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Kazuhisa Kodama

Publications and source records attributed to Kazuhisa Kodama.

At least 19 recordsLinked to original sources
PubMed2006

Multislice computed tomographic findings of the anomalous origins of the right coronary artery: evaluation of possible causes of myocardial ischemia.

BACKGROUND: Anomalous right coronary arteries (RCA) arising from the left sinus of Valsalva may cause myocardial ischemia. OBJECTIVE: We evaluated morphological features of anomalous RCA by using multislice computed tomography (MSCT) in relation to myocardial ischemia provoked by myocardial perfusion single-photon emission computed tomography. METHODS: MSCT was performed in a total of 3, 212 patients by using an Aquillion 16 and a Light Speed Ultra. Retrospective ECG-gated image reconstruction was performed. Volume rendering, axial and curved multiplanar reformatted images were analyzed for the determination of the origin and course of the RCA, the take-off angle of the RCA from the aorta, and size of the RCA orifice. Furthermore, virtual angioscopic images were also used for the evaluation of the RCA orifice structure. RESULTS: Anomalous origins of the RCA were found in 15 patients. In 13 patients, the RCA arose from the left sinus of Valsalva, and in 2 patients it arose from the left main coronary artery as a single coronary artery. The RCA coursed anteriorly between the ascending aorta and pulmonary artery in 14 patients, whereas it had a retroaortic course in 1 patient. Acute angle take-off (<30 degrees ) of the RCA from the aorta and the left main coronary artery was observed in 8 patients, intramural course of the RCA within the aortic wall was observed in 6 patients and a small RCA orifice was observed in 4 patients. Exercise-induced myocardial ischemia was present in 5 patients. CONCLUSION: Coursing between the aorta and pulmonary artery, acute angle take-off and intramural course were thought to be major causes of exercise-induced ischemia in patients with anomalous origins of the RCA.

Aged↗
PubMed2006

Usefulness of plasma brain natriuretic peptide concentration for predicting subsequent left ventricular remodeling after coronary angioplasty in patients with acute myocardial infarction.

To determine the relation between plasma brain natriuretic peptide (BNP) and remodeling in terms of infarct-related artery (IRA) patency, 106 patients with a first anterior wall acute myocardial infarction with a patent IRA at 1 month were studied. The IRA reoccluded at 6 months in 17 patients (reoccluded IRA) and was patent in 89 patients (patent IRA). The 2 groups did not differ with respect to clinical characteristics, hemodynamic variables, and left ventricular function at 1 month, except for left ventricular end-diastolic and systolic volumes, which were significantly greater in the reoccluded IRA group. Plasma BNP concentration in the reoccluded IRA group (336 +/- 288 pg/ml) was significantly higher than that in the patent IRA group (116 +/- 106 pg/ml) at 1 month. BNP concentration decreased significantly at 6 months in the 2 groups (reoccluded IRA vs patent IRA 152 +/- 162 vs 44 +/- 58 pg/ml, p <0.05). The increase in left ventricular volume from 1 to 6 months was significantly correlated with plasma BNP concentration at 1 month in the patent IRA group (r = 0.314, p < 0.01) and the reoccluded group (r = 0.634, p < 0.01). Linear regression analysis showed that the correlation between the 2 parameters in the 2 groups was similar. Based on stepwise multivariate linear regression analysis, only plasma BNP concentration was significantly correlated with the increase in left ventricular volume from 1 to 6 months in the 2 groups. In conclusion, these results suggest that plasma BNP concentration predicts left ventricular dilation independently of IRA patency.

Angioplasty, Balloon, Coronary↗
PubMed2006

Number of yellow plaques detected in a coronary artery is associated with future risk of acute coronary syndrome: detection of vulnerable patients by angioscopy.

OBJECTIVES: We sought to test whether the risk of acute coronary syndrome (ACS) can be estimated by angioscopy. BACKGROUND: Disruption of vulnerable plaque and subsequent thrombosis is regarded as a major mechanism of ACS. Although yellow plaques are supposedly vulnerable, the association between angioscopically determined extent of coronary atherosclerosis and risk of ACS events has not been reported. METHODS: Patients (n = 552) who received catheterization and angioscopic examination for the diagnosis of coronary artery diseases were prospectively included and followed up for new onset of ACS events. Yellow color intensities of all detected yellow plaques were graded as 1, 2, or 3 according to the standard colors. Number of yellow plaques (NYP) in a coronary artery and maximum color grade of detected yellow plaques (maxYP) were determined. Association between the incidence of ACS events and angioscopic findings were analyzed. RESULTS: Follow-up interval was 57.3 +/- 22.1 months. Acute coronary syndrome events were detected in 39 patients (7.1%). Although maxYP was not statistically different (2.0 +/- 0.7 vs. 1.8 +/- 0.9; p = 0.18), NYP was higher in the patients with an ACS event than those without the event (3.1 +/- 1.8 vs. 2.2 +/- 1.5; p = 0.008). Patients with NYP > or =2 and those with NYP > or =5 had 2.2- and 3.8-fold higher event rates, respectively, than those with NYP 0 or 1 (9.0% and 15.6%, respectively, vs. 4.1%; p = 0.02). Multivariate logistic regression analysis revealed NYP and multivessel disease as the independent risk factors of ACS events. CONCLUSIONS: Patients with multiple yellow plaques per vessel have a higher risk of suffering ACS events than those with NYP 0 or 1. Angioscopy would be useful to detect vulnerable patients.

Acute Disease↗
PubMed2006

Angioscopic evaluation of neointima coverage: sirolimus drug-eluting stent versus bare metal stent.

BACKGROUND: The process of neointima formation after bare metal stent (BMS) implantation has been previously elucidated by angioscopic observations; however, that after drug-eluting stent (DES) implantation has not been clarified. Therefore, we compared the angioscopic appearance of neointima over DESs with that over BMSs 6 months after implantation. METHODS AND RESULTS: Patients who received an implantation of a BMS (n = 13) or a sirolimus DES (n = 24) were included in this study. Angiographic and angioscopic examinations were performed at 6 months. The color of the stented lesion (white or yellow), coverage of stent by neointima (not covered, covered by a thin layer, or buried under neointima), and thrombus at the stented lesion (presence or absence) were angioscopically evaluated. Of the 24 lesions in which a DES was implanted, 11 (46%) had a part where the stent strut had no coverage, 21 (88%) had a part where it was covered by a thin layer, and 11 (46%) had a part where it was buried under neointima. Of the 13 lesions in which a BMS was implanted, 1 (8%) lesion had a part where the stent strut had no coverage, 4 (31%) lesions had a part where it was covered by a thin layer, and 13 (100%) lesions had a part where it was buried under neointima. The prevalence of a stent buried under neointima (46% vs 100%, P = .001) was lower and that of thrombus (42% vs 8%, P = .03) was higher in DES-implanted lesions as compared with BMS-implanted lesions. The prevalence of thrombus (64% vs 17%, P = .005) was higher in the yellow area than in the white area when a DES was implanted. CONCLUSION: Sirolimus DESs, as compared with BMSs, were poorly covered by neointima and were accompanied by thrombus especially when there was a yellow plaque under the stents. Thus, the thrombogenic potential in DES-implanted lesions may be sustained by the inhibition of neointima formation over thrombogenic plaques.

Aged↗
PubMed2006

[Acute coronary syndrome diagnosed by the intravascular imaging].

Coronary plaque rupture and the following formed thrombus have been revealed the cause of acute coronary syndrome. This evidence had been proposed by the pathologists 100 years ago; however, the intravascular imaging such as intravascular ultrasound (IVUS) or coronary angioscopy has revealed the clinical evidences in live human being. Thrombus and yellow plaque detected by coronary angioscopy as well as the ruptured fibrous cap detected by IVUS are the characteristics for the lesion of ACS, which does not show the significant stenosis. Thus, ACS lesion should be diagnosed by IVUS or coronary angioscopy.

Angina, Unstable↗
PubMed2006

Angioscopically-determined extent of coronary atherosclerosis is associated with severity of acute coronary syndrome.

OBJECTIVE: Some patients with acute coronary syndrome (ACS) have large myocardial infarction but others have small or no infarction. However, what makes this difference has not been clarified. We compared the angioscopic findings between those two categories of ACS patients and examined the association between the severity of ACS and the morphology of both culprit lesion and nonculprit coronary segments. METHODS: Prospectively and consecutively enrolled patients with ACS were classified as CK-elevation-ACS (CKE-ACS; n = 54) or non-CK-elevation-ACS (NCKE-ACS; n = 22). Patients were diagnosed as CKE-ACS when the elevation (greater than twice the normal upper limit) of CK-MB was detected; otherwise, patients were diagnosed as NCKE-ACS. They all underwent emergent catheterization and PCI of the culprit lesion. The entire culprit artery was observed by angioscopy, and the prevalence of thrombus and the color grade of yellow plaques were evaluated. The color grade of yellow plaques were classified as 0 (white), 1 (slight yellow), 2 (yellow), or 3 (intense yellow) according to the standard colors. The color grade of culprit plaque (CC), number (NP) and maximum (MC) color grade of yellow plaques in the nonculprit segments, plaque index (PI = N x MC), and prevalence of thrombus at the culprit lesion (CT) and in the nonculprit segments (NT) were compared between CKE-ACS and NCKE-ACS patients. RESULTS: CC (1.9 +/- 0.9 vs. 1.7 +/- 0.8; p = 0.3) and CT (93% vs. 77%; p = 0.06) were not significantly different between CKE-ACS and NCKE-ACS patients, however, NP (2.2 +/- 1.6 vs. 1.4 +/- 1.2; p = 0.03), MC (1.8 +/- 0.9 vs. 1.2 +/- 0.9; p = 0.008), PI (4.8 +/- 4.4 vs. 2.4 +/- 3.1; p = 0.03), and NT (39% vs. 11%; p = 0.02) were significantly higher in CKE-ACS than in NCKE-ACS patients. CONCLUSION: Although the culprit lesions of CKE- and NCKE-ACS had similar yellow color grades, the culprit lesions of CKE-ACS showed a trend towards a higher prevalence of thrombus. A greater number of yellow plaques of higher color grades and a higher prevalence of thrombosis in the nonculprit segments were detected in CKE-ACS compared to NCKE-ACS patients. The angioscopically-determined extent of coronary atherosclerosis appeared advanced in CKE-ACS patients compared to NCKE-ACS patients.

Acute Disease↗