PubMed Health⌕ Search

Biomedical subjects

T Iwasaka

Publications and source records attributed to T Iwasaka.

At least 19 recordsLinked to original sources
PubMed2006

Effect of nifedipine on adiponectin in hypertensive patients with type 2 diabetes mellitus.

Nifedipine, a dihydropyridine calcium antagonist, improves endothelial function in patients with hypercholesterolaemia by enhancing nitric oxide (NO) activity, and increases endothelial NO bioavailability by antioxidant mechanisms. We administered a long-acting nifedipine formulation (controlled release (CR) nifedipine: 20 mg/day) to hypertensive patients for 6 months. There were no other changes of drug treatment during therapy with CR nifedipine. Clinical and biochemical data obtained before and after CR nifedipine administration were compared. All markers were measured by enzyme-linked immunosorbant assay. The levels of soluble markers (soluble CD40 ligand, soluble P-selectin, and soluble E-selectin), microparticles (MP) (platelet-derived MP, monocyte-derived MP, and endothelial cell-derived MP), and adiponectin differed between the control group and the hypertension group. The levels of these markers were also different in hypertensive patients with and without type 2 diabetes compared with the control group. In the hypertensive patients with type 2 diabetes, all markers except adiponectin decreased significantly after 3 months of CR nifedipine treatment. In contrast, markers were unchanged in the hypertensive patients without type 2 diabetes. Adiponectin was increased after 6 months of CR nifedipine treatment in hypertensive patients with type 2 diabetes. The effects of CR nifedipine on platelet/monocyte activation and adiponectin levels demonstrated in the present study indicate the potential effectiveness of calcium antagonist therapy for hypertensive patients with type 2 diabetes.

Adiponectin↗
PubMed2006

Genetic analysis of HLA, NA and HPA typing in type 2 diabetes and ASO.

We examined the genetic status of human leucocyte antigens (HLA), human platelet alloantigens (HPA) and neutrophil-specific antigens (NA) in patients with type 2 diabetes mellitus and diabetic arteriosclerosis obliterans (ASO). To our knowledge, the present study is the first report showing the relationship among three genetic factors in type 2 diabetes mellitus and ASO patients. HLA typing was performed by the polymerase chain reaction (PCR)-restriction fragment length polymorphism method. HPA-typing and NA-typing were by a PCR-sequence-specific primer method. The incidence of HLA-DRB1*1501 was found to be significant in type 2 diabetes and non-diabetic, particularly ASO-positive patients, compared to control subjects. There were no differences in NA1/NA2 between the control and diabetic or non-diabetic ASO groups. However, the frequency of NA2/NA2 in ASO-positive diabetes and non-diabetic ASO patients was significantly higher than controls. The a/b genotype of HPA-5a/5b was significantly lower in type 2 diabetes and non-diabetic ASO-positive patients than in controls. These findings suggest that genetic studies of HLA, NA and HPA could be useful to understand the pathogenesis of type 2 diabetes and ASO.

Adult↗
PubMed2005

Benidipine improves oxidized LDL-dependent monocyte and endothelial dysfunction in hypertensive patients with type 2 diabetes mellitus.

We investigated the effects of long-term benidipine treatment on levels of monocyte and endothelial cell activation markers in hypertensive patients with (n = 28) and without (n = 10) type 2 diabetes mellitus. Benidipine, 4 mg/day, was administered for 6 months; there were no other changes in any of the patients pharmacologic regimens during benidipine treatment. Clinical and biochemical data obtained before and after benidipine administration were compared; all markers were measured by ELISA. The levels of platelet activation markers (CD62P, CD63, and PAC-1), microparticles (monocyte-derived microparticles: MDMPs, and endothelial cell-derived microparticles: EDMPs), chemokines (monocyte chemotactic peptide 1: MCP-1, regulated on activation normally T-cell expressed and secreted: RANTES) and soluble adhesion markers (soluble E-selectin and soluble ICAM-1) differed in the control and hypertension groups. In addition, levels of platelet, monocyte, and endothelial cell activation markers, microparticles, chemokines, and soluble adhesion molecules were higher in hypertensive patients than in those without type 2 diabetes. Furthermore, benidipine administration decreased the concentrations of all these markers. The effect of this drug was significant in diabetes patients with high levels of antioxidized low-density lipoprotein (LDL) antibody. These results suggest that benidipine is effective for the treatment of oxLDL-dependent vascular disorders in hypertensive patients with type 2 diabetes.

Aged↗
PubMed2005

Association of leukocyte activation, but not the common cold, with restenosis after percutaneous coronary intervention in patients with angina pectoris.

We investigated the relationship between the common cold and restenosis after percutaneous coronary intervention (PCI) in Japanese patients with angina pectoris, because suffering from a common cold during the follow-up period after PCI may be involved in the development of restenosis. In addition, we measured the soluble (s) L-selectin level early after PCI in patients with and without restenosis. The study group included 104 effort angina pectoris patients. We examined whether or not they had had a common cold in the 6 months following angioplasty. Finally, 88 patients, whose common cold status was known, were selected as the study subjects. Twelve patients caught a common cold after PCI. All of these patients were given antibiotics and/or anti-inflammatory agents and recovered within 2 weeks. None had clinically detectable influenza infection. Thirty-three patients suffered from restenosis and 55 did not. There was no significant difference in the restenosis frequency between effort angina pectoris patients with and without a common cold. The sL-selectin level was significantly increased in patients with restenosis early after PCI, whereas in patients without restenosis, sL-selectin remained unchanged. These findings suggest that restenosis development after PCI in patients with effort angina pectoris may involve leukocyte activation early after PCI, while suffering from a common cold during the follow-up period after PCI has no effect.

Aged↗
PubMed2004

Membranous glomerulonephritis associated with hepatitis C virus infection: case report and literature review.

We describe the case of a 51-year-old man with hepatitis C virus (HCV) infection and a 3-month history of facial edema. Laboratory tests upon admission for renal biopsy showed normal renal function and normocomplementemia. Serum HCV antibody (Ab) and cryoglobulin were positive. Renal biopsy specimens showed features of membranous glomerulonephritis. The likely cause was immune complex-mediated glomerulonephritis associated with HCV infection. Reports of similar cases in the literature show the normocomplementemia and negative or slightly positive cryoglobulins observed in our case as well as seropositivity for circulating immune complexes containing HCV RNA. In our case, electron microscopic examination of the subepithelial glomerular lesions revealed massive virus-like particles within unusual multilayers of electron-dense deposits (EDDs), suggesting the existence of HCV in the glomeruli. In the addition to the unique histopathological feature the presence of La/SS-B antibody in his serum indicated an abnormal immune response associated with HCV. We advise him to undergo the therapy with new type of IFN such as pegIFN-alpha2a and/or anti-viral agent like ribavirin to achieve clinical and histopathological improvement.

Glomerulonephritis, Membranous↗
PubMed2003

Renal blood flow measurement with contrast-enhanced harmonic ultrasonography: evaluation of dopamine-induced changes in renal cortical perfusion in humans.

BACKGROUND: An accessible non-invasive method for evaluating renal regional blood flow in real time is highly desirable in the clinical setting. Recent progress in ultrasonography with microbubble contrast has allowed quantification of regional blood flow in animal models. AIMS: Goal ofthis study was to establish a convenient contrast--enhanced harmonic ultrasonography (CEHU) method for evaluating renal cortical blood flow in humans. METHODS: We carried out intermittent second harmonic imaging in 9 healthy volunteers. Pulse interval was progressively decreased from 4 s - 0.2 s during continuous venous infusion of the microbubble contrast agent. RESULTS: Pulse interval versus CEHU-derived acoustic intensity plots provided microbubble velocity (MV) and fractional vascular volume (FVV) during renal cortical perfusion in humans. Low-dose dopamine infusion (2 microg/min/kg) resulted in a significant increase in MV which correlated well with the increase in total renal blood flow (RBF) determined by a conventional study of p-aminohippurate clearance (C(PAH)) (r = 0.956, p < 0.0001). Although FVV was not significantly increased, alterations in CEHU-derived renal cortical blood flow calculated by the products of MV and FVV were also correlated with alterations in total RBF (r = 0.969, p < 0.0001). Thus, low-dose dopamine infusion increases renal cortical blood flow observed in CEHU, mainly by increasing MV. CONCLUSIONS: The present study shows that renal cortical blood flow in humans can be measured non-invasively by CEHU and that CEHU can be used for quantitatively evaluating changes induced by a therapeutic agent such as dopamine in flow velocity and in FVV.

Adult↗
PubMed2002

Detection of monocyte-derived microparticles in patients with Type II diabetes mellitus.

AIMS/HYPOTHESIS: The role of plasma monocyte-derived microparticles (MDMPs) and platelet-activation markers (platelet-derived microparticle [PDMP], platelet-bound CD62P [plt-CD62P], and platelet-bound CD63 [plt-CD63]) in diabetic vascular complications is not clear. We measured and compared plasma concentrations of MDMPs and the platelet-activation markers to investigate their possible contribution to diabetic vascular complications. METHODS: Activated platelets and microparticles (PDMP and MDMP) were analysed by flow cytometry. Concentrations of serum sE-selectin were measured with enzyme-linked immunosorbent assay. RESULTS: The concentration of MDMPs in diabetic patients was higher than in normal subjects. We found no differences in the binding of anti-GPIIb/IIIa and anti-GPIb monoclonal antibodies between groups. There were differences, however, in the concentrations of PDMPs, plt-CD62P, and plt-CD63 between Type II (non-insulin-dependent) diabetes mellitus patients and control subjects (PDMPs: 585 +/- 25 vs 263 +/- 9, p < 0.01; plt-CD62P: 28.1 % +/- 1.4 % vs 9.4 % +/- 0.6 %, p < 0.001; plt-CD63: 28.1 % +/- 1.4 % vs 8.6 % +/- 0.5 %, p < 0.001). Amounts of MDMPs correlated positively with these platelet activation markers, and the relation between PDMP and MDMP was the most significant. The concentration of MDMP in patients who had diabetes complicated with nephropathy, retinopathy, or neuropathy was higher than in those without diabetes-related complications. The increase in MDMP was particularly significant in patients with nephropathy. Concentrations of sE-selectin were higher in Type II diabetes patients than in control subjects, and correlated with MDMP, PDMP, plt-CD62P, and plt-CD63 levels in nephropathy patients. CONCLUSION/INTERPRETATION: In Type II diabetes patients, we detected increased activation of monocytes, which could have been stimulated by activated platelets and PDMPs. Because the activation of monocytes is associated with vascular endothelial damage, high concentrations of MDMPs could indicate vascular complications in diabetes patients, especially those who have diabetes-related nephropathy.

Antigens, CD↗
PubMed2002

Association of parvovirus B19 infection with acute glomerulonephritis in healthy adults: case report and review of the literature.

An otherwise healthy 20-year-old woman presented with an erythematous rash on her face as well as arthralgia and anemia. She also had systemic edema, proteinuria and hypertension. Laboratory data on admission showed hypocomplementemia, human parvovirus B 19 (HPV) DNA and both immunoglobulin (Ig) M and IgG antibodies to HPV in her serum. Renal biopsy specimens showed features of endocapillary glomerulonephritis under light microscopy. Electron microscopy showed massive subendothelial electron-dense deposits. No cause was probable other than immune complex-mediated glomerulonephritis associated with HPV infection. In a review of this and similar cases reported in the literature, several characteristic features come to light: female dominance, onset in the second or third decade of life, hypocomplementemia, histologic renal endocapillary and/or mesangioproliferative glomerulonephritis with subendothelial deposits and spontaneous recovery.

Adult↗
PubMed2001

Endometrioid adenocarcinomas of the uterine corpus in women younger than 50 years of age can be divided into two distinct clinical and pathologic entities based on anatomic location.

BACKGROUND: This study used the clinicopathologic profiles of Japanese women younger than 50 years of age with endometrial carcinoma to distinguish the clinicopathologic features of carcinomas of the lower uterine segment (LUS) from those of carcinomas of the corpus mucosa proper (CMP). METHODS: Eighty-eight endometrial carcinomas in women younger than 50 years old (25.3%) were selected from our file of 348 Japanese women with endometrial carcinoma. Seventy-two were classified as carcinomas of the CMP and 16 carcinomas of the LUS. A tumor was judged to be a carcinoma of the LUS when it involved a continuous area ranging from the lower corpus to the upper cervix with or without intervention of a portion of uninvolved LUS. RESULTS: The mean ages of women with carcinomas of the CMP and LUS were 41.2 and 39.0 years, respectively. In comparison to carcinomas of the LUS, carcinomas of the CMP were more strongly associated with reproductive risk factors including parity (P = 0.01) and polycystic ovary syndrome (P = 0.02). There was no significant difference in body mass index or the incidence of diabetes mellitus and hypertension between women presenting with carcinomas of the CMP and LUS. Histologically, carcinomas of the LUS more frequently showed a high-grade endometrioid tumor (P = 0.02) with deep myometrial invasion (P < 0.01) and were less associated with endometrial hyperplasia (P < 0.01) than those of the CMP. CONCLUSIONS: Carcinomas of the LUS occurred predominantly in women younger than 50 years of age and had clinicopathologic features distinct from carcinomas of the CMP in women younger than 50 years of age.

Adenocarcinoma↗
PubMed2001

Early identification of impaired myocardial reperfusion with serial assessment of ST segments after percutaneous transluminal coronary angioplasty during acute myocardial infarction.

To evaluate the relation between ST-segment analysis and microvascular reperfusion in patients with acute myocardial infarction (AMI), we studied 51 patients with first AMI who were successfully treated by percutaneous transluminal coronary angioplasty (PTCA). The lead showing the greatest ST-segment elevation on the 12-lead electrocardiogram (ECG) was serially investigated until 24 hours after PTCA. Successful reperfusion was determined by technetium-99m tetrofosmin single-photon emission computed tomography. Impaired reperfusion (group 1: < 4 change in the sum of the defect score from before to immediately after PTCA) was observed in 24 patients, and successful reperfusion (group 2) was observed in 27 patients. Although ST-segment elevation was reduced significantly at 30 minutes after PTCA in group 2 (2.2 +/- 1.4 to 1.7 +/- 1.3 mm, p = 0.01), there was no significant change in group 1 (1.9 +/- 1.9 to 2.4 +/- 1.7 mm). Ten of 14 patients (71%) with persistent ST-segment elevation (DeltaST > 0 mm change in ST segment from before to 30 minutes after PTCA > 0) were in group 1, whereas 23 of 37 patients (62%) with ST-segment resolution (DeltaST < or = 0) were in group 2. The sensitivity and specificity of persistent ST-segment elevation for predicting impaired microvascular reperfusion were 42% and 85%, respectively. Thus, persistent ST-segment elevation 30 minutes after primary PTCA was a highly specific electrocardiographic marker of impaired reperfusion in patients with AMI.

Aged↗
PubMed2001

Implantation of bone marrow mononuclear cells into ischemic myocardium enhances collateral perfusion and regional function via side supply of angioblasts, angiogenic ligands, and cytokines.

BACKGROUND: Bone marrow implantation (BMI) was shown to enhance angiogenesis in a rat ischemic heart model. This preclinical study using a swine model was designed to test the safety and therapeutic effectiveness of BMI. METHODS AND RESULTS: BM-derived mononuclear cells (BM-MNCs) were injected into a zone made ischemic by coronary artery ligation. Three weeks after BMI, regional blood flow and capillary densities were significantly higher (4.6- and 2.8-fold, respectively), and cardiac function was improved. Angiography revealed that there was a marked increase (5.7-fold) in number of visible collateral vessels. Implantation of porcine coronary microvascular endothelial cells (CMECs) did not cause any significant increase in capillary densities. Labeled BM-MNCs were incorporated into approximately 31% of neocapillaries and corresponded to approximately 8.7% of macrophages but did not actively survive as myoblasts or fibroblasts. There was no bone formation by osteoblasts or malignant ventricular arrhythmia. Time-dependent changes in plasma levels for cardiac enzymes (troponin I and creatine kinase-MB) did not differ between the BMI, CMEC, and medium-alone implantation groups. BM-MNCs contained 16% of endothelial-lineage cells and expressed basic fibroblast growth factor>>vascular endothelial growth factor>angiopoietin 1 mRNAs, and their cardiac levels were significantly upregulated by BMI. Cardiac interleukin-1beta and tumor necrosis factor-alpha mRNA expression were also induced by BMI but not by CMEC implantation. BM-MNCs were actively differentiated to endothelial cells in vitro and formed network structure with human umbilical vein endothelial cells. CONCLUSIONS: BMI may constitute a novel safety strategy for achieving optimal therapeutic angiogenesis by the natural ability of the BM cells to secrete potent angiogenic ligands and cytokines as well as to be incorporated into foci of neovascularization.

Angiopoietin-1↗
PubMed2001

Conservative therapy for adenocarcinoma and atypical endometrial hyperplasia of the endometrium in young women: central pathologic review and treatment outcome.

Thirty-nine patients with endometrioid adenocarcinoma (EA) and atypical hyperplasia (AH) of the endometrium who received conservative treatment to preserve fertility were collected from member institutions of the Japan Gynecologic Oncology Study Group. Twenty-nine and ten were originally diagnosed with EA without myometrial invasion and AH, respectively. We performed a central pathological review to make definite diagnoses, and the diagnosis of EA in 29 cases was changed to AH in ten, complex hyperplasia in three and atypical polypoid adenomyoma in three, and AH in ten was changed to EA in one and simple hyperplasia in one. Nine of 12 women (75%) with EA and 15 of 18 women (83%) with AH had an initial response to medroxyprogesterone acetate (MPA) treatment. Two of nine responders with EA later developed relapse, and one of them had metastasis to the left obturator lymph node. Two became pregnant, and one delivered one full-term infant. One of the responders with AH had a relapse in the endometrium. Five became pregnant, and four delivered four normal infants. The young women with endometrial carcinoma localized in the endometrium who wish to preserve fertility may be treated as successfully with MPA as those with AH.

Adenocarcinoma↗
PubMed2001

Effect of angiotensin II type 2 receptor on tyrosine kinase Pyk2 and c-Jun NH2-terminal kinase via SHP-1 tyrosine phosphatase activity: evidence from vascular-targeted transgenic mice of AT2 receptor.

Angiotensin II (Ang II) has two major receptor isoforms, AT1 and AT2. AT1 transphosphorylates Ca(2+)-sensitive tyrosine kinase Pyk2 to activate c-Jun NH2-terminal kinase (JNK). Although AT2 inactivates extracellular signal-regulated kinase (ERK) via tyrosine phosphatases (PTP), the action of AT2 on Pyk2 and JNK remains undefined. Using AT2-overexpressing vascular smooth muscle cells (AT2-VSMC) from AT2-transgenic mice, we studied these undefined actions of AT2. AT1-mediated JNK activity was increased 2.2-fold by AT2 inhibition, which was abolished by orthovanadate. AT2 did not affect AT1-mediated Pyk2 phosphorylation, but attenuated c-Jun mRNA accumulation by 32%. The activity of src-homology 2 domain-containing PTP (SHP-1) was significantly upregulated 1 min after AT2 stimulation. Stable overexpression of SHP-1 dominant negative mutant in AT2-VSMC completely abolished AT2-mediated inhibition of JNK activation and c-Jun expression. These findings suggest that AT2 inhibits JNK activity by affecting the downstream signal of Pyk2 in a SHP-1-dependent manner, leading to a decrease in c-Jun expression.

Angiotensin Receptor Antagonists↗
PubMed2001

Angiotensin AT(1) and AT(2) receptors differentially regulate angiopoietin-2 and vascular endothelial growth factor expression and angiogenesis by modulating heparin binding-epidermal growth factor (EGF)-mediated EGF receptor transactivation.

Angiotensin II (Ang II)-mediated signals are transmitted via heparin binding epidermal growth factor (EGF)-like growth factor (HB-EGF) release followed by transactivation of EGF receptor (EGFR). Although Ang II and HB-EGF induce angiogenesis, their link to the angiopoietin (Ang)-Tie2 system remains undefined. We tested the effects of Ang II on Ang1, Ang2, or Tie2 expression in cardiac microvascular endothelial cells expressing the Ang II receptors AT(1) and AT(2). Ang II significantly induced Ang2 mRNA accumulations without affecting Ang1 or Tie2 expression, which was inhibited by protein kinase C inhibitors and by intracellular Ca(2+) chelating agents. Ang II transactivated EGFR via AT(1), and inhibition of EGFR abolished the induction of Ang2. Ang II caused processing of pro-HB-EGF in a metalloproteinase-dependent manner to stimulate maturation and release of HB-EGF. Neutralizing anti-HB-EGF antibody blocked EGFR phosphorylation by Ang II. Ang II also upregulated vascular endothelial growth factor (VEGF) expression in an HB-EGF/EGFR-dependent manner. AT(2) inhibited AT(1)-mediated Ang2 expression and phosphorylation of EGFR. In an in vivo corneal assay, AT(1) induced angiogenesis in an HB-EGF-dependent manner and enhanced the angiogenic activity of VEGF. Although neither Ang2 nor Ang1 alone induced angiogenesis, soluble Tie2-Fc that binds to angiopoietins attenuated AT(1)-mediated angiogenesis. These findings suggested that (1) Ang II induces Ang2 and VEGF expression without affecting Ang1 or Tie2 and (2) AT(1) stimulates processing of pro-HB-EGF by metalloproteinases, and the released HB-EGF transactivates EGFR to induce angiogenesis via the combined effect of Ang2 and VEGF, whereas AT(2) attenuates them by blocking EGFR phosphorylation. Thus, Ang II is involved in the VEGF-Ang-Tie2 system via HB-EGF-mediated EGFR transactivation, and this link should be considerable in pathological conditions in which collateral blood flow is required.

Angiopoietin-1↗
PubMed2001

Correlates of bundle-branch block in patients undergoing primary angioplasty for acute myocardial infarction.

BACKGROUND: Early reperfusion therapy has reduced the infarct size and mortality rate in patients with acute myocardial infarction (AMI). The occurrence of bundle-branch block in AMI is related to the amount of myocardial damage and the insult to the conduction system. HYPOTHESIS: To evaluate the clinical and angiographic factors related to the occurrence of bundle-branch block (BBB) in patients with primary percutaneous transluminal coronary angioplasty (PTCA), we investigated consecutive series of patients with their first Q-wave AMI and successful PTCA. METHODS: Coronary angiogram at the time of admission, electrocardiogram, and echocardiogram were evaluated in 279 patients with their first Q-wave AMI and successful PTCA. RESULTS: Bundle-branch block was detected in 26 patients (9%); 16 patients had transient and 10 patients had persistent block, while 16 patients had bifascicular block and 10 patients had right BBB. The patients with BBB had a significantly larger number of left ventricular asynergic segments, higher incidence of total occlusion of infarct-related artery, angiographic no reflow, and pericardial rub than those without BBB. When the multivariate analysis was performed using five clinical markers of infarct severity, angiographic no reflow (F = 20.2, p < 0.001) and total occlusion of infarct-re-lated artery (F = 4.2, p = 0.04) were found to be the significant variables related to BBB. CONCLUSIONS: Despite successful primary PTCA, absence of antegrade flow in the infarct-related artery at the onset of AMI and/or angiographic no reflow resulted in more severe transmural myocardial damage and, hence, the occurrence of BBB.

Aged↗
PubMed2001

Inhibition of cardiac delayed rectifier K+ currents by an antisense oligodeoxynucleotide against IsK (minK) and over-expression of IsK mutant D77N in neonatal mouse hearts.

The IsK (minK or KCNE1) protein is known to co-assemble with the KvLQT1 (KCNQ1) protein to form a channel underlying the slowly activating delayed rectifier K+ current (IKs). Controversy remains as to whether the IsK protein assembles with ERG (the ether-a-go-go-related gene) products to form or modulate the channel-underlying the rapidly activating delayed rectifier K+ current (IKr). We investigated the effects of antisense oligodeoxynucleotides (AS-ODN) against IsK and its mutant D77N [which underlies a form of long QT syndrome (LQT5) in humans] on the delayed rectifier K+ current (IK) of neonatal mouse ventricular myocytes in primary culture. Patch-clamp experiments on these cells showed that IK consists of IKs and IKr. IK was not recorded from ventricular cells transfected with AS-ODN, while it was recorded from cells transfected with the corresponding sense oligodeoxynucleotides (S-ODN). IK was not recorded from cells transfected with the D77N mutant, and the action potential duration was much longer than in cells transfected with wild-type IsK. Furthermore, HERG could not induce currents in COS-1 cells co-expressed with the D77N mutant and HERG (the human form of ERG). These results indicate that the IsK protein associates with both KvLQT1 and ERG products to modulate IKr and IKs in cardiac myocytes.

Action Potentials↗
PubMed2001

Evidence for infection with Helicobacter pylori in patients with acute myocardial infarction.

BACKGROUND: Anti-Helicobacter pylori (HP) IgA and IgG antibody titers were measured in patients with ischemic heart diseases. METHODS: There were 60 healthy individuals that served as control subjects, and 21 patients with acute myocardial infarction (AMI), 34 with old myocardial infarctions (OMI), 35 with effort angina (AP) and 41 with vasospastic angina (VSA). RESULTS: In the control group, the IgA and IgG anti-HP antibody titers were positively correlated with age. When the IgA and IgG antibody titers were compared among patient groups, IgG did not significantly differ between each patient group and the control group, whereas IgA was significantly higher in the AMI group (5.10+/-1.25 EV) than in the OMI (p<0.01), AP, or the control (p<0.05). Moreover, the positivity rate for IgA anti-HP antibody was the highest in the AMI group (90%), with an odds ratio to the age-matched control group of 4.09, whereas the positivity rate for IgG did not significantly differ between the groups when either the 10 or 55 U/ml cut-off value was used. CONCLUSIONS: These results suggest that an increased IgA antibody titer, which is an index of the active phase of HP infection, should be an etiological marker for acute myocardial infarction.

Antibodies, Bacterial↗