The association between microalbuminuria (MAU) and the indices of macrovascular complication in patients with newly diagnosed type 2 diabetes (D) or essential hypertension (H) was evaluated. Total 446 patients were classified into four groups according to the urinary albumin-to-creatinine ratio: MAU-D (n = 104), normoalbuminuria (NAU)-D (n = 114), MAU-H (n = 116), and NAU-H (n = 112). The indices of macrovascular complication including arterial stiffness evaluated by pulse-wave-velocity (PWV), carotid intima-media thickness (IMT), and vascular inflammation marked by high-sensitivity C-reactive protein (hsCRP) were assessed. PWV, IMT, and hsCRP were higher in patients with MAU than in those with NAU in both diabetes and hypertension groups. In both MAU-D and MAU-H groups, PWV and hsCRP levels were positively correlated with MAU level (MAU-D: r = 0.47, 0.41, MAU-H: r = 0.36, 0.62, respectively, P < 0.05). Additionally, PWV and hsCRP were independent factors predicting MAU (diabetes group: OR 1.85, 1.54, hypertension group: OR 1.38, 1.51, respectively, P < 0.001), but not IMT. MAU is independently associated with arterial stiffness and vascular inflammation but not with IMT in patients with newly diagnosed type 2 diabetes or essential hypertension, which emphasizes the importance of proactive clinical investigations for atherosclerotic complications in patients with MAU, even in newly diagnosed diabetes or hypertension.
Albuminuria ; Area Under Curve ; C-Reactive Protein/analysis ; Cardiovascular Diseases/etiology ; Carotid Intima-Media Thickness ; Creatinine/urine ; Diabetes Mellitus, Type 2/complications/*diagnosis/physiopathology ; Female ; Humans ; Hypertension/complications/*diagnosis/physiopathology ; Logistic Models ; Male ; Middle Aged ; Multivariate Analysis ; Odds Ratio ; Risk Factors ; Vascular Stiffness

BACKGROUND AND OBJECTIVES: Chlamydia pneumoniae (CP) has been linked with atherosclerosis. While several studies have shown that CP contributes to the acceleration of atherosclerotic lesions, any studies on the initiation of atherosclerosis are sparse. The present study investigated whether CP infection could initiate atherosclerotic lesions in rats that are known to be resistant to atherosclerosis; further, we investigated if these lesions do form, then how does the CP participate in this and develop of atherosclerosis in these rats. MATERIALS AND METHODS: Thirty 11-week-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats, thirty type 2 diabetic rats and thirty age-matched Long-Evans Tokushima Fatty (LETO) rats that were maintained on a high-cholesterol diet were either mock-inoculated or inoculated intranasally 3 times at 11, 13 and 15 weeks of age. The serum levels of the lipid profiles, plasminogen activator inhibitor-1 (PAI-1), monocyte chemoattractant protein-1 (MCP-1) and C-reactive protein (CRP) were measured by performing ELISA at 24 weeks and 40 weeks of age. The atherosclerotic lesion areas were analyzed, and immunohistochemical staining using chlamydia genus-specific monoclonal antibody and PDGF-B was performed in the ascending aorta at 40 weeks of age. RESULTS: Immunohistochemical staining with using specific monoclonal antibody demonstrated CP infection in the vessel walls. The serum PAI-1 level of the OLETF rats was higher than that of the LETO rats (p<0.05) regardless of the state of the CP infection, but there were no differences in the serum MCP-1 and CRP levels between the OLETF rats and the LETO rats. While no atherosclerotic lesion was observed in the mock-infected LETO rats, early-to-advanced atherosclerotic lesions were found in the other rat groups. CP-infected OLETF rats showed more advanced atherosclerotic lesions and greater mean lesion areas than the other rat groups (LT-N, 0 mm2; LETO-CP, 3.29+/-1.23 mm2; OT-N, 4.91+/-2.11 mm2; OT-CP, 9.20+/-4.62 mm2)(p<0.05). The characteristics of the atherosclerotic lesions in the rats were intimal thickening that was mainly composed of smooth muscle cells. The atherosclerotic lesion area positively correlated with the presence and the extent of PDGF-B staining in the aortic wall (p<0.01). CONCLUSION: Chronic infection of CP in the vessel walls initiated the development of atherosclerosis in the LETO rats and it accelerated the atherosclerosis in the OLETF rats. CP-induced smooth muscle proliferation and the resultant intimal thickening may be mediated by PDGF-B in these atherosclerotic lesions.
Acceleration ; Animals ; Aorta ; Atherosclerosis* ; C-Reactive Protein ; Chemokine CCL2 ; Chlamydia* ; Chlamydophila pneumoniae* ; Diet ; Enzyme-Linked Immunosorbent Assay ; Muscle, Smooth ; Myocytes, Smooth Muscle ; Plasminogen Activator Inhibitor 1 ; Plasminogen Activators ; Rats* ; Rats, Inbred OLETF

Although neurologic complications of multiple myeloma are common, brain-involvement is rare, despite the high frequency of the cranial lesions. The cranial plasmacytoma grows only from bone, dura mater or adjacent mucous membrane and cerebral structures are affected secondarily. It is less likely that a solitary cranial plasmacytoma exists, and patients who harbor these neoplasms should undergo complete evaluations to exclude multiple myeloma. Solitary plasmacytoma is radiosensitive and the definite treatment for the cranial plasmacytoma usually consists of complete surgical resection with adjacent radiation therapy. However, the treatment and prognosis of the cranial plasmacytoma depends on whether this neoplasm is primary or secondary. Most of patients develop cranial plasmacytoma as the presenting form of multiple myeloma and the treamtment of in these speical cases is usually unsatisfatory. We report a case of multiple myeloma presented with the motor weakness of both upper and lower extremities by a bulky cranial plasmacytoma invading cerebrum treated with surgery, radiation therapy and chemotherapy.
Cerebrum* ; Drug Therapy ; Dura Mater ; Humans ; Lower Extremity ; Mucous Membrane ; Multiple Myeloma* ; Plasmacytoma* ; Prognosis

BACKGROUND AND OBJECTIVES: Connective tissue growth factor (CTGF) is a profibrotic cytokine, which may play an important role in the development of diabetic cardiovascular complications. ACE inhibition significantly prevents cardiovascular events in diabetics, although the mechanism remains obscure. The purpose of this study was to explore the effect of ACE inhibitors on the expression of CTGF and oxidative stress in the diabetic heart, and determine the effects of long term treatment with ACE inhibitors on diabetic cardiomyopathy. MATERIALS AND METHODS: Thirty OLETF (Otsuka Long Evans Tokushima Fatty) diabetic and thirty LETO (Long Evans Tokushima Otsuka) nondiabetic control rats were randomized into four groups for 24 weeks of treatment with either ramipril (5 mg/kg/day, n=15, each groups) or saline (n=15, each groups). RESULTS: The OLETF diabetic rats had prominent perivascular fibrosis, as shown by picrosirius red stains, compared to the LETO nondiabetic rats. ACE inhibition significantly prevented perivascular fibrosis in OLETF rats (p<0.01). Immunohistochemical stains were used to detect proteins for the receptors of advanced glycation end products (RAGE), CTGF, collagen III and nitrotyrosine. Although there were no significant differences in the myocardiac collagen contents, as found by measuring the hydroxyproline concentration among the four groups, the OLFTF diabetic rats had significantly increased cardiac CTGF and collagen III protein expression compared with the nondiabetic rats. The ACE inhibitor attenuated the increases in RAGE (-50.3%; p<0.01), CTGF (-37.5%; p<0.01) and collagen III (-52.3%; p<0.01) expression in the diabetic heart microvascular area. The OLFTF rats showed marked an increment in cardiac nitrotyrosine, a marker of protein oxidation. Ramipril also inhibited the expression of cardiac nitrotyrosine (-78.3%; p<0.01). CONCLUSION: The present study shows a possible role of RAGE/nitrotyrosine/CTGF in the diabetic cardiomyopathy of OLETF rats. The long term treatment of high dose ACE inhibitors may have beneficial effects on the diabetic heart through both antioxidant and antifibrotic mechanisms.
Angiotensin-Converting Enzyme Inhibitors ; Animals ; Collagen ; Coloring Agents ; Connective Tissue Growth Factor* ; Connective Tissue* ; Diabetic Cardiomyopathies ; Fibrosis* ; Glycosylation End Products, Advanced ; Heart* ; Hydroxyproline ; Oxidative Stress ; Rage ; Ramipril* ; Rats* ; Rats, Inbred OLETF

BACKGROUND AND OBJECTIVES: Coronary flow reserve (CFR) is the capability of coronary arteriolar bed to dilate in response to increased cardiac metabolic demand. Nocorandil, a hybrid of ATP-sensitive K+ channel opener and nitrates, causes coronary vasodilation of both epicardial and resistance vessels. We investigated the feasibility and safety of nicorandil as compared to adenosine in the measurement of CFR using a Doppler guide wire. SUBJECTS AND METHODS: We measured CFR in 26 consecutive patients (mean age 52+/-19 years, M:F=16:10) during coronary intervention with a 0.014-inch Doppler guide wire. We recorded the baseline average peak velocity (APV) and the hyperemic APV induced by intracoronary adenosine or nicorandil. The heart rate, mean aortic pressure and the time interval from maximal APV to baseline APV were also recorded. RESULTS: There were no significant differences between APV, diastole/systole velocity ratio and CFR induced by adenosine and those induced by nicorandil (44.4 +/- 17.3 vs 45.5 +/- 17.6, p=0.78, 1.59 +/- 0.51 vs 1.57 +/- 0.52 p=0.78, 2.22 +/- 0.89 vs 2.27 +/- 0.94, p=0.36). The CFR and diastole/systole velocity ratio induced by nicorandil showed a strong positive linear correlation with those by adenosine (r2=0.77, p=0.0001, r2=0.83, p=0.0001). Adenosine significantly decreased the heart rate as compared to nicorandil =-25.5 +/- 9.7 vs -8.7 +/- 4.9 bpm, p=0.001). There were no differences in the changes of mean aortic pressure between adenosine and nicorandil (-7 +/- 9 vs -2 +/- 3 mmHg, p=0.17). Nicorandil prolonged the time interval from maximal APV to baseline APV compared to adenosine (194 +/- 62 vs 37 +/- 12 sec, p=0.001). CONCLUSION: Nicorandil is feasible and safe for use in measuring CFR using a Doppler guide wire and may replace adenosine.
Adenosine* ; Arterial Pressure ; Blood Flow Velocity ; Heart Rate ; Humans ; Nicorandil* ; Nitrates ; Ultrasonography ; Vasodilation

BACKGROUND AND OBJECTIVES: Matrix metalloproteinase-9 (MMP-9) plays an important role in the genesis of atherosclerotic plaque rupture and acute coronary syndrome (ACS), including an acute myocardial infarction (AMI). A single nucleotide polymorphism (SNP) in the MMP-9 promoter (-1562C>T) has recently been identified. This study investigated whether the SNP of the MMP-9 promoter is a significant risk factor for an AMI due to plaque rupture and if SNPs affect the transcription of the gene that elevates the MMP-9 expression level. SUBJECTS AND METHODS: A polymerase chain reaction, followed by a restriction fragment length polymorphism analysis, was performed in 173 control participants and 206 AMI patients. The serum levels of MMP-9 in the groups with or without the SNP were measured, using ELISA, and compared. RESULTS: There was a significantly higher incidence of the -1562C>T MMP-9 polymorphism in the AMI compared to the control group (27.6% vs. 17.9%, p=0.04). A multiple logistic regression analysis of the risk factors for coronary artery disease and the MMP-9 polymorphism showed the MMP-9 polymorphism to be an important factor in the prediction of an AMI (odds ratio 1.67, 95% confidence interval 1.02-2.67, p=0.04). CONCLUSION: The -1562C>T polymorphism in the MMP-9 promoter is a definite risk factor for an AMI, and is associated with elevated MMP-9 expression. These results suggest that a SNP in the MMP-9 promoter is strongly associated with an Acute Myocardial Infarction.
Acute Coronary Syndrome ; Coronary Artery Disease ; Enzyme-Linked Immunosorbent Assay ; Humans ; Incidence ; Logistic Models ; Matrix Metalloproteinase 9* ; Myocardial Infarction* ; Plaque, Atherosclerotic ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic* ; Risk Factors ; Rupture

BACKGROUND AND OBJECTIVES: Vasospastic angina (VA) is a specific type of coronary artery disease and develops as a result of coronary artery spasm. Recently, a few studies have revealed that VA caused by coronary artery spasm is related to genetic traits. The objective of this study was to use the recently developed technique of array comparative genomic hybridization (CGH) to screen the genetic aberrations of VA. SUBJECTS AND METHODS: To identify candidate genes that might be causally involved in the pathogenesis of VA, genomic deoxyribonucleic acids were extracted from whole blood of 28 patients with VA who presented at Department of Cardiology at Seoul St. Mary's Hospital, Seoul, Korea. The copy number profiles of these patients was then analyzed using array CGH and reverse transcriptase (RT) quantitative polymerase chain reaction (PCR). RESULTS: Array CGH revealed gains in 31 different regions, with losses in the 4q35.2, 7q22.1, 10q26.3, 15q11.2, 16p13.11, 17p11.2 and 19q13.3 regions (more than 32% aberration in these regions). Several loci were found to be frequently including gains of 5p and 11q (50% of samples). The most common losses were found in 7q (54% of samples). Copy number aberrations in chromosomal regions were detected and corresponding genes were confirmed by RT quantitative PCR. The fold change levels were highest in the CTDP1 (18q23), HDAC10 (22q13.33), KCNQ1 (11p15.5-p15.4), NINJ2 (12p13.33), NOTCH2 (1p12-p11.2), PCSK6 (15q26.3), SDHA (5p15.33), and MUC17 (7q22.1) genes. CONCLUSION: Many candidate chromosomal regions that might be related to the pathogenesis of VA were detected by array CGH and should be systematically investigated to establish the causative and specific genes for VA.
Cardiology ; Coat Protein Complex I ; Comparative Genomic Hybridization ; Coronary Artery Disease ; Coronary Vessels ; DNA ; Humans ; Korea ; Polymerase Chain Reaction ; RNA-Directed DNA Polymerase ; Spasm

Kawasaki Disease (KD) is an acute, febrile, multisystem disease of children. More severe complications in 15~25% of cases include, the development of coronary aneurysms, ischemic heart disease, and sudden cardiac death. The standard treatment for significant coronary artery stenosis has generally been aortocoronary bypass surgery, although percutaneous transluminal coronary angioplasty (PTCA) has been described in a small number of patients. This report describes a 14 year old boy with a history of KD who developed multiple coronary aneurysms and stenosis. We performed PTCA, which was successful in relieving the stenosis of the left circumflex artery.
Adolescent ; *Angioplasty, Transluminal, Percutaneous Coronary ; Coronary Aneurysm/diagnosis/etiology/therapy ; Coronary Angiography ; Coronary Stenosis/diagnosis/etiology/*therapy ; Coronary Vessels/ultrasonography ; Endosonography ; Follow-Up Studies ; Humans ; Male ; Mucocutaneous Lymph Node Syndrome/*complications/diagnosis

No abstract available.
Heart* ; Pericardial Effusion*

BACKGROUND AND OBJECTIVES: The treadmill exercise test (TMT) is used as a first-line test for diagnosing coronary artery disease (CAD). However, the findings of a TMT can be inconclusive, such as incomplete or equivocal results. Aortic valve sclerosis (AVS) is known to be a good predictor of CAD. We determined the usefulness of assessing AVS on 2-dimensional (2D) echocardiography for making the diagnosis of CAD in patients with inconclusive results on a TMT. SUBJECTS AND METHODS: This prospective study involved 165 consecutive patients who underwent a TMT that resulted in inconclusive findings, 2D echocardiography to detect AVS, and coronary angiography to detect CAD. Following echocardiography, AVS was classified as none, mild, or severe. CAD was defined as > or =70% narrowing of the luminal diameter on coronary angiography. RESULTS: CAD was more common in patients with AVS than in patients without AVS (75% vs. 47%, respectively, p<0.01). Multiple logistic regression analysis showed that AVS was the only independent predictor of CAD {odds ratio=8.576; 95% confidence interval (CI), 3.739-19.672}. The sensitivity, specificity, accuracy, positive predictive value, and negative predictive value of the presence of AVS for predicting CAD in a patient with an inconclusive TMT were 62%, 67%, 64%, 75%, and 53%, respectively. During a 1-year clinical follow-up, patients with and without AVS were similar in terms of event-free survival rates. CONCLUSION: If the results of TMT for patients with chest pain on exertion are inconclusive, the presence of AVS on echocardiography is a good predictor of CAD.
Aortic Valve ; Chest Pain ; Coronary Angiography ; Coronary Artery Disease ; Coronary Vessels ; Disease-Free Survival ; Echocardiography ; Exercise Test ; Follow-Up Studies ; Humans ; Logistic Models ; Phenobarbital ; Prospective Studies ; Sclerosis ; Sensitivity and Specificity