of N(G)-monomethyl-L-arginine inhibited this response. With or without endothelium, norepinephrine contracted arterioles to a greater extent in the hypercholesterolemic group than in controls. We concluded that severe hypercholesterolemia decreased endothelially dependent factors by injuring endothelium and independently increased contractility of vascular smooth muscle.
Acetylcholine↗
[Reverse redistribution of technetium-99m-tetrofosmin after acute coronary revascularization in patients with myocardial infarction].
This study qualified the severity and localization of reverse redistribution of technetium-99 m (Tc)-tetrofosmin rest imaging. Both Tc-tetrofosmin and thallium-201 (Tl) rest imaging with early images and delayed images were obtained in the subacute phase of myocardial infarction in 21 patients with first anterior myocardial infarction and with successful transluminal angioplasty (including stenting). Relative myocardial uptake (%uptake), degree of reverse redistribution (%), and washout rate (%) were evaluated quantitatively in 6 left ventricular segments (inferoseptal, anteroseptal, anterior, anterolateral, lateral, inferolateral and inferior) by circumferential profile analysis. The percentage reverse redistribution in the infarct area was larger in Tc-tetrofosmin imaging than in Tl imaging (p = 0.013). Reverse redistribution was most prominent in the anterior wall (anterior > anteroseptal > inferoseptal, p = 0.020). This suggests that infradiaphragmatic scatter is unlikely as the mechanism of reverse redistribution. The washout rate of Tc-tetrofosmin in the infarct area (reverse redistribution area) was higher than that in the normal area (non-reverse redistribution area), and was also higher than the washout rate of Tl imaging in the infarct area. The %uptake of delayed images in the infarct area was larger in Tc-tetrofosmin than that in Tl imaging, whereas %uptake of early images did not differ. The percentage reverse redistribution did not correlate with the degree of collateral circulation and the residual stenosis. In conclusion, reverse redistribution of Tc-tetrofosmin was more prominent in the infarct area, and this was due to the relatively lower uptake of reverse redistribution of Tc-tetrofosmin than delayed Tl images.
Angioplasty, Balloon, Coronary↗
Monoclonal anti-cardiolipin antibodies from New Zealand Black x New Zealand White F1 mice react to thrombomodulin.
The reactivity with and affinity for thrombomodulin (TM) of monoclonal anti-cardiolipin Abs (MoaCL), derived from a New Zealand Black x New Zealand White F1 (NZB/W F1) mouse, were studied to investigate the pathogenicity of anti-cardiolipin Abs (aCL). Four of eighteen MoaCL were found to react with rabbit TM when examined using ELISA. These four MoaCL also reacted with synthetic peptide that included the epidermal growth factor-like domain of human TM, a binding site for thrombin. The reaction with TM of these four MoaCL was inhibited by bovine thrombin. When the affinity for TM of the MoaCL was determined, the dissociation constants (Kd) ranged from 4.8 x 10(-9) to 4.7 x 10(-8) M. By contrast, examination of the affinity for cardiolipin (CL) gave values from 8.3 x 10(-6) to 7.4 x 10(-5) M. Thus, these MoaCL reacted to TM with a higher affinity than to CL. Moreover, these MoaCL also bound to TM on HUVEC and down-regulated the expression level of TM on the surface of HUVEC due to internalization of TM. The binding of thrombin to TM is known to initiate rapid protein C activation, and complexes of activated protein C and protein S show anticoagulatory activity. Thus, the present studies suggest that certain pathogenic aCL cross-react with TM and induce down-regulation of TM on endothelial cells, followed by induction of thrombosis.
Animals↗
Enhanced myogenic response in resistance small arteries from spontaneously hypertensive rats: relationship to the voltage-dependent calcium channel.
To characterize the myogenic response during the development of hypertension, we evaluated the myogenic response of small arteries isolated from the cremaster muscle of spontaneously hypertensive rats (SHR) aged 4-5 and 7-8 weeks, as compared with age-matched Wistar-Kyoto rats (WKY), using an in vitro system. The myogenic response of SHR aged 7-8 weeks (but not those aged 4-5 weeks) significantly exceeded that of WKY. Measurement of intracellular levels of free calcium ([Ca2+]i) in small arteries of the 7-8-week-old SHR and WKY loaded with a calcium-sensitive dye showed that the increase in [Ca2+]i in SHR was significantly greater than that in WKY during the myogenic response. The inhibitory effects of nitrendipine on the increased myogenic response and [Ca2+]i were greater in SHR. Thus, the myogenic response was enhanced in SHR and may be explained in part by an increase in Ca2+ entry through the voltage-dependent calcium channel (VDCC). The myogenic response and Ca2+ entry through the VDCC may be increased in association with the elevation of blood pressure.
Animals↗
Stimulatory guanine nucleotide-binding protein in failing heart of hamsters and rats.
The role of the stimulatory guanine nucleotide-binding protein (Gs) in heart failure is unclear. We therefore determined the amount of protein and mRNA of Gs in the failing myocardium using two animal models: the BIO 53.58 hamster, a model of genetic cardiomyopathy, and adriamycin-treated rats (ADR rats), a model of secondary cardiomyopathy. The maximal number of myocardial beta-adrenoceptors in the BIO 53.58 hamsters as well as in the ADR rats was significantly lower than that in the respective controls, indicating that the beta-adrenoceptors were down-regulated in heart failure. Analysis by Western blot and Northern blot revealed a significant decrease in Gs protein and mRNA in the BIO 53.58 hamsters relative to the control. There were no differences in the level of Gs protein or mRNA in the ADR rats vs the controls. The functional activity of Gs was investigated by measuring adenylate cyclase activity. The activity of adenylate cyclase in response to stimulation by sodium fluoride or forskolin was decreased in the BIO 53.58 hamsters relative to control animals, whereas no differences were observed in the ADR rats vs the controls. Thus, alterations in Gs in the failing heart appear to differ according to its cause.
Adenylyl Cyclases↗