Biomedical subjects

Kazuo Haze

Publications and source records attributed to Kazuo Haze.

22 records · Page 2Linked to original sources

PubMed2002

Neutrophil infiltration of culprit lesions in acute coronary syndromes.

BACKGROUND: Neutrophils in unstable atherosclerotic lesions have not received much consideration, despite accumulating evidence suggesting a link between systemic inflammation and acute coronary syndromes. METHODS AND RESULTS: Coronary artery segments were obtained at autopsy from 13 patients with acute myocardial infarction (AMI); 8 had a ruptured and 5 an eroded plaque. Patients (n=45) who had died of noncardiovascular diseases served as reference. Atherectomy specimens were obtained from 35 patients with stable angina pectoris (SAP) and from 32 patients with unstable angina pectoris (UAP). Antibodies against CD66b, elastase, myeloperoxidase, and CD11b identified neutrophils; CD10 identified neutral endopeptidase (NEP). CD66b-positive and NEP-positive neutrophils were counted and expressed as a number per square millimeter of tissue. All specimens with plaque rupture or erosion showed distinct neutrophil infiltration; the number did not differ between ruptured and eroded plaques. However, the number of NEP-positive neutrophils was significantly higher (P<0.0001) in ruptured plaques than in eroded plaques. UAP patients showed neutrophils in 14 of 32 culprit lesions; in SAP only 2 of 35 lesions contained neutrophils. The number of neutrophils and NEP-positive cells in patients with UAP was significantly higher (neutrophils, P<0.0005; NEP-positive cells, P<0.005) than in patients with SAP. CONCLUSIONS: The observations suggest that neutrophil infiltration is actively associated with acute coronary events. The high number of NEP-positive neutrophils in ruptured plaques, compared with eroded plaques, may reflect differences in the underlying pathophysiological mechanisms.

Acute Disease↗

PubMed2002

The impact of tranilast on restenosis after coronary angioplasty: the Second Tranilast Restenosis Following Angioplasty Trial (TREAT-2).

BACKGROUND: The Tranilast Restenosis Following Angioplasty Trial showed that oral administration of 600 mg/day of tranilast for 3 months markedly reduced the restenosis rate after percutaneous transluminal coronary angioplasty (PTCA) for de novo lesions. METHODS: We conducted the second multicenter, randomized, double-blinded placebo-controlled trial. A total of 297 patients with 329 lesions were randomly assigned to treatment with tranilast or a placebo for 3 months after successful PTCA for both de novo and restenotic lesions. Angiographic follow-up examination was done at 3 months, and angiograms were interpreted with a quantitative approach. RESULTS: Two hundred thirty-nine lesions (72.6%) in 216 of the patients (72.7%) met the criteria and were included in the assessment of restenosis. Lesion restenosis was defined as a loss of 50% or more of the initial gain, and the restenosis rates were 18.8% in the tranilast group (n = 112) and 44.1% in the placebo group (n = 127; P =.00005). The restenosis rate, defined as a percent stenosis of > or = 50% at follow-up examination, was also significantly lower in the tranilast group (25.9% versus 41.9%; P =.012). The numbers of restenotic lesions were 38 (33.9% of 112) in the tranilast group and 30 (23.6% of 127) in the placebo group. In restenotic lesions, the lesion restenosis rate was significantly lower in the tranilast subgroup (18.4% versus 53.3% with the first restenosis criterion; P =.004). CONCLUSION: The oral administration of tranilast for 3 months markedly reduced the restenosis rate after PTCA, even in restenotic lesions.

Administration, Oral↗

PubMed2002

Impact of diabetes on coronary stenosis and coronary artery calcification detected by electron-beam computed tomography in symptomatic patients.

OBJECTIVE: Ischemic heart disease is a pivotal complication for diabetic patients. Electron-beam computed tomography (EBCT) represents the only noninvasive method that allows for accurate quantification of coronary artery calcification that reflects underlying atherosclerotic disease. Although coronary calcium score (CCS) cut points that predict the presence of angiographic stenosis have been established in nondiabetic individuals, it is not known whether coronary calcifications in diabetic patients are associated with the presence of significant coronary stenoses. In this study, we evaluated the relationship between coronary calcifications and angiographic stenosis in symptomatic patients with or without type 2 diabetes. RESEARCH DESIGN AND METHODS: In this study, 282 patients (204 men and 78 women) with chest pain, including 101 diabetic patients and 181 nondiabetic patients (mean age 63 +/- 9.6 years), underwent coronary angiography and EBCT with determination of CCS using Agatston's method. Luminal stenosis >or= 50% was defined as significant coronary stenosis. RESULTS: Angiography identified 205 patients with significant stenoses (89 of 101 diabetic patients, 114 of 181 nondiabetic patients). The sensitivity and specificity of EBCT to detect significant coronary stenosis were not significantly different between diabetic and nondiabetic patients. In diabetic patients, a CCS >or=90 was associated with 75% sensitivity and 75% specificity, whereas a CCS >or=200 was associated with 64% sensitivity and 83% specificity. CONCLUSIONS: We demonstrated that calcification of the coronary arteries in symptomatic diabetic patients is well associated with severity of coronary stenosis, as in nondiabetic patients.

Adult↗

PubMedDate not supplied

Pathophysiological role of oxidized low-density lipoprotein in plaque instability in coronary artery diseases.

Oxidized low-density lipoprotein (ox-LDL) is considered to play a key role in the genesis of inflammatory processes in atherosclerotic lesions. It has also been shown that LDL isolated from patients with diabetes mellitus (DM) has an enhanced susceptibility to oxidation. Recently, a sandwich ELISA method for measurement of plasma ox-LDL levels has been developed. To elucidate the role of ox-LDL in plaque instability in coronary artery disease, we measured the plasma ox-LDL levels in patients with acute myocardial infarction (AMI), unstable angina pectoris (UAP), and stable angina pectoris (SAP), and moreover assessed whether a relationship is present between plasma ox-LDL levels and DM. We also measured the plasma ox-LDL level in a patient who died of AMI, thus enabling us to study the presence of ox-LDL and CD 36, which is one of the ox-LDL receptors, in the culprit lesion. Plasma ox-LDL levels were measured in 210 patients (AMI: 70, UAP: 70, SAP: 70), and in 55 control subjects. Plasma ox-LDL levels in AMI patients were significantly higher than in UAP patients (P<.0001), SAP patients (P<.0001), or controls (P<.0001). In the UAP group, plasma ox-LDL levels in patients with DM were significantly higher than those without DM (P<.005). The autopsied patient who died of AMI revealed an increased plasma level of ox-LDL, and immunohistochemically, the culprit coronary lesion contained abundant macrophage-derived foam cells, showing distinct positivity for ox-LDL and CD 36. These results strongly suggest an important role for ox-LDL in the genesis of plaque instability in human coronary atherosclerotic lesions.

Angina Pectoris↗