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Biomedical subjects

Kimio Kamimori

Publications and source records attributed to Kimio Kamimori.

8 recordsLinked to original sources

Method analysis for optimal continuous imaging using intravascular optical coherence tomography.

OBJECTIVES: Optical coherence tomography(OCT)is a high-resolution imaging method that can clearly visualize vessels through the displacement of blood with flushing agents. Continuous imaging methods have not been established. This study investigated optimal methods for continuous OCT imaging. METHODS: Thirty-four arteries with stent implantation (24 peripheral and 10 coronary arteries)in 14 pigs were examined using OCT with a motorized pullback device. Two imaging methods (flush alone by liquid substance and flush with occlusion) were compared. Adequate image acquisition was defined as the entire circumferential intimal layer being detectable within continuous segments. To investigate factors that could influence image quality, stented regions were divided into 4-5 mm segments. RESULTS: The flush with occlusion method provided better OCT images compared to flush alone (flush with occlusion: 60.9%, flush alone: 8.7%, p = 0.0002). Using the flush with occlusion method, the rate of adequate image acquisition was 64.4% and visualization of > 75% intimal circumference was 83.5%. Intravascular ultrasound could detect all stented regions. Segmental analyses found more adequate images were detected in smaller vessels (adequate segment: 3.8 +/- 0.4 mm, inadequate segment: 4.2 +/- 0.8 mm, p < 0.0001) or with centered image wire position (adequate segment: center 35%, inadequate segment: center 14%, p = 0.003). In addition, side branches did not affect image quality. CONCLUSIONS: To acquire continuous OCT images, the flush with occlusion method was more effective compared to flush alone. Moreover, image quality is affected by vessel size and imaging wire position. These results suggest that optimized OCT imaging can provide continuous vessel detection.

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Left ventricular remodeling after myocardial infarction in antecedent hypertensive patients.

Antecedent hypertension adversely affects mortality and heart failure after myocardial infarction (MI). In addition, accelerated ventricular remodeling is a contributor to the increased mortality observed after MI. The purpose of this study was to assess the relationship of antecedent hypertension to ventricular remodeling after MI. Ninety-four patients presenting with a first acute MI who were treated with reperfusion therapy within 12 h of their symptom onset were enrolled in this study. All of them underwent left ventriculography immediately after reperfusion therapy and again at 6 months after the occurrence of MI. Patients were divided into two groups: a hypertensive group and a normotensive group. End-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) values in the acute phase were compared to those at 6 months after acute MI in either group. The hypertensive group showed a significant increase in both EDVI and ESVI after 6 months, whereas the normotensive group did not. In addition, there was no change in EF in the hypertensive group, whereas EF increased significantly after 6 months in the normotensive group. As a result, the percent changes in ESVI and EF were significantly different between the hypertensive group and normotensive group. The results demonstrated that antecedent hypertension interacts with ventricular cavity dilatation after MI.

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Convalescent stage coronary flow reserve and late myocardial morphologic outcomes in patients with first anterior acute myocardial infarction.

BACKGROUND: Microvascular damage immediately after reperfusion therapy is an independent predictor of left ventricular function in patients with acute myocardial infarction (AMI). However, its recovery may vary among individuals and the relationship between convalescent stage microvasculature and late myocardial morphologic change is unclear. METHODS AND RESULTS: Patients treated with coronary angioplasty within 12 h of their first anterior AMI were enrolled in this study. Coronary flow reserve (CFR) was measured 3 weeks post AMI, in both branches of the left coronary artery: culprit (left anterior descending artery: LAD) and non-culprit (left circumflex artery: LCX). Left ventriculography was performed at 3 weeks and 6 months post AMI and compared. Seventeen patients showed abnormal CFR in the LAD (Group 1: CFR<2), whereas 20 patients showed normal CFR (Group 2: CFR >/=2). Percent changes of end-diastolic volume tended to be higher in Group 1 than in Group 2 (11.8+/-21.6% vs -1.3+/-14.4%, p=0.056), and %changes of end-systolic volume was significantly smaller in Group 2 (11.8+/-22.1% vs -8.7+/-25.1%, p<0.05). A statistically significant correlation was found between absolute and relative CFR in the LAD and %change of end-systolic volume (r=-0.58: p<0.001, and r=0.40: p<0.05, respectively). CONCLUSIONS: Microvascular function in the convalescent stage may be related to these favorable changes.

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Antecedent hypertension interacts with adverse ventricular remodeling after myocardial infarction.

BACKGROUND: Ventricular remodeling is an independent predictor of left ventricular function in patients with myocardial infarction (MI). Accelerated ventricular remodeling is a probable contributor to the increased mortality observed after MI in hypertensive patients. The purpose of this study is to assess the relationship of antecedent hypertension to ventricular remodeling after MI. METHODS: Seventy-nine patients presenting with a first acute MI (AMI) who were treated and attained Thrombolysis In Myocardial Infarction (TIMI) flow grade 3 with re-perfusion therapy within 12 hours of their symptom onset were enrolled in this study. All of them underwent left ventriculography (LVG) immediately after re-perfusion therapy and again at 6 months after the occurrence of MI. Patients were divided into two groups; hypertensive group and normotensive group. End-diastolic volume index (EDVI), end-systolic volume index (ESVI), and EF were compared between acute phase and 6 months after AMI in each group. RESULTS: The hypertensive group showed a significant increase in both EDVI and ESVI after 6 months, whereas the normotensive group did not. In addition, there was no change in EF in the hypertensive group, whereas EF increased significantly after 6 months in the normotensive group. As a result, percent change in ESVI and EF showed significantly differences between the hypertensive group and normotensive group, whereas percent change in EDVI showed no significant difference between the two groups. CONCLUSIONS: Antecedent hypertension interacts with ventricular remodeling after MI.

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Impact of HMG-CoA reductase inhibitors for non-treated coronary segments.

BACKGROUND: HMG-CoA reductase inhibitors (statin) have been reported to decrease coronary artery events in several angiographic studies. However, the mechanism by which statin achieve this is still unclear. The purpose of this study was to identify the effect of statin on coronary plaque using serial intravascular ultrasound analysis. METHODS AND RESULTS: In this study, 48 patients with 48 lesions were divided into the prescribed group (statin group, n = 22) or the non-prescribed group (control group, n = 26) after successful coronary artery stenting. IVUS images were obtained at consecutive 5 mm segments, 5 mm from the proximal stent edge, immediately after stenting and at 6 months follow up. External elastic membrane volume (EEMV), lumen volume (LV) and plaque volume (PV) were measured using Simpson's method. The control group revealed no significant serial change in EEMV, PV, and LV during 6 months. On the other hand, the statin group revealed significant reductions of PV (35.5 +/- 12.7 mm3 vs 30.9 +/- 15.6 mm3, p = 0.001), resulting in increase of LV (47.7 +/- 19.8 mm3 vs 52.5 +/- 22.2 mm3, p = 0.003) without EEMV change (82.8 +/- 21.8 mm3 vs 83.9 +/- 25.7 mm3, p = NS). Although percent EEMV and percent LV changes showed no differences between the two groups, a larger percent PV change was observed in the statin group compared to the control group (control; 5.8 +/- 20.3% vs statin; -20.4 +/- 21.8%, p = 0.02). CONCLUSION: The results of this study suggest that statin administration for 6 months reduces coronary plaque without positive vessel remodeling.

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The impact of IVUS guided bare metal stent implantation for non-small vessel.

UNLABELLED: Previous studies have shown larger target vessel or greater stent area contribute to reduced restenosis rate. Thus, intravascular ultrasound (IVUS)-guided bare metal stent (BMS) implantation for selected lesions might achieve drug-eluting stent-like outcomes. The aim was to examine the long-term outcomes of BMS using IVUS-guided optimization. METHODS: Consecutive 103 coronary artery lesions suitable for IVUS were enrolled. Using IVUS, final stent balloon size selected was 90 percent of media-to-media diameter at the lesion or distal reference. The balloon size was listed as follows: group A (3.0-3.5 mm, n = 15), group B (3.5-3.75 mm, n = 64), and group C (3.75-4.5 mm, n = 24). RESULTS: At post-intervention, average stent area increased by the balloon size (A: 7.2 +/- 1.4 mm2, B: 8.9 +/- 1.5 mm2, and C: 12.1 +/- 2.0 mm2, respectively p < 0.001). At 6 month follow up, the average lumen area increased by balloon size (A: 4.1 +/- 1.7 mm2, B: 5.7 +/- 1.2 mm2, and C: 8.1 +/- 2.0 mm2, respectively p < 0.001). Accordingly, group B and C revealed lower restenosis, compared to group A (A: 46.7%, B: 10.9%, C: 8.3%, A vs B: p = 0.001; C vs A: p = 0.015). Moreover, target lesion revascularization was less in group B and C than group A (A 26.6%, B 3.1%, C 0%, A vs B: p = 0.011; C vs A: p = 0.017). CONCLUSIONS: For non-small vessels, IVUS-guided BMS implantation showed less restenosis and target lesion revascularization compared to small vessels, mainly due to larger initial gain. These study results suggest that IVUS-guided optimal BMS implantation for selected lesions might result in favorable long-term outcomes similar to those seen using drug-eluting stents. For a decade, coronary stenting has become a standard therapy for coronary artery disease due to favorable long-term outcomes and simple treatment procedure. Furthermore, for the last two years, drug-eluting stents (DES), releasing antiproliferative agents from bare metal backbone, revealed the restenosis rates less than half of those seen using conventional bare metal stents (BMS). While target lesions especially suitable for DES continue to be identified, earlier BMS studies showed that larger target vessel or greater stent area contributed to less restenosis. Thus, optimal IVUS-guided BMS implantation for selected lesions might achieve DES-like long-term outcomes. This study was designed to examine the long-term outcomes of BMS with intravascular ultrasound (IVUS)-guided optimization, using coronary angiography and IVUS data.

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Percutaneous transluminal angioplasty and stent placement for subclavian steal syndrome with concomitant anterograde flow in the left internal mammary artery graft for coronary artery bypass--case report.

A 63-year-old man presented with subclavian steal syndrome associated with left internal mammary artery (IMA) bypass graft to a coronary artery. He was admitted with a history of oppressive sensation in the chest, dizziness, and light headedness on exertion for 2 weeks in March 2002. He had undergone myocardial revascularization consisting of a left IMA-to-left anterior descending coronary artery graft in April 1988. His blood pressure was 140/70 mmHg in the right arm and 80/64 mmHg in the left arm. Aortic arch arteriography revealed complete occlusion of the left subclavian artery proximal to the left IMA takeoff and subclavian steal with anterograde flow of the left IMA. Percutaneous angioplasty and stent placement with protection of the left IMA bypass graft using a balloon catheter was successfully performed without complication by cerebral or myocardial ischemia. Complete recanalization of the occluded left subclavian artery and anterograde flow of the left vertebral artery were achieved. His symptoms disappeared and blood pressure in the left arm recovered. This variant of coronary subclavian steal might require protection of the left IMA during angioplasty and stent placement.

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Hepatocyte growth factor production may be related to the inflammatory response in patients with acute myocardial infarction.

Hepatocyte growth factor (HGF) is a well-known powerful proliferative factor of vascular endothelial cells and it has been reported that plasma HGF concentrations are increased in acute myocardial infarction (AMI), although the mechanisms are not yet well delineated. Serum HGF levels and C-reactive protein (CRP) were measured in 22 patients with unstable angina pectoris (UAP) (15 males, 7 females; class IIb or IIIb of the Braunwald classification), 60 patients with AMI (37 males, 23 females; average time from the onset of symptoms to admission 4.6+/-0.7h, range, 0.5-12h), and 20 normal subjects. Immediate angioplasties were performed in 51 patients with AMI, and the time course of the HGF levels were measured in 31 patients among them. Heparin dramatically increased the HGF level and it declined to the normal range 18h after heparin injection. Blood samples were taken before heparin treatment, or at least 24h after. Serum HGF levels on admission was significantly increased in UAP (mean+/-SE: 0.30+/-0.03ng/ml, p<0.01), and AMI (0.27+/-0.02ng/ml, p<0.01) compared with the normal subjects (0.19+/-0.01 ng/ml). Even in the early stage (within 3 h of onset of symptoms to admission, average time was 1.8+/-0.1 h), serum HGF levels were already elevated (0.25+/-0.02 ng/ml, p<0.05). There was no significant difference between the HGF levels in UAP and AMI. Fifty-one of the 60 patients with AMI underwent immediate percutaneous transluminal coronary angioplasty and blood samples were obtained from 31 of them on days 7, 14, and 21 after MI. Serum HGF levels peaked on day 7 (0.34+/-0.04ng/ml, p<0.01) and there was a weak relationship between peak creatine kinase and serum HGF levels at that time. A statistically significant correlation was found between peak CRP and serum HGF levels on day 7 (r=0.62: p<0.001). Serum HGF levels decreased to nearly normal by day 21 (0.22+/-0.01 ng/ml). The study shows that serum HGF levels during the early stage of AMI increased significantly and peaked by day 7 after the onset, at which time there was a strong correlation with peak CRP levels. These data suggest that HGF production may be related to the inflammatory response in AMI.

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