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Biomedical subjects

Akira Kitabatake

Publications and source records attributed to Akira Kitabatake.

At least 73 records · Page 4Linked to original sources
PubMed2003

Serial changes in BMIPP uptake in relation to thallium uptake in the rat myocardium after ischaemia.

Several clinical studies have shown that iodine-123 labelled 15-(p-iodophenyl)-3-(R, S)-methylpentadecanoic acid (BMIPP) uptake is often lower than the uptake of perfusion tracers in patients with ischaemic heart disease. However, BMIPP accumulation may not decrease during the acute phase of a stunned myocardium in patients with acute coronary syndrome. We evaluated serial changes in BMIPP and perfusion tracer uptake in the myocardium after ischaemia. We performed a 20-min left coronary artery occlusion followed by reperfusion in male Wistar rats. One hour after the reperfusion, echocardiography was performed. Intravenous injection of iodine-125 labelled BMIPP and thallium-201 was performed 1 day (acute group) and 5 days (subacute group) after the operation. To determine the myocardial distribution of 125I-BMIPP and 201Tl, dual-tracer autoradiography was conducted. We identified regions of interest in the anterolateral wall as an area at risk and in the inferoseptum as a remote control area. The anterolateral wall/inferoseptum ratio (A/I ratio) was calculated to compare the distributions of 125I-BMIPP and 201Tl. Coronary occlusion induced hypokinesia in the anterolateral region 1 h after the reperfusion. The A/I ratio of 125I-BMIPP was significantly higher than that of 201Tl in the acute group (1.01 +/- 0.15 vs 0.80 +/- 0.23, P<0.001). On the other hand, there was no significant difference between the A/I ratios of 125I-BMIPP and 201Tl in the subacute group (0.88 +/- 0.18 vs 0.85 +/- 0.18). Two rats showed a significantly lower A/I ratio of 125I-BMIPP than 201Tl in the subacute phase. These data suggest that BMIPP uptake is preserved despite a decrease in perfusion in the acute phase after ischaemia. In the subacute phase, on the other hand, BMIPP uptake is similar to or even lower than thallium uptake. Since BMIPP uptake may change with time after ischaemia, careful interpretation of BMIPP uptake after ischaemia is required in a clinical setting.

Animals↗
PubMed2003

Intracellular signal transduction modulating expression of plasminogen activator inhibitor-1 in adipocytes.

The concentrations in blood of plasminogen activator inhibitor-1 (PAI-1), an inhibitor of fibrinolysis and proteolysis, are elevated in obese and insulin-resistant subjects, predispose them to the risk of thrombosis, and may accelerate atherogenesis. Adipose tissue is a prominent source. Accordingly, intracellular signaling pathways that may influence PAI-1 expression in adipocytes have been the focus of considerable study. Rho, a small GTP binding and GTPase protein, when activated in turn activates its target, Rho-associated coiled-coil forming protein, to yield an active kinase, Rho-kinase, an effector in the Rho pathway. Rho-kinase exerts calcium-sensitizing effects in vascular smooth muscle cells and inhibitory effects on transforming growth factor-beta (TGF-beta) expression in chicken embryonic heart cells. Because TGF-beta is a powerful agonist of PAI-1 expression, we characterized the effects of inhibition of Rho-kinase in 3T3-L1 adipocytes. PAI-1 mRNA was determined by Northern blotting, and PAI-1 protein was determined by Western blotting. The Rho-kinase inhibitor, Y-27632 [(R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide], increased PAI-1 expression markedly. Although genistein, a flavonoid tyrosine kinase, attenuated the increase of PAI-1 induced by Y-27632, other non-flavonoid tyrosine kinase inhibitors did not. However, another flavonoid, daidzein, which lacks tyrosine kinase activity, decreased basal PAI-1 expression and attenuated the induction of PAI-1 expression by Y-27632. Thus, the Rho/Rho-kinase system inhibits PAI-1 expression by a flavonoid-sensitive mechanism in adipocytes. Therefore, flavonoids may be useful in decreasing elevated PAI-1 expression in adipose tissue and its consequent pathophysiologic sequelae.

3T3 Cells↗
PubMed2003

Osteopontin deficiency attenuates atherosclerosis in female apolipoprotein E-deficient mice.

OBJECTIVE: Osteopontin (OPN), a noncollagenous adhesive protein, is implicated in atherosclerosis, in which macrophages within atherosclerotic plaques express OPN. However, it is not known whether the elevated OPN expression is a cause or result of atherosclerosis. METHODS AND RESULTS: We generated mice that lacked OPN and crossed them with apolipoprotein (apo) E-deficient mice and analyzed these mice with a mixed C57BL/6x129 background after 36 weeks on a normal chow diet. In female mice, OP+/-E-/- and OP-/-E-/- mice had significantly smaller atherosclerotic and inflammatory lesions compared with OP+/+E-/- mice, and that was reflected by smaller area of MOMA-2-positive staining. In male mice, however, there was no significant difference in the atherosclerosis lesion areas among 3 genotypes. In both OP-/-E-/- and OP+/+E-/- mice, typical atherosclerotic lesions were detected, which include necrotic core, foamy cell collections, and cholesterol clefts. However, we found that vascular mineral-deposited areas in 60-week-old male OP-/-E-/- mice were significantly increased compared with those in OP+/+E-/- male mice. CONCLUSIONS: These results suggest that OPN plays a promoting effect in atherosclerosis and inhibitory effect in vascular calcification. The suppression of OPN expression in females should be considered a therapeutic possibility in atherosclerosis.

Animals↗
PubMed2003

Adenovirus-mediated gene transfer of ICOSIg fusion protein ameliorates ongoing experimental autoimmune myocarditis.

Experimental autoimmune myocarditis (EAM) has been used as a model for human myocarditis. We previously demonstrated that blockade of B7/CD28 or CD40/CD40 ligand (CD40L) had a potential preventive effect on EAM, but less therapeutic effect on ongoing EAM. Thus, we searched for the involvement of other costimulatory molecules in EAM. We demonstrated the expression of inducible costimulator (ICOS)/ICOSL molecules in the lymph nodes, spleen, and heart in the EAM rat. We constructed adenovirus vectors containing ICOSIg (Adex1CAICOSIg) to achieve effective inhibition of ICOS/ICOSL interaction, and examined the effects of Adex1CAICOSIg on EAM. Adex1CAICOSIg treatment shortly after the immunization did not inhibit the onset and severity of EAM compared to control rats. On the other hand, delayed treatment with Adex1CAICOSIg significantly inhibited ongoing EAM. The survival rate in rats treated with Adex1CAICOSIg was significantly higher than that of the control group. Furthermore, the affected area ratio of the Adex1CAICOSIg treatment group was significantly lower than that of the control group. This study indicates that ICOS/ICOSL costimulation makes an important contribution to the progression of EAM and that the blockade of this pathway by gene transfer has therapeutic potential for ongoing autoimmune myocarditis.

Adenoviridae↗
PubMed2003

VEGF-mediated angiogenesis is impaired by angiotensin type 1 receptor blockade in cardiomyopathic hamster hearts.

OBJECTIVE: Coronary microcirculation plays an important role in the progression of cardiac remodeling. Among angiogenic factors, it has been reported that angiotensin II may contribute to neovascularization. However, it is unknown whether inhibition of the renin-angiotensin system suppresses angiogenesis, especially within the heart. Our aim was to evaluate the effects of the angiotensin-converting enzyme inhibitor enalapril and the angiotensin II receptor type I blocker valsartan on cardiac microvasculature, function, vascular endothelial growth factor (VEGF) expression, and survival in cardiomyopathic hamsters. METHODS: Male cardiomyopathic hamsters (BIO TO2) were administered either a placebo (group C), enalapril (30 mg/kg/day) (group E), or valsartan (40 mg/kg/day) (group V), starting at the age of 6 weeks. This continued until death. Hemodynamic study, histological analysis, and northern blot analysis were performed at 39 weeks. RESULTS: Group V showed significant increases in percent fibrosis, end diastolic pressure, and LV dP/dt min, and significant decreases in percent fractional shortening, LV dP/dt max, capillary density, and the level of mRNA expression of VEGF compared with group C. Group E showed significant increases in percent fractional shortening while the capillary density and level of mRNA expression of VEGF were unchanged. The 300-day survival rate was significantly lower in group V (25.0%) but higher in group E (100%) than that of group C (66.7%). CONCLUSIONS: Therapy with valsartan may have adverse effects on survival rate concomitant with the progression of cardiac remodeling owing to impaired VEGF-mediated angiogenesis. Therapy with enalapril has a neutral effect on VEGF-mediated angiogenesis, leading to the suppression of cardiac remodeling and an increase in life expectancy.

Angiotensin Receptor Antagonists↗
PubMed2003

A 44-kDa of protein identical to the N-terminal amino acid sequence of MCT1 in human circulation.

A family of specific carrier protein designated as monocarboxylate transporter (MCT) has been known to transport the lactate and other moncarboxylates in mammalian cells. We hypothesized the presence of serum protein in human circulation that may works as a lactate carrier and that biochemical structure would possesses common structure with MCT on the plasma membrane. Immunoblot analysis with an anti-MCT1 polyclonal antibody suggested the presence of a 44-kDa protein in human circulation and N-terminal amino acid sequencing exhibited a stretch of 14 amino acids which is completely identical to MCT1. The unbound fractions from the GST-MCTI fusion protein-immobilized glutathione sepharose 4B column demonstrated that lactic acid concentration began to increase with one fraction delay compared to Sepharose 4B and GST-immobilized column. When lactic acid was washed away with PBS, lactic acid concentrations in the effuluent constantly decreased in both Sepharose 4B and GST-immobilized column. However, GST-MCT1-immobilized column showed specific convex curve from fraction approximately 3 mM of lactate and demonstrated wash out delay compared to Sepharose 4B and GST-immobilized column. These observations demonstrated biochemical and immunological similarities between a 44-kDa protein purified from human serum and MCT1 present on the plasma membrane. The studies on MCT1-fusion protein suggested possible functional properties of a 44-kDa protein as a lactate buffer by holding and unhand a lactate according to the lactate concentration in human blood. The experiments described herein have suggested the existence of lactate carrier in human circulation which is free from plasma membrane.

Animals↗
PubMed2003

Coronary capillary network remodeling and hypofibrinolysis in aged obese diabetic rats: implications for increased myocardial vulnerability to ischemia.

Despite the known abnormalities of cardiac function in patients with overt non-insulin dependent diabetes mellitus (NIDDM) the temporal changes of coronary capillary network remodeling leading to potential microcirculatory dysfunction have not been elucidated. To this end, left ventricular subendocardial capillary network of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, characterized by hypertension, obesity, hyperglycemia, hyperinsulinemia and mild NIDDM, and control Long-Evans Tokushima (LETO) rats were investigated. Total capillary density in OLETF was significantly higher than that in LETO at 20 weeks, suggesting compensatory improvement of O2 transport at early stages of NIDDM. The increase in capillary density in OLETF was lost at 40 and 60 weeks due to the decreases of intermediate capillary portions and venular capillary portions. Although capillary domain area (area innervated by single capillary) in OLETF was lower than that in LETO at 20 weeks, the values were similar between OLETF and LETO at 40 and 60 weeks, suggesting that adaptive improvement in the capacity for 02 transport with a high perfusion was lost in late stages of NIDDM. Activity of plasma plasminogen activator inhibitor-1 (PAI-1), the major physiologic inhibitor of proteo(fibrino)lysis, in OLETF was higher than that in LETO at 40 and 60 weeks, suggesting that increase of PAI-1 may downregulate compensatory adaptive capillary network remodeling by inhibiting proteolysis and angiogenesis in the cardiac interstitium. Loss of adaptive myocardial microcirculation may therefore contribute to increased vulnerability in ischemic injury and to cardiac dysfunction in NIDDM.

Animals↗
PubMed2003

Increased cycle length variability during ventricular fibrillation: a novel predictor of arrhythmia recurrence.

To evaluate the clinical value of cycle length (CL) variability during ventricular fibrillation (VF), 26 patients who underwent implantable cardioverter defibrillator (ICD) implantation were enrolled. In VF induced for defibrillation testing, mean and SD of VFCL, mean successive differences (MSD) of VFCL, and coefficient of variations of the VFCL (CV(FF)) (SD x 100/mean VFCL) were calculated. During the follow-up period of 20 +/- 2 months, ventricular arrhythmias recurred in 13 patients. MSD and CV(FF) were 31 +/- 3(*) ms and 15.6 +/- 1.3(**) in recurrence group (n = 13), and 17 +/- 2 ms and 9.0 +/-1.1 in non-recurrence group (n = 13) ((*)P <.005, (**)P <.001 vs. nonrecurrence group). Relatively good repeatability of mean VFCL, MSD and CV(FF) in each patient was confirmed by the Bland-Altman method. In VF induced by programmed ventricular stimulation before ICD implantation, MSD and CV(FF) in recurrence group were also increased significantly. Kaplan-Meier estimates revealed that MSD >or= 20 ms and CV(FF) >or= 12 predicted higher arrhythmia recurrence (MSD, P =.039; CV(FF), P =.0069 by the log-rank test). By multivariate analysis, CV(FF) >or= 12 was a significant predictor of recurrent arrhythmic events (P =.019). In conclusion, the CL variability of VF, which was evaluated as MSD and CV(FF), is increased in patients with arrhythmia recurrence. These values may reflect the degree of electrical heterogeneity, and appears to be useful indexes of the future arrhythmic events.

Arrhythmias, Cardiac↗
PubMed2003

Estrogen deprivation and replacement modulate cerebral capillary density with vascular expression of angiogenic molecules in middle-aged female rats.

The effect of postmenopausal estrogen replacement therapy (ERT) on the risk or severity of cerebrovascular disorders is as yet unclear, and the evidence for flow preservation being a mechanism of estrogen neuroprotection remains elusive. The authors examined whether estrogen-mediated flow-preserving neuroprotective mechanisms, if any, may involve its angiogenic action. This study was conducted using middle-aged (44 weeks) female rats because of the importance of aging in cerebrovascular disease in women. Middle-aged female rats were subjected to sham operation, ovariectomy, or ovariectomy with ERT. The anatomic cerebral capillary morphology showed a significant reduction in the total capillary density in the frontal cortex after ovariectomy. This was associated with marked decreases in protein and gene expression of vascular endothelial growth factor and its angiogenic receptors in cerebral vessels, as demonstrated by immunohistochemistry and hybridization. The expression levels of both estrogen receptor (ER) subtypes, ERalpha and ERbeta, in cerebral vessels were significantly reduced after ovariectomy, but ERbeta was more dramatically downregulated as assessed by the ERbeta/ERalpha ratio. These ovariectomy-induced changes were completely prevented by ERT. Vascular endothelial growth factor appears to be a critical regulatory molecule for physiologic cerebral angiogenesis in middle-aged female rats and may play an important role in the flow-preserving neuroprotective action of estrogen through its angiogenic and antiapoptotic properties.

Aging↗
PubMed2003

Effects of angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade on beta-adrenoceptor signaling in heart failure produced by myocardial Infarction in rabbits: reversal of altered expression of beta-adrenoceptor kinase and G i alpha.

Both angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type 1 (AT1) receptor blockers have been demonstrated to improve symptoms and prognosis in heart failure (HF). We compared the effects of ACE inhibition and AT1 receptor blockade on myocardial beta-adrenoceptor desensitization in rabbits with HF established 3 weeks after myocardial infarction (MI) with left circumflex coronary artery ligation. Rabbits with MI were randomized to no treatment, the ACE inhibitor temocapril (0.5 mg/kg/day) or AT1 receptor blocker valsartan (3 mg/kg/day). Echocardiographic examinations showed that, relative to rabbits with untreated MI, rabbits receiving temocapril or valsartan had a limitation of cardiac remodeling and prevention of the development of systolic dysfunction. Circulating plasma norepinephrine levels that were markedly elevated in MI animals were strongly inhibited by temocapril or valsartan therapy. beta-Adrenoceptor density, beta-adrenoceptor proportion showing high-affinity agonist binding, and basal and isoproterenol-stimulated adenylate cyclase activities were significantly reduced in MI rabbits. These defects were similarly reversed by temocapril or valsartan. Importantly, as found in human HF, myocardial protein levels of beta-adrenoceptor kinase 1 and G(i alpha) were significantly elevated in MI rabbits, suggesting that these molecules are contributing to the defects in myocardial beta-adrenoceptor signaling. The expression levels of these molecules were normalized equally by both treatments. The results suggest that pharmacologically different interventions in the renin-angiotensin system can equivalently improve the derangements in the beta-adrenoceptor signaling system in the failing heart. This may be important for the beneficial effects of these agents in HF.

Adenylyl Cyclases↗
PubMed2003

Sensitive method of detecting myocardial ischemia during dobutamine stress echocardiography.

To test the hypothesis that dobutamine-induced myocardial ischemia causes early-systolic asynchrony predominantly in the regional left ventricular wall, color kinesis (CK) images during dobutamine stress echocardiography (DSE) were recorded in 13 patients with coronary artery disease and in 10 patients without, all of whom showed normal wall motion at rest. Based on the visual interpretation of DSE and the angiographic findings, 21 segments in the short-axis images at the papillary muscle level were defined as ischemic, and 60 segments of the patients without coronary artery disease were defined as normal. The incremental fractional segmental area change (IFAC) was calculated at 33-ms intervals from the CK images. At the peak dose, IFACs during the first 33 and 33-67 ms were significantly lower in the ischemic segments than in the normal ones, and IFACs during 133-167, 200-233 and 233-267 ms were significantly higher in the ischemic segments. The ratio (peak/low dose) of the cumulative fractional area change at 100 ms gave the best sensitivity (= specificity) for differentiating the 2 groups (86%). Dobutamine-induced ischemia is characterized by an early-systolic asynchrony rather than a change in overall wall excursion and CK can provide an objective assessment of ischemia developing during DSE.

Aged↗
PubMed2003

Increased expression of plasminogen activator inhibitor-1 by mediators of the acute phase response: a potential progenitor of vasculopathy in hypertensives.

Hypertension is an important risk factor for coronary atherosclerosis, which is accelerated by inflammation and diminished fibrinolysis. We have previously shown that levels of plasminogen activator inhibitor-1 (PAI-1), the major physiologic inhibitor of fibrinolysis, are increased with atherogenic metabolic derangement. Because the liver is one of the major sources of circulating PAI-1, we here examined the effects of two proinflammatory cytokines, interleukin (IL)-1beta, and IL-6, on PAI-1 production in a human hepatoma cell line, HepG2. IL-1beta (1 ng/ml) and IL-6 (1 ng/ml) increased the accumulation of PAI-1 in the conditioned media over 24 h (IL-1beta: 2.1 +/- 0.2 (mean +/- SD) fold over the control; IL-6:1.4 +/- 0.2 fold; Western blot, p < 0.05). The increase in PAI-1 protein accumulation correlated with the increased expression of PAI-1 mRNA (Northern blot). An HMG-CoA reductase inhibitor (mevastatin, 10 micromol/l) attenuated the PAI-1 production induced by IL-1beta and IL-6. The plasma PAI-1 activity level was higher in hypertensives than in normotensives (10.0 +/- 9.8 AU/ml vs. 6.2 +/- 4.5 AU/ml, p < 0.05). The plasma PAI-1 antigen level was also higher in hypertensives than in normotensives (30.9 +/- 22.4 ng/ml vs. 24.4 +/- 13.3 ng/ml, p < 0.05). Thus, 1) IL-1beta and IL-6 can increase PAI-1 production in hepatic cells and 2) mevastatin may exert anti-thrombotic effects by decreasing the PAI-1 protein production induced by these proinflammatory cytokines. These results provide further insights into how inflammation is involved in the atherothrombotic complications observed in hypertensives, which may be ameliorated by HMG-CoA reductase inhibitors.

Acute-Phase Reaction↗
PubMed2003

A newly developed angiotensin II type 1 receptor antagonist, CS866, promotes regression of cardiac hypertrophy by reducing integrin beta1 expression.

Previous studies have demonstrated that integrins link the extracellular matrix to the hypertrophic response pathway of cardiac myocytes in vitro. To examine the direct relation between integrin beta1 and cardiac hypertrophy in vivo, we studied the effects of a newly developed angiotensin II type 1 (AT1) blocker, CS866 (ARB; 10 mg/kg/day), an angiotensin-converting enzyme inhibitor, temocapril (ACEI, 10 mg/kg/day), or both on modulation of integrin beta1 in the hypertrophied hearts of stroke-prone spontaneously hypertensive rats (SHRSP) 6 to 12 weeks of age. Treatments with ARB, ACEI, and combination therapy significantly reduced systolic blood pressure. However, the reduction in cardiac hypertrophy was greater in SHRSP treated with ARB or combination therapy than in those treated with ACEI. Multiplex reverse transcription-polymerase chain reaction revealed significantly higher mRNA expression of atrial natriuretic factor, AT1 receptor, and integrin beta1 in untreated SHRSP than in normotensive Wistar-Kyoto rats (WKY). The mRNA levels of ANP, AT1 receptor, and integrin B1 in SHRSP were significantly decreased by treatment with ARB, ACEI, or combination therapy. Decreased mRNA expression of ANP, AT1 receptor, and integrin beta1 in the treated SHRSP was associated with reductions in blood pressure; ARB and combination therapy produced greater decreases in expression than did ACEI. These observations suggest that CS866 has a beneficial effect on myocyte hypertrophy and that down-regulation of AT1 receptor and suppression of integrin beta1 participate in the regression of pressure-induced cardiac hypertrophy in vivo. The correlation between the expression of integrin beta1 and AT1 receptor was significant. Our results also suggest that integrin expression by myocytes might be modulated by angiotensin II via AT1 receptor.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2003

Different coronary blood flow increase in left ventricular hypertrophy due to hypertension compared to hypertrophic cardiomyopathy at elevated heart rate.

Coronary vasodilator reserve (CVR) is reduced in patients with left ventricular hypertrophy (LVH). However, it is not clear whether there is any difference between the coronary blood flow increase in LVH caused by hypertension (HTH) and that caused by hypertrophic cardiomyopathy (HCM) when the heart rate increases. In this study, 16 subjects with HTH, 10 subjects with HCM, and 10 subjects with normotension (NT) were investigated. Average peak velocities at rest, at pacing, and at dilatation were measured using a Doppler catheter placed at the left descending coronary artery to calculate coronary blood flow (CBF) and CVR. CVR at rest was identical in the HTH and HCM groups, and in both cases was lower than the resting CVR in NT subjects. There were significant differences in the CVR values at a pacing rate of 120 beats/min among the groups. These values were lowest in HCM, highest in NT, and intermediary in HTH subjects. And the percent increase in CBF in HCM at that pacing rate was higher than that in HTH (p < 0.05) or NT (p < 0.05). There was no difference in the percent increase in CBF at this pacing rate between the HTH and NT groups. The effects of elevated heart rate on the percent increase in CBF were different between the HTH and HCM groups. We conclude that cardiac hypertrophy has qualitatively different effects on coronary circulation depending on whether patients have HTH or HCM.

Aged↗
PubMed2003

Altered microvasculature is involved in remodeling processes in cardiomyopathic hamsters.

UNLABELLED: The cardiomyopathic hamster (BIO TO2) is a well-established model of heart failure. Deterioration of cardiac function in BIO TO2 is attributed to a defect in delta-sarcoglycan, whereas cardiac dysfunction in delta-sarcoglycan knockout mice is caused by microvascular abnormalities. We examined the relation between cardiac function and the microvasculature, including angiogenic factors, in BIO TO2. METHODS AND RESULTS: At the age of 5 weeks, percent fractional shortening (%FS) and positive rate of change in left ventricular pressure over time (dP/dt max) were lower in BIO TO2 than in age-matched F1B controls. Capillary density, capillary/myocyte (CM) ratio, capillary domain area (CDA), and myocyte density were similar between BIO TO2 and F1B controls. At the ages of 13 and 20 weeks, BIO had significantly lower capillary and myocyte densities and a significantly higher CM ratio and CDA. Myocyte density positively correlated with %FS and dP/dt max. There were no significant differences in mRNA expression for VEGF, Flt-1, angiopoietin-1, or angiopoietin-2 between BIO TO2 and F1B control. CONCLUSION: Progressive myocyte loss is responsible for deterioration of cardiac function in BIO TO2. The impaired neovascularization may be involved in the progress of cardiac remodeling in cardiomyopathic hamsters.

Animals↗
PubMed2003

Side branch protection with hydrophilic polymer coated guide wire during cutting balloon angioplasty of a bifurcated lesion.

Cutting balloon angioplasty (CBA) was performed in a patient with in-stent restenosis (ISR) which had an important side branch. We used a hydrophilic polymer-coated guide wire for side branch protection during CBA. After CBA was successfully performed, the cutting balloon and guide wire were microscopically examined and proven to have suffered minor damage which, in itself, did not disturb the procedure. Hydrophilic polymer-coated wire might be an effective and safe choice for ISR which needs to be treated by CBA while protecting an important side branch.

Aged↗