Synuclein Motor Dysfunction Composite Scale for the Discrimination of Dementia With Lewy Bodies From Alzheimer's Disease.

Background: An abnormal increase of α-synuclein in the brain is the hallmark of dementia with Lewy bodies (DLB). However, the diagnostic power of plasma α-synuclein in DLB is not yet confirmed. Parkinsonism is highly associated with and is one of the core clinical features of DLB. We studied plasma α-synuclein and developed a novel tool that combined plasma α-synuclein level and Motor Dysfunction Questionnaire (MDQ), namely Synuclein Motor Dysfunction Composite Scale (SMDCS), for the clinical discrimination of DLB from Alzheimer's disease (AD). Methods: This cross-sectional study analyzed participants' demographical data, plasma α-synuclein level, MDQ, structured clinical history questionnaire, neuropsychological and motor function tests, and neuroimaging studies. The power of plasma α-synuclein level, MDQ, and SMDCS for discriminating DLB from non-demented controls (NC) or AD were compared. Results: Overall, 121 participants diagnosed as 58 DLB, 31 AD, and 31 NC were enrolled. Patients with DLB had significantly higher mean plasma α-synuclein level (0.24 ± 0.32 pg/ml) compared to the NC group (0.08 ± 0.05 pg/ml) and the AD group (0.08 ± 0.05 pg/ml). The DLB group demonstrated higher MDQ (2.95 ± 1.60) compared to the NC (0.42 ± 0.98) or AD (0.44 ± 0.99) groups. The sensitivity/specificity of plasma α-synuclein level, MDQ, and SMDCS for differentiating DLB from non-DLB were 0.80/0.64, 0.83/0.89, and 0.88/0.93, respectively. Conclusion: Both plasma α-synuclein and MDQ were significantly higher in patients with DLB compared to the NC or AD groups. The novel SMDCS, significantly improved accuracy for the clinical differentiation of DLB from AD or NC.

Type A Aortic Dissection Presenting with Inferior ST-Elevation Myocardial Infarction.

UNLABELLED: Type A aortic dissection with concurrent ST-elevation myocardial infarction (STEMI) is relatively rare. However, it can be potentially fatal and easily misdiagnosed as STEMI alone. Misdiagnosis will lead to inappropriate administration of anticoagulant and thrombolytic therapy and delayed surgical repair of the aorta. In patients with STEMI, short reperfusion time is associated with improved survival, and minimizing the door-to-balloon time is the goal of therapy worldwide. However, signs critical for differential diagnosis may be overlooked in the rush to primary percutaneous coronary intervention. When a patient is encountered who presents with chest pain and ST elevation on electrocardiogram, STEMI should not be the only diagnosis considered. By using bedside available information, detailed history taking and focused physical examination, it is possible to avoid a mistaken diagnosis. Here we report a case of Stanford type A aortic dissection with STEMI that was initially misdiagnosed as sole acute inferior wall myocardial infarction. Patient mortality may have resulted from delayed diagnosis and surgical treatment. KEY WORDS: Acute myocardial infarction; Aortic dissection.

Changes in left atrial functional indexes in ischemic stroke patients.

BACKGROUND: Increased left atrial (LA) size has been proposed as a predictor of multiple adverse cardiovascular events including stroke. LA dysfunction can occur in the absence of increased LA size. However, the relationship between stroke and changes in LA function is not well known. METHODS: Patients with acute ischemic stroke and healthy controls were enrolled prospectively. Stroke patients received standard work-ups to determine the etiology of their strokes. Those patients with significant cardiac arrhythmia and heart failure were excluded. All participants received echocardiography examination. Conventional echocardiographic parameters were calculated and cardiac contractile characteristics of the left atrium and left ventricle were analyzed using vector velocity imaging (VVI) technique. RESULTS: In total, 87 patients with acute ischemic stroke and 20 controls were recruited. The mitral inflow E-wave velocities were lower and A-wave velocities were higher in stroke patients (0.76 ± 0.19 vs. 0.84 ± 0.16, p = 0.048; and 0.97 ± 0.20 vs. 0.76 ± 0.11, p < 0.001 respectively). Stroke patients had a higher active emptying percent of total LA emptying (60.5 ± 19.0%) compared with that in controls (33.5 ± 11.7%, p < 0.001). The minimal LA volume was larger in stroke patients (15.0 ± 10.5 mL) than that in controls (9.9 ± 4.2 mL, p = 0.021), whereas there was no difference in maximal LA volume between stroke patients (37.3 ± 16.5 mL) and controls (33.3 ± 9.9 ml, p = 0.366). The diastolic emptying index of the LA was significantly lower in stroke patients compared with that in controls (61.4 ± 14.6% vs. 70.2 ± 11.0%, p = 0.016). The mitral A-wave velocity and active emptying percent of total LA emptying were significantly higher in all stroke subtypes than those in controls. CONCLUSION: Acute ischemic stroke patients had altered mitral inflow velocities and emptying function of the left atrium. VVI is convenient for quantitative assessment of left atrial volumes and contractile characteristics. Functional changes of LA may occur without significant structural changes. Therefore, the clinical implications of LA functional indexes require further study.

Recurrent stress cardiomyopathy with different electrocardiographic abnormalities on each presentation in a depressed post-menopausal woman.

Stress cardiomyopathy (SCM) is a syndrome of transient cardiac abnormalities precipitated by intense emotional or physical stress. Differentiating SCM from acute myocardial infarction is often difficult but vital to avoid subjecting SCM patients to unnecessary reperfusion therapy and invasive coronary angiography. For accurate diagnosis, it is important that physicians be familiar with the current diagnostic criteria, most susceptible populations, and typical triggers for SCM. SCM occurs almost exclusively in post-menopausal women, a group with a high frequency of psychiatric disorders. Thus, in addition to typical trigger events, comorbid psychiatric disorders may contribute to SCM onset. We report a rare case of recurrent SCM with distinct electrocardiographic abnormalities during each presentation in a post-menopausal woman with depression. .

Repeated massive pulmonary air embolism during pacemaker implantation.

Pacemaker implantation is associated with the potential for various acute and late complications. Though they rarely occur, massive pulmonary air embolisms are lethal. We report the case of a 72-year old male with sick sinus syndrome who underwent permanent pacemaker implantation. Sedation was administered due to back pain with the resultant appearance of snoring. The procedure was complicated with repeated massive pulmonary air embolisms. The events occurred after the leads had been placed in the sheaths. The patient was successfully resuscitated with fluid challenge, O(2) supplement, vasopressor and catheter aspiration. This case illustrates that in a heavily sedated, snoring patient, the marked negative intrathoracic pressure can overcome the frictional resistance of air to being sucked into the gap between the lead body and sheath's wall. Careful manipulation alone is not enough to prevent pulmonary air embolisms. Aggressive treatment for upper airway obstruction is important. The use of a sheath with a haemostatic valve is strongly recommended if the upper airway obstruction cannot be treated adequately.

Inhibitory effect of α-lipoic acid on platelet aggregation is mediated by PPARs.

Peroxisome proliferator-activated receptors (PPARs) isoforms (α, ß/δ, and γ are present in human platelets, and activation of PPARs inhibits platelet aggregation. α-Lipoic acid (ALA), occurring naturally in human food, has been reported to exhibit an antiplatelet activity. However, the mechanisms underlying ALA-mediated inhibition of platelet aggregation remain unknown. The aim of this study was to investigate whether the antiplatelet activity of ALA is mediated by PPARs. ALA itself significantly induced PPARα/γ activation in platelets and increased intracellular amounts of PPARα/γ by blocking PPARα/γ secretion from arachidonic acid (AA)-activated platelets. Moreover, ALA significantly inhibited AA-induced platelet aggregation, Ca(2+) mobilization, and cyclooxygenase-1 (COX-1) activity, but increased cyclic AMP production in rabbit washed platelets. Importantly, ALA also enhanced interaction of PPARα/γ with protein kinase Cα (PKCα) and COX-1 accompanied by an inhibition of PKCα activity in resting and AA-activated platelets. However, the above effects of ALA on platelets were markedly reversed by simultaneous addition of selective PPARα antagonist (GW6471) or PPARγ antagonist (GW9662). Taken together, the present study provides a novel mechanism by which ALA inhibition of platelet aggregation is mediated by PPARα/γ-dependent processes, which involve interaction with PKCα and COX-1, increase of cyclic AMP formation, and inhibition of intracellular Ca(2+) mobilization.

Immediate change in pulmonary venous flow pattern after deployment of occluder device for atrial septal defect.

Transcatheter closure of a secundum defect using a septal occluder is a safe and effective procedure based on long-term follow-up, but no clinical studies have examined immediate hemodynamic changes. We evaluated pulmonary venous flow velocity pattern before and immediately after deployment of the Amplatzer septal occluder for closure of atrial septal defect. From May 2003 to January 2005, 48 patients with secundum atrial septal defect received transcatheter closure with complete occlusion. Patients were divided into two groups according to age: pediatric group, under 16 years (n = 30, age 7.3 +/- 3.2 years), and adult group, 16 years or older (n = 18, age 30.1 +/- 11.4 years). Pulmonary venous flow pattern was recorded by transesophageal echocardiography before and immediately after occluder deployment. Immediately after deployment in both patient groups, pulmonary vein systolic (S) and diastolic (D) wave velocity decreased, but atrial reversal (AR) wave velocity increased. In the pediatric group, S-wave was 56.1 +/- 17.1 versus 35.5 +/- 11.3 cm/sec (P < 0.001); D-wave was 57.6 +/- 12.5 versus 42.9 +/- 11.8 cm/sec (P < 0.001); and AR wave velocity was 12.2 +/- 3.8 versus 15.5 +/- 4.1 cm/sec (P < 0.001). In the adult group, S-wave was 48.4 +/- 13.7 versus 32.7 +/- 10.3 cm/sec (P < 0.001); D-wave was 51.9 +/- 11.7 versus 38.0 +/- 8.5 m/sec (P < 0.001); and AR wave velocity was 12.1 +/- 4.1 versus 16.2 +/- 4.9 cm/sec (P < 0.001). Comparison of pulmonary venous flow before and immediately after deployment of the Amplatzer septal occluder provides an excellent model to evaluate the influence of an atrial communication on pulmonary venous flow. Pulmonary venous forward flow decreases following atrial septal defect (ASD) closure.

Activated matrix metalloproteinase and disrupted myocardial collagen matrix in increased sympathetic activity following stimulation of dorsal medulla in the vagotomized feline model.

Sympathetic hyperactivation in many kinds of neurocardiogenic injury can result in obvious heart failure. We generated a vagotomized feline model in which sympathetic hyperactivation was induced by electrical stimulation of dorsal medulla (ESDM) of brain stem to investigate the relationship between disruption of extracellular collagen matrix (ECM) and activation of matrix metalloproteinases (MMPs) in myocardium in the sympathetic hyperactivity. Mean blood pressure, heart rate and plasma norepinephrine were all significantly increased from baseline to a peak at 5 min after ESDM. Echocardiographic study showed significant left ventricular dilatation and hypokinesia (ejection fraction: from 87.7 +/- 6.3% to 39.4 +/- 7.8%) from baseline to 180 mm after ESDM. Histopathological finding revealed significant overstretching or spring-like disappearance and disruption of ECM. MMP-2 expression was significantly increased in left ventricular myocardium as compared to sham. These results suggest that ESDM-induced sympathetic hyperactivity causes the expression of MMP-2 that disrupts myocardial ECM, contributing to the development of cardiac dysfunction.

Decreased circulating protective adiponectin level is associated with angiographic coronary disease progression in patients with angina pectoris.

Adipocyte cytokines regulate glucose metabolism and insulin resistance and adiponectin is thought to have a protective effect against atherosclerosis. Studies have shown that adiponectin expression is decreased in obese subjects and those with metabolic syndrome or diabetes mellitus. The purpose of this study was to investigate the relationship between circulating adipocyte cytokine concentrations and angiographic coronary artery disease (CAD) progression in patients with chest pain. Patients with stable angina pectoris who underwent repeat coronary angiograms and had serum samples at the time of first catheterization between March 1999 and January 2004 were enrolled. A modified Gensini scoring system was used to define angiographic coronary artery progression between the index and follow-up angiograms. Those who had significant angiographic progression of coronary lesions were classified into the progression group (N=55). Those who did not have CAD progression were classified into the non-progression group (N=102). Univariate analysis showed that CAD progression was associated with male gender (93% vs. 78%, p=0.038), higher baseline total cholesterol (187+/-43 vs. 173+/-39 mg/dl, p=0.037) and higher baseline fasting blood glucose (128+/-57 vs. 110+/-40 mg/dl, p=0.037). Patients in the progression group had a significantly lower serum adiponectin level (14.3+/-7.9 vs. 18.9+/-13.2 mug/ml, p=0.007) than, but resistin (28.9+/-13.4 vs. 34.4+/-26.0 ng/ml, p=0.142) and leptin (7.4+/-4.6 vs. 7.7+/-6.5 ng/ml, p=0.675) levels similar to, those in the non-progression group. In a multivariate binary logistic regression model, male gender (odds ratio 4.283, p=0.015), higher serum cholesterol (odds ratio 1.010, p=0.032) and lower serum adiponectin (odds ratio 0.959, p=0.030) were all significant independent predictors of CAD progression. In conclusion, we found that a decreased circulating level of adiponectin is associated with angiographic CAD progression in patients with angina pectoris.

Diabetes exacerbates angiographic coronary lesion progression in subjects with metabolic syndrome independent of CRP levels.

BACKGROUND: Metabolic syndrome is gaining more attention as a special cluster of cardiovascular risks. However, its role, with or without diabetes, in predicting atherosclerosis progression, remains largely undetermined. We investigated the predictors for angiographic coronary atherosclerosis progression in patients with metabolic syndrome and angina pectoris. METHODS: Patients with metabolic syndrome and angina pectoris who underwent repeat coronary angiograms and had serum samples at the time of first catheterization were enrolled for analysis (N=113). A modified Gensini scoring system was used to define CAD progression between the index and follow-up angiograms. Those who had significant angiographic progression of coronary disease were classified as the progression group (N=42) and those who did not as the non-progression group (N=71). RESULTS: There were more cases of diabetes mellitus (52% vs. 31%, p=0.040) in the CAD progression group. The progression group also had higher baseline fasting blood glucose (150+/-73 vs. 117+/-46 mg/dl, p=0.010) but similar LDL cholesterol (114+/-38 vs. 109+/-33 mg/dl, p=0.421) than the non-progression group. In terms of inflammatory markers, there was no difference in hs-CRP (p=0.208), MCP-1 (p=0.514), or sCD40L (p=0.549) between the groups. In binary logistic regression, diabetes mellitus remained a significant predictor of CAD progression (OR 2.43, p=0.030) for patients with metabolic syndrome and angina pectoris, but hs-CRP and LDL-C were not. CONCLUSION: Diabetes mellitus, but not inflammatory marker hs-CRP or LDL-C, is a significant predictor of angiographic CAD progression in patients with metabolic syndrome and angina pectoris.

Circulating hepatocyte growth factor level but not basic fibroblast growth factor level is elevated in angiography-proven symptomatic peripheral artery disease.

Circulating vasogenic factors may be up-regulated in response to ischemia to promote angiogenesis in patients with peripheral artery disease (PAD). Studies on this are limited in number and size, and results are inconsistent, especially regarding basic fibroblast growth factor (bFGF) level. From March 1999 to April 2004, all consecutive patients with lower limb PAD having serum samples at the time of intervention were recruited. The diameter of the primary PAD lesion had to be at least 70% stenotic at the lower limb artery. Control subjects, who underwent angiography, were free of PAD, coronary disease, and other major medical diseases. Serum samples were analyzed for circulating hepatocyte growth factor (HGF) and bFGF levels. Patients with PAD (n = 60) had higher circulating HGF levels (mean +/- SEM, 1,544 +/- 238 vs 970 +/- 129 pg/mL; P = .04) but similar bFGF distribution tertiles (P = .55) compared with control subjects (n = 30). Thirty-six patients with summed PAD lesion lengths exceeding 5 cm demonstrated a significantly higher circulating HGF level compared with control subjects (mean +/- SEM, 1,701 +/- 335 vs 970 +/- 129 pg/mL; P = .048). Patients with concurrent coronary artery disease tend to have a higher circulating HGF level (mean +/- SEM, 1,606 +/- 365 vs 970 +/- 129 pg/mL; P = .06) but not a higher bFGF level compared with control subjects. Circulating HGF level, but not bFGF level, is significantly elevated in patients with symptomatic angiographically documented PAD, especially in those with more extensive involvement.

C-reactive protein gene polymorphism 1009A>G is associated with serum CRP levels in Chinese men: a TCVGHAGE study.

BACKGROUND: Increased concentrations of high-sensitivity CRP (hs-CRP) are associated with increased risk of cardiovascular disease. This increase might be caused by low-grade inflammation, but a number of studies have suggested that serum CRP concentrations are under genetic control. Since the relation between CRP concentration and cardiovascular diseases occurs across ethnicities, we determined whether CRP gene variants affect fasting hs-CRP concentrations in a cohort of Chinese men. METHODS: High-sensitivity CRP concentrations were measured in 369 Chinese men. Six polymorphisms were identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and direct sequencing within the CRP gene: 969T>C, 1009A>G, and a 3-allele polymorphism 1440C>A>T in the 5' UTR (promoter region), 2667G>C in exon 2, and 3872A>G and 5992T>A in the 3' UTR. RESULTS: In a group of participants (n=328) whose fasting serum hs-CRP concentrations were within the 5th to 95th percentile, we found that the genetic polymorphism 1009A>G was significantly associated with fasting serum hs-CRP concentrations (GG vs. AG or AA genotypes, CRP concentrations 0.072+/-0.062 vs. 0.176+/-0.166 and 0.166+/-0.185 mg/dl, mean+/-S.D., both P=0.023). Furthermore, subjects carrying the 1009G bearing haplotype exhibited the lowest CRP concentrations (P=0.05). CONCLUSION: The CRP 1009A>G genotypes and associated haplotypes were associated with lower fasting serum hs-CRP concentrations in a group of elderly Chinese men.

An adult with aortic arch interruption associated with sinus venosus atrial septal defect and partial anomalous pulmonary venous connection.

Interruption of the aortic arch is a rare and usually lethal congenital anomaly that is often associated with multiple cardiac malformations. Most neonates with aortic arch interruption perish once the ductus arteriosus closes after birth. However, sporadic cases have been reported to survive into adulthood uneventfully. Here, we report a 19-year-old male with a 3-month history of exertional dyspnea. A series of cardiovascular studies confirmed the presence of aortic arch interruption in conjunction with sinus venosus atrial septal defect and partial anomalous pulmonary venous connection. To the best of our knowledge, such an association has not been previously reported in adults.

Intra-cardiac echocardiography guided trans-septal puncture in patients with dilated left atrium undergoing percutaneous transvenous mitral commissurotomy.

Percutaneous transvenous mitral commissurotomy (PTMC) is an effective treatment for mitral stenosis, but trans-septal puncture carries a certain risk of complications. There have been few reports on phase-array intra-cardiac echocardiography (ICE) guidance in trans-septal puncture for PTMC, especially in patients with dilated left atrium or distorted anatomy. Herein, we report our preliminary experience with ICE-guided trans-septal puncture in patients with dilated left atrium (>or=5.5 cm) who underwent PTMC. From June 2005 to March 2006, there were nine consecutive patients with symptomatic mitral stenosis and left atrium size larger than 5.5 cm who underwent trans-septal puncture for PTMC with the ICE guidance in this institution by a same operator. The procedural and catheterization results were analyzed. Using ICE guidance, the success rate for trans-septal puncture was 100% for all patients with dilated left atrium (>or=5.5 cm). The trans-septal procedures were free of major and minor complications and the patients were not exposed to contrast medium. Mitral valve area increased significantly from 1.0+/-0.2 cm(2) to 1.9+/-0.2 cm(2). Our preliminary result showed that ICE safely and effectively guided trans-septal puncture for PTMC in patients with dilated left atrium (>or=5.5 cm), thus eliminating contrast medium usage and avoiding unnecessary longer X-ray exposure.

Positive associations of bone mineral density with body mass index, physical activity, and blood triglyceride level in men over 70 years old: a TCVGHAGE study.

It is known that osteoporosis decreases physical function in older males. However, the role of metabolic parameters and physical activity influencing older men's bone status remains unclear. Thus, this study was designed to evaluate calcaneus bone mass by ultrasonic screening and the associated physical and metabolic functions in older men. This was a cross-sectional study. Three hundred sixty-eight older men (average age, 78.8 years) living in a veterans' home were enrolled. We measured body height and weight, waist and hip circumference, body fat, lean body mass, blood pressure, 6-min walking distance, complete blood count, and blood biochemical profile. Broadband ultrasound attenuation (BUA) and T-score were recorded using Soundscan quantitative ultrasound over the right calcaneus. The range of calcaneus BUA was 27.3-134.0; T-score was from -4.78 to 3.43. Of the total participants, 36.4% were osteopenic (-2.5 < T-score < -1.0) and 16.3% were osteoporotic (T-score

High-dose norepinephrine induces disruption of myocardial extracellular matrix and left ventricular dilatation and dysfunction in a novel feline model.

BACKGROUND: Intravenous norepinephrine (NE) at a dose of 1-6 microg/kg/minute can induce increased extracellular matrix (ECM) and hypertrophic cardiomyopathy. This study aimed to investigate the effects of a higher dose of NE on cardiac remodeling. METHODS: After intraperitoneal urethane-chloralose anesthesia, 7 cats (3.03 +/- 0.58 kg) received intravenous infusion of NE 30 microg/kg/minute for 3 hours. Aortic blood pressure and heart rate (HR) were measured by polygraphy at 0, 5, 15, 30, 60, 90, 120, and 180 minutes. Left ventricular size and ejection fraction (EF) were measured by M-mode echocardiography before and after NE administration. Histopathology was performed by hematoxylin-eosin, silver impregnation, and Sirius red staining. Activity of matrix metalloproteinases (MMP) in the left ventricle was measured by zymography. RESULTS: Mean blood pressure (mmHg) increased from 139 +/- 20 to 198 +/- 19, 187 +/- 23, and 166 +/- 16 at 15, 30, and 60 minutes, respectively, during NE infusion. HR (beats/minute) decreased from 214 +/- 10 to 158 +/- 28 at 15 minutes and then recovered gradually. The left ventricles showed significant dilatation (end-diastolic diameter: from 1.20 +/- 0.18 to 1.58 +/- 0.23cm, p=0.003; end-systolic diameter: from 0.62 +/- 0.23 to 1.35 +/- 0.29cm, p=0.002) and hypokinesia (EF: from 86.2 +/- 5.2 to 33.1 +/- 16.5%, p < 0.001). Histopathology revealed that left ventricular myocytes were elongated, wavy, and fragmented, while collagen fibers were overstretched, straightened, and disrupted. MMP-9 activity was significantly elevated (p = 0.003 vs. control), while MMP-2 activity was unchanged. CONCLUSION: High-dose NE increases MMP-9 activity and causes ECM disruption, left ventricular dilatation and dysfunction.

The presence of metabolic syndrome is independently associated with elevated serum CD40 ligand and disease severity in patients with symptomatic coronary artery disease.

Nontraditional atherosclerotic risk factors have become the focus of attention in recent years. In addition, metabolic syndrome is gaining recognition as another multiplex cardiovascular risk factor. However, to date, no studies have investigated the effect of metabolic syndrome on circulating soluble CD40 ligand (sCD40L), monocyte chemoattractant protein 1, cellular adhesion molecules, and disease severity in patients with symptomatic coronary artery diseases. This study was conducted to address this issue. Patients with stable angina who received percutaneous coronary interventions for significant (> or = 70% diameter stenosis) de novo lesions between January 1999 and January 2004 and had preprocedural serum samples were enrolled. Metabolic syndrome was defined by the National Cholesterol Education Program criteria with waist criterion modified into body mass index of more than 25 kg/m2. The serum samples were thawed and analyzed for circulating sCD40L, monocyte chemoattractant protein 1, adhesion molecules, and high sensitivity C-reactive protein (hs-CRP). Coronary severity was assessed by a modified version of Gensini scoring system. A total of 313 patients, 248 males and 65 females, were studied. Among them, 222 (70.9%, 170 males and 52 females) had metabolic syndrome. Patients with metabolic syndrome had higher serum creatinine level and lower low-density lipoprotein cholesterol despite higher triglyceride concentration. In multivariate analysis, patients with metabolic syndrome had higher sCD40L (6057 +/- 275 vs. 5051 +/- 423 pg/mL, P = .037) and more hs-CRP in higher tertiles (P = .005) than patients without, but similar levels of intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and P selectin. Metabolic syndrome was also significantly associated with multiple coronary vessel involvements with 70% or higher diameter stenosis (36.5% double-vessel and 14% triple-vessel diseases vs 30.8% double-vessel and 5.5% triple-vessel diseases, P = .026) and multiple coronary segment involvements with 50% or higher diameter stenosis (P = .014) in multivariate analysis. In conclusion, the presence of metabolic syndrome is independently associated with elevated sCD40L, hs-CRP, and coronary disease severity in patients with coronary artery disease requiring interventional treatment of stable angina.

Coronary artery disease progression is associated with C-reactive protein and conventional risk factors but not soluble CD40 ligand.

BACKGROUND: Coronary artery disease (CAD) is a major cause of death worldwide. Epidemiological studies have documented conventional risk factors; however, no studies to date have addressed the roles of soluble CD40 ligand (sCD40L) and monocyte chemoattractant protein-1 (MCP-1), and there have been few reports on other novel risk factors in CAD progression. The aim of the present study was to explore the roles of novel and conventional risk factors in CAD progression. METHODS: Patients with stable angina pectoris who underwent repeat coronary angiograms and had serum samples at the time of their first catheterization between March 1999 and January 2004 were enrolled. Those who had progression of coronary atherosclerosis were classified into the progression group (n = 66). Those who did not have CAD progression were classified into the nonprogression group (n = 124). RESULTS: There were more cases of diabetes mellitus (36% versus 20%; P = 0.024) and more men (92% versus 81%; P = 0.040) in the CAD progression group than in the nonprogression group, respectively. The progression group also had poorer lipid profiles than the nonprogression group, including higher total cholesterol (188+/-42 mg/dL versus 173+/-39 mg/dL, respectively; P = 0.014) and low density lipoprotein cholesterol (122+/-38 mg/dL versus 112+/-36 mg/dL, respectively; P = 0.025). In terms of inflammatory markers, progression patients had higher baseline high-sensitivity C-reactive protein (hs-CRP) concentrations (P = 0.018), which was also related to the subsequent angiographic severity score changes; however, sCD40L (6182+/-4352 pg/mL versus 6244+/-4602 pg/mL; P = 0.961), MCP-1 (427+/-540 pg/mL versus 341+/-128 pg/mL; P = 0.580) and adhesion molecules concentrations were indifferent between the progression group and the nonprogression group, respectively. Using a multivariate logistical regression model, the ORs for predicting progression were 2.19 for diabetes mellitus, 2.04 for hypercholesterolemia and 1.52 for hs-CRP (P < 0.05). CONCLUSION: In the present study, only conventional risk factors, and particularly hs-CRP, were markers for predicting CAD progression. Novel risk factors, such as concentrations of sCD40L, MCP-1 and adhesion molecules, did not play significant roles.

Iso-osmolar contrast medium better preserves short- and long-term renal function after cardiovascular catheterizations in patients with severe baseline renal insufficiency.

BACKGROUND: Iso-osmolar iodixanol was shown to least affect very-short-term renal function. However, its short- and long-term renal effects after cardiovascular catheterizations in severe renal insufficiency remain unknown. METHODS: Patients undergoing elective cardiovascular catheterizations and having pre-procedural serum creatinine (Scr) > or =2.5 mg/dl were prospectively studied. The results were compared to those of historical controls who received iopromide. RESULTS: The iodixanol group included 27 patients, aged 73+/-1 years, and the case-matched control group consisted of another 27 patients, aged 71+/-1 years. The baseline Scr were 3.0+/-0.3 and 3.0+/-0.2 mg/dl respectively. Although the Scr at 3 months was similar, the Scr at 6 months was lower in the iodixanol group (2.7+/-0.3 vs 4.2+/-0.5 mg/dl, p = 0.017). The absolute and percentage increments in Scr at 3 months (0.0+/-0.2 vs 0.6+/-0.2 mg/dl, p = 0.014, and 1+/-4% vs 24+/-6%, p = 0.003, respectively) and 6 months (-0.3+/-0.2 vs 1.3+/-0.4 mg/dl, p = 0.001, and -10+/-5% vs 47+/-12%, p < 0.001, respectively) were lower in the iodixanol group. CONCLUSIONS: Iodixanol better preserves short- and long-term renal outcomes in patients with severe baseline renal insufficiency.

Caveolin-1 expression is associated with plaque formation in hypercholesterolemic rabbits.

Caveolin-1, the major structural protein of caveolae, is present in several cell types known to play a role in the development of atherosclerosis. In this study, the distribution and expression of caveolin-1 in the arterial walls were studied in hypercholesterolemic rabbits. Immunohistochemical results indicated that the staining intensity of caveolin-1 reached a high level in the arterial intima at 5 weeks after high-cholesterol-diet treatment and decreased to a very low level at 8 weeks when atheromatous plaques appeared. Western blot analysis showed that in rabbits fed a high-cholesterol diet for 5 weeks, the expression of caveolin-1 reached its highest level and then decreased from 8 to 12 weeks. The proliferative activity of smooth muscle cells (SMCs) decreased to the lowest level at 5 weeks and then increased at 8 and 12 weeks. Nitric oxide synthase activity gradually decreased in animals fed a high-cholesterol diet throughout the experiment. These studies demonstrate that the change in abundance of caveolin-1 is associated with SMC proliferation in the formation of atheromatous plaque after hypercholesterolemia insult.