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Yasunori Ueda

Publications and source records attributed to Yasunori Ueda.

25 records · Page 2Linked to original sources
PubMed2003

Plaque characterization and atherosclerosis evaluation by coronary angioscopy.

When observed by angioscopy, the culprit lesions of acute coronary syndrome (ACS) have a common appearance of a yellow plaque with irregular surface covered by a thrombus. Angioscopy is a powerful device to detect not only the ruptured plaques at ACS lesions but also the yellow plaques in their early stages. The culprit lesions of ACS are sometimes detected by angioscopy even in the angiographically normal segments of coronary arteries. Angioscopy can further classify the culprit lesions of ACS as (1) vasospasm, (2) plaque rupture, or (3) plaque erosion according to the angioscopic definitions. These classifications may be beneficial to determine the treatment strategy. Anti-vasospastic medications rather than stenting may be more suitable for the treatment of vasospasm-induced ACS. Percutaneous coronary intervention (PCI) of ruptured plaque rather than of erosive plaque tends to cause more distal embolization with thrombus and plaque contents. Therefore, distal protection device may be more beneficial for those cases. Although angioscopy may be able to identify vulnerable plaques as the plaques of intensive yellow color, it may be more practical to identify the patients at high risk of suffering ACS by evaluating the extent of coronary atherosclerosis. The process and the time course of plaque formation, maturation, and disruption are left to be clarified, however, the number of yellow plaques or the yellow color intensity of those plaques may be a marker of coronary atherosclerosis. Angioscopy should be useful not only as a diagnostic tool but also as an investigational tool. The effect of medications that regress coronary atherosclerosis may be evaluated by the angioscopically determined markers of coronary atherosclerosis.

Acute Disease↗
PubMed2003

Celiprolol increases coronary blood flow and reduces severity of myocardial ischemia via nitric oxide release.

Celiprolol is a selective beta(1)-adrenoceptor antagonist with antihypertensive actions, which causes renal vasodilation by increasing tissue nitric oxide (NO) levels. The authors tested whether celiprolol increases coronary blood flow (CBF) by increasing cardiac NO release in the ischemic heart in vivo. In open-chest dogs, coronary perfusion pressure of the left anterior descending coronary artery was reduced so that CBF decreased to 60% of control levels, and thereafter, coronary perfusion pressure was maintained constant. Ten minutes after the reduction of coronary perfusion pressure, we infused celiprolol into the left anterior descending coronary artery and measured fractional shortening and lactate extraction ratio as indices of regional myocardial contractility and metabolism. CBF significantly increased from 51.5 mL/100 g/min +/- 1.9 to 67.0 mL/100 g/min +/- 5.1 20 minutes after celiprolol infusion without changes in coronary perfusion pressure, while fractional shortening and lactate extraction ratio increased. Celiprolol also increased cardiac NO release. The L omega-nitroarginine methyl ester, the inhibitor of NO synthase, attenuated the increases in CBF, fractional shortening, lactate extraction ratio, and cardiac NO release due to celiprolol. ICI 118551, a beta(2)-adrenoceptor antagonist, did not blunt the effects of celiprolol and a nonselective beta-adrenoceptor antagonist, propranolol, increased neither CBF nor cardiac NO release, indicating that the effect of celiprolol is independent of beta-adrenoceptor blockade. It was concluded that celiprolol mediates coronary vasodilation and improves myocardial ischemia through NO-dependent mechanisms.

Animals↗
PubMed2002

Comparison of time of reperfusion during anterior wall acute myocardial infarction to left ventricular volume one month and 20 months later.

We studied 95 patients with a first anterior wall acute myocardial infarction who received successful reperfusion within 72 hours after the onset. The patients were divided into 4 groups based on the time required to achieve reperfusion; <3 hours (n = 23), 3 to 6 hours (n = 42), 6 to 24 hours (n = 17), and >24 to 72 hours (n = 13). The infarct size, as evaluated by thallium-201 single-photon emission computed tomography, at 1 month after the infarct was significantly larger (p <0.05) in >24 to 72 hours (1,593 +/- 652 U) than that in <3 hours (749 +/- 650 U), but was not significantly different from that at 3 to 6 hours (1,353 +/- 770 U) or 6 to 24 hours (1,371 +/- 561 U). The end-diastolic volume index at 1 month did not differ among the 4 groups. However, the end-diastolic volume index during the follow-up period (20 +/- 8 months) in >24 to 72 hours (93 +/- 23 ml/m(2)) was significantly larger than that in the other 3 groups (<3 hours [65 +/- 21 ml/m(2)], 3 to 6 hours [65 +/- 22 ml/m(2)], and 6 to 24 hours [70 +/- 25 ml/m(2)]). Similar findings were observed in end-systolic volume index. In conclusion, although infarct size reduction was not observed by late reperfusion, left ventricular volumes at 1 month were comparable among patients with successful reperfusion within 3 and up to >24 hours. Left ventricular volumes 2 years after acute myocardial infarction were significantly larger in patients who did not under reperfusion for >24 hours.

Aged↗
PubMed2002

Aplastic anaemia with 13q-: a benign subset of bone marrow failure responsive to immunosuppressive therapy.

In an attempt to determine the pathological significance of a long arm deletion of chromosome 13 (13q-) in bone marrow failure syndrome, we reviewed the clinical records of nine patients who were initially diagnosed with aplastic anaemia due to bone marrow hypoplasia without dysplasia. Six patients responded to immunosuppressive therapy and the other three improved with steroids. None of the patients developed acute leukaemia (follow up: 54-129 months) and the estimated 5-year survival was 78%. These findings indicate that pancytopenia with 13q- represents bone marrow failure of a benign nature, similar to aplastic anaemia without karyotypic abnormalities, rather than preleukaemia.

Adult↗
PubMed2002

[Usefulness of coronary angioscopy for the evaluation of hyperlipidemia].

Hyperlipidemia is one of the major coronary risk factors, which leading to the clinical worse outcome in patients with coronary artery disease, that is, acute coronary syndrome. Coronary plaque rupture followed by the formation of thrombus has been revealed to be a major cause of acute coronary syndrome. It would be important to detect the vulnerable plaque before its rupture, but there were no ways to detect by the conventional methods except coronary angioscopy. Yellow plaque and thrombus are mostly observed at the culprit lesion by the coronary angioscopy, which suggests that vulnerable plaque is dark yellow. Coronary angioscopy may diagnose the high-risk group among patients with hyperlipidemia.

Angioscopy↗