Early detection of myocardial infarction following blunt chest trauma by computed tomography: a case report.

BACKGROUND: Blunt cardiac trauma encompasses a wide range of clinical entities, including myocardial contusion, cardiac rupture, valve avulsion, pericardial injuries, arrhythmia, and even myocardial infarction. Acute myocardial infarction due to coronary artery dissection after blunt chest trauma is rare and may be life threatening. Differential diagnosis of acute myocardial infarction from cardiac contusion at this setting is not easy. CASE PRESENTATION: Here we demonstrated a case of blunt chest trauma, with computed tomography detected myocardium enhancement defect early at emergency department. Under the impression of acute myocardial infarction, emergent coronary angiography revealed left anterior descending artery occlusion. Revascularization was performed and coronary artery dissection was found after thrombus aspiration. Finally, the patient survived after coronary stenting. CONCLUSION: Perfusion defects of myocardium enhancement on CT after blunt chest trauma can be very helpful to suggest myocardial infarction and facilitate the decision making of emergent procedure. This valuable sign should not be missed during the initial interpretation.

Glossogyne tenuifolia Extract Inhibits TNF-α-Induced Expression of Adhesion Molecules in Human Umbilical Vein Endothelial Cells via Blocking the NF-kB Signaling Pathway.

Chronic inflammation plays a pivotal role in the development of atherosclerosis, where the pro-inflammatory cytokine-induced expression of endothelial adhesion molecules and the recruitment of monocytes are the crucial events leading to its pathogenesis. Glossogyne tenuifolia ethanol extract (GTE) is shown to have potent anti-inflammatory and antioxidant activities. We evaluated the effects of GTE and its major components, luteolin (lut), luteolin-7-glucoside (lut-7-g), and oleanolic acid (OA) on TNF-α-induced expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs). The results demonstrated that GTE, lut, and lut-7-g attenuated the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in TNF-α-activated HUVECs, and inhibited the adhesion of monocytes to TNF-α-activated HUVECs. The TNF-α-induced mRNA expression of ICAM-1 and VCAM-1 was also suppressed, revealing their inhibitory effects at the transcriptional level. Furthermore, GTE, lut, and lut-7-g blocked the TNF-α-induced degradation of nuclear factor-kB inhibitor (IkB), an indicator of the activation of nuclear factor-kB (NF-kB). In summary, GTE and its bioactive components were effective in preventing the adhesion of monocytes to cytokine-activated endothelium by the inhibition of expression of adhesion molecules, which in turn is mediated through blocking the activation and nuclear translocation of NF-kB. The current results reveal the therapeutic potential of GTE in atherosclerosis.

Quantitation of the mitral tetrahedron in patients with ischemic heart disease using real-time three-dimensional echocardiography to evaluate the geometric determinants of ischemic mitral regurgitation.

BACKGROUND: Ischemic mitral regurgitation (IMR) is common in ischemic heart disease and results in poor prognosis. However, the exact mechanism of IMR has not been fully elucidated. HYPOTHESIS: Quantitation of the mitral tetrahedron using three-dimentianl (3D) echocardiography is capable of evaluating the geometric determinants and mechanisms of IMR. METHODS: Forty patients with a history of ST-elevation myocardial infarction at least 6 months earlier were studied. Parameters of mitral deformation and global left ventricular (LV) function and shape were evaluated by 2-dimensional echocardiography. The effective regurgitant orifice (ERO) of IMR was obtained by the quantitative continuous-wave Doppler technique. Three-dimensional (3D) echocardiography was applied to assess the mitral tetrahedron. RESULTS: Mitral valvular tenting area (P < 0.001), mitral annular area (P = 0.032), dilation of the LV in diastole, impairment of the LV ejection fraction, and volume of the spherically shaped LV in systole were greater in patients with an ERO ≥20 mm(2) than in those with an ERO <20 mm(2). In the mitral tetrahedron, only the interpapillary muscle roots distance showed a significant difference (P = 0.004). Multivariate analysis with the logistic regression model showed the systolic mitral tenting area (odds ratio [OR]: 280.49, 95% confidence interval [CI]: 4.59-1.72 × 10(4), P = 0.007) and interpapillary muscle distance (OR: 1.50, 95% CI: 1.03-2.19, P = 0.036) to be independent factors in predicting significant IMR (ERO ≥20 mm(2)). CONCLUSIONS: 3D echocardiography can be effectively applied in measuring the mitral tetrahedron and evaluating the mechanism of IMR. Mitral valvular tenting and interpapillary muscle distance are 2 independent factors of significant IMR.

Brugada-type electrocardiogram in the Taiwanese population--is it a risk factor for sudden death?

BACKGROUND/PURPOSE: People receive electrocardiogram (ECG) examination for various reasons in a hospital setting. An important clinical practice issue may be that cardiologists need to be consulted for Brugada-type ECGs identified through routine screening. We investigated the prevalence and prognosis of patients with Brugada-type ECG in a hospital-based population in an attempt to improve the management of these patients. METHODS: In 20,562 patients seeking medical care for non-cardiovascular reasons, 74,955 ECGs were performed from December 1999 to February 2001. The diagnostic criteria for Brugada-like ECG from the European Society of Cardiology were used. International Statistical Classification of Diseases codes and city residents' records were documented to indicate the reasons for visiting clinics or hospitalization and mortality outcome. Medical records were reviewed and telephone interviews were conducted. RESULTS: Twenty-six (0.13%) of the 20,562 patients were confirmed to have Brugada-type ECGs. None of these patients had ever experienced syncope, near syncope or sudden cardiac death. After 57.1 ± 15.8 months of follow-up, there were four deaths out of the 26 patients with Brugada-type ECG (15.4%, 95% CI: 1.53-2.9%) compared with 2899 of those without (14.1%, 95% CI: 13.6-14.5%; p=0.89, log-rank test). Neither sudden cardiac death (p=0.61) nor hospitalized death (p=0.55) was different between patients with and without Brugada-type ECG. CONCLUSION: Patients with Brugada-type ECGs are not rare in a hospital-based population. The presence of Brugada-type ECGs in patients without syncope or sudden cardiac death was not associated with hospitalized mortality.

Continuous intravenous infusion of prostaglandin E1 improves myocardial perfusion reserve in patients with ischemic heart disease assessed by positron emission tomography: a pilot study.

OBJECTIVE: Recent investigation has demonstrated that prostaglandin E(1) (PGE(1)) therapy increased capillary density in explanted hearts. Dynamic (13)N-ammonia positron emission tomography (PET) is reliable for non-invasive measurement of myocardial blood flow and myocardial perfusion reserve (MPR). The aim of this study was to investigate the effects of PGE(1) therapy during 4 weeks on reduction of myocardial perfusion abnormalities and increase of MPR in the patients with ischemic heart disease. METHODS: In this double-blind, placebo-controlled trial, we randomly assigned 11 patients who had symptomatic heart failure and documented myocardial ischemia to 4 weeks intravenous infusion of PGE(1) (2.5 ng/kg/min; 8 patients, age 60 ± 13 years) or saline (3 patients, age 57 ± 13 years). Dynamic (13)N-ammonia PET scans at rest and during adenosine stress were obtained at baseline and 12 weeks after treatment completion. Quantitative size/severity of perfusion defects and MPR change from baseline to follow-up PET were determined using a 17-segment model. RESULTS: Compared with the control group, baseline MPR in the PGE(1) group was significantly lower (1.96 ± 0.78 vs. 2.71 ± 0.73; P < 0.001). MPR significantly improved 12 weeks after completion of PGE(1) infusion (1.96 ± 0.78 to 2.16 ± 0.77; P < 0.001). In contrast, MPR declined significantly in the placebo group (2.71 ± 0.73 to 2.01 ± 0.58, P < 0.001). CONCLUSION: Four weeks of PGE(1) infusion sustained MPR improvement in patients with ischemic heart disease. This may be an attractive therapeutic approach for no-option patients with severe ischemic cardiomyopathy.

Efficacy and safety of valsartan in hypertensive Taiwanese patients: post-marketing surveillance study.

OBJECTIVE: To evaluate the efficacy and safety of valsartan in Taiwanese patients with essential hypertension. METHODS: This 12-week multi-center, open-label, observational, post-marketing surveillance study enrolled 2046 hypertensive patients who were prescribed valsartan 80 or 160 mg as monotherapy or in combination with other antihypertensives based on clinical judgment. The primary endpoint was the incidence rate of dizziness with valsartan 160 mg monotherapy or combination therapy at Week 4. Secondary endpoints included the blood-pressure-lowering efficacy and the overall safety and tolerability of valsartan at Weeks 4 and 12. RESULTS: The monotherapy and combination groups had comparable baseline characteristics. At Week 4, monotherapy was found non-inferior to combination for incidence rate of dizziness (monotherapy, 9.25%; combination, 10%; difference in incidence of dizziness, 0.75%; 95% CI - 0.61% to 2.12%; non-inferiority margin, -1.33%;WaldTest approach). Greater blood pressure (BP) reduction was noted atWeek 12 than atWeek 4.The antihypertensive effect was greater with combination therapy and the 160-mg dose. BP control (systolic <140 mmHg or diastolic <90 mmHg) was achieved in 80-90% patients.Valsartan was well tolerated; most commonly reported adverse events included dizziness, headache, constipation and cough. CONCLUSION: Valsartan is an effective treatment option for essential hypertension in Taiwanese patients.

Effect of physical activity on the prevalence of metabolic syndrome and left ventricular hypertrophy in apparently healthy adults.

BACKGROUND/PURPOSE: Metabolic syndrome and left ventricular hypertrophy (LVH) carry high cardiovascular risks. We performed a cross-sectional study to evaluate the effect of different amounts of physical activity (PA) on the prevalence of metabolic syndrome and LVH in our study population. METHODS: This study was a cross-sectional survey of 1494 apparently healthy subjects: 776 men with a mean age of 57.6 + 12.3 years, and 718 women with a mean age of 56.4+ 11.0 years. The metabolic syndrome was defined according to modified criteria of the National Cholesterol Education Program Adult Treatment Panel III. LVH was diagnosed by electrocardiography voltage criteria. The amount of PA was determined with a questionnaire and stratified into low, moderate or high levels. RESULTS: The prevalence of metabolic syndrome and its components was as follows: metabolic syndrome, 15.5%; obesity, 29.7%; high triglyceride level, 21.7%; low high-density lipoprotein-cholesterol level, 35.9%; high blood pressure, 56.9%; and impaired fasting glucose, 13.1%. A high amount of PA (> 14 km per week walking distance) was significantly associated with lower prevalence of metabolic syndrome [odds ratio (OR) = 0.53, p = 0.001], lower prevalence of obesity (OR = 0.56, p = 0.001), triglyceridemia (OR = 0.58, p = 0.007) and LVH (OR=0.37, p = 0.006). CONCLUSION: This study suggests that high amounts of PA are inversely correlated with the prevalence of metabolic syndrome and LVH in men and women.

Transcatheter embolization of a huge renal arteriovenous fistula with Amplatzer Vascular Plug.

A large renal arteriovenous fistula (RAF) may lead to heart failure, renal insufficiency, hematuria, and progressive increase in size of renal vessels. Here we present the case of a 67-year-old man with a huge left RAF, who suffered from exertional dyspnea, nocturnal orthopnea, and impaired renal function. The left renal vein and inferior vena cava were dilated to 4 cm. An Amplatzer Vascular Plug with the largest size of 30 mm in disk diameter was deployed to block the fistula, with balloons inflated at renal artery and vein in advance, to reduce the renal flow in order to prevent plug migration. The decrease of shunt flow after embolization was suboptimal. However, dyspnea ameliorated, which was associated with decreased cardiac murmur, subsided abdominal bruit, normalization of the lowered diastolic pressure, and better renal function. In addition, more microcoils can be applied, using the lodged plug as a framework, to achieve the best clinical improvement.

Effects of acetyl-L-carnitine and oxfenicine on aorta stiffness in diabetic rats.

BACKGROUND: We compared the haemodynamic and metabolic effects of acetyl-L-carnitine (one of the carnitine derivatives) and of oxfenicine (a carnitine palmitoyltransferase-1 inhibitor) in streptozotocin-induced diabetes in male Wistar rats. MATERIALS AND METHODS: Diabetes was induced by a single tail vein injection of 55mgkg(-1) streptozotocin. The diabetic animals daily treated with either acetyl-L-carnitine (150mgkg(-1) in drinking water) or oxfenicine (150mgkg(-1) by oral gavage) for 8weeks,were compared with the untreated age-matched diabetic controls. Arterial wave reflection was derived using the impulse response function of the filtered aortic input impedance spectra. Thiobarbituric acid reactive substances (TBARS) measurement was used to estimate malondialdehyde (MDA) content. RESULTS: Oxfenicine, but not acetyl-L-carnitine, increased total peripheral resistance in diabetes, which paralleled its elevation in plasma levels of free fatty acids. By contrast, acetyl-L-carnitine, but not oxfenicine, resulted in a significant increase in wave transit time and a decrease in wave reflection factor, suggesting that acetyl-L-carnitine may attenuate the diabetes-induced deterioration in systolic loading condition for the left ventricle. This was in parallel with its lowering of MDA/TBARS content in plasma and aortic walls in diabetes. Acetyl-L-carnitine therapy also prevented the diabetes-related cardiac hypertrophy, as evidenced by the reduction in ratio of the left ventricular weight to body weight. CONCLUSION: Acetyl-L-carnitine, but not oxfenicine, attenuates aortic stiffening and cardiac hypertrophy, possibly through its decrease of lipid oxidation-derived MDA/TBARS in the rats with insulin deficiency.

The effect of surgical weight reduction on left ventricular structure and function in severe obesity.

The aim of this study was to examine the effect of surgical weight reduction on cardiac structure and function and to seek the determinants of these changes. Sixty-six severely obese adults (BMI >or=35 kg/m(2)) who received bariatric surgery underwent echocardiographic examination before and 3 months after surgery. At 3 months after surgery, BMI and systolic blood pressure (BP) decreased (43.3 +/- 6.3 to 34.1 +/- 5.6 kg/m(2), P < 0.001, and 146 +/- 12 to 130 +/- 14 mm Hg, P < 0.001, respectively). In left ventricular (LV) geometry, the relative wall thickness (RWT) and LV mass index decreased significantly (0.43 +/- 0.05 to 0.35 +/- 0.05, P < 0.001, and 50 +/- 11 to 39 +/- 11 g/m(2.7), P < 0.001, respectively) without changes in chamber size. Multivariate analyses showed change in systolic BP to be an independent predictor for the changes in RWT and LV mass index. In myocardial performance, peak systolic mitral annular velocity and all diastolic indexes showed significant improvements. We concluded that LV hypertrophy and function improved rapidly after bariatric surgery in severely obese adults. BP reduction was the major determinant for the regression of LV hypertrophy in the early stage of surgical weight reduction.

Factors associated with behavior modification for cardiovascular risk factors in patients with coronary artery disease in northern Taiwan.

BACKGROUND: Studies have demonstrated that improvement in cardiovascular risk factors may contribute to reduced coronary artery disease (CAD) morbidity and mortality, improved patient outcomes, and lower medical costs associated with treating heart disease. PURPOSE: The purpose of this study was to understand the coronary risk factor profile, to have the knowledge of risk factors, to understand the modifying behaviors, and to understand the factors associated with modifying behaviors of cardiovascular risk factors among patients with CAD in northern Taiwan. METHODS: A cross-sectional design was used in this study. Using nonprobability sampling, 156 patients diagnosed with CAD were interviewed and asked to complete a structural questionnaire in cardiovascular clinics at three medical centers in northern Taiwan. Data were analyzed by descriptive analysis, Pearson's correlation, chi-square tests, and stepwise multiple regression. RESULTS: A total of 38% of variance of modifying behaviors was explained by self-efficacy, actual risk factors, work status, and health beliefs. Self-efficacy was the strongest predictor of behavior to modify cardiovascular risk factors. Age and type "A" personality were the two leading cardiovascular risk factors for the participants. Most participants could perform modifying behaviors such as taking medications, eating an appropriate diet, and following specific lifestyle recommendations. However, participants had relatively lower adherence to monitoring blood pressure, exercising regularly, and controlling weight. CONCLUSIONS/IMPLICATIONS FOR PRACTICE: Nurses should assess patient cardiovascular risk factors, health beliefs, and self-efficacy and then provide comprehensive and adequate instruction to each based on his or her specific risk factors.

Prevention of arterial stiffening by pyridoxamine in diabetes is associated with inhibition of the pathogenic glycation on aortic collagen.

BACKGROUND AND PURPOSE: Our team previously demonstrated that diabetes induces a deterioration in vascular dynamics, in parallel with the enhanced formation of advanced glycation end products. The aim of this study was to determine whether prevention of the arterial stiffening by pyridoxamine in diabetes is associated with inhibition of the pathogenic glycation on aortic collagen. EXPERIMENTAL APPROACH: Diabetes was induced in rats by a single tail vein injection with 55 mg.kg(-1) steptozotocin (STZ). After induction of hyperglycaemia, animals were treated for 8 weeks with pyridoxamine (1 g.L(-1) in drinking water) and compared with the age-matched untreated diabetic controls. Pulse wave reflection along the vasculature was derived using the impulse response function of the filtered aortic input impedance spectra. KEY RESULTS: Treatment of this experimental diabetes with pyridoxamine resulted in a significant increase in wave transit time and a decrease in wave reflection factor, indicating that pyridoxamine attenuates the diabetes-induced augmentation in systolic load of the left ventricle coupled to its arterial system. Meanwhile, pyridoxamine therapy ameliorated the diabetes-related cardiac hypertrophy, as evidenced by the reduction in ratio of the left ventricular weight to body weight. Glycation-derived modification of aortic collagen was also found to be attenuated by administration of pyridoxamine to the STZ-induced diabetic rats. CONCLUSIONS AND IMPLICATIONS: Pyridoxamine imparts significant protection against the diabetes-induced deterioration in pulsatile arterial load imposed on the heart, at least partly through inhibition of the formation of advanced glycation end products and their accumulation on aortic collagen of the STZ-treated rats.

Protein kinase C-Fyn kinase cascade mediates the oleic acid-induced disassembly of neonatal rat cardiomyocyte adherens junctions.

Oleic acid (OA) affects assembly of gap junctions in neonatal cardiomyocytes. Adherens junction (AJ) regulates the stability of gap junction integrity; however, the effect of OA on AJ remains largely unexplored. The distribution of N-cadherin and catenins at cell-cell junction was decreased by OA. OA induced activation of protein kinase C(PKC)-alpha and -epsilon and Src family kinase, and all three kinases were involved in the oleic acid-induced disassembly of the adherens junction, since it was blocked by pretreatment with Gö6976 (a PKCalpha inhibitor), epsilonV1-2 (a PKCepsilon inhibitor), or PP2 (a Src family kinase inhibitor). Src family kinase appeared to be the downstream of PKC-alpha and -epsilon, as blockade of either PKC-alpha or -epsilon activity prevented the OA-induced activation of Src family kinase. Immunoprecipitation analyses showed that OA activated Fyn and Fer. OA promoted the association of p120 catenin/beta-catenin with Fyn and Fer and caused increased tyrosine phosphorylation of p120 catenin and beta-catenin, resulting in decreased binding of the former to N-cadherin and of the latter to alpha-catenin. Pretreatment with PP2 abrogated this OA-induced tyrosine phosphorylation of p120 catenin and beta-catenin and restored the association of N-cadherin with p120 catenin and that of beta-catenin with alpha-catenin. In conclusion, these results show that OA activates the PKC-Fyn signaling pathway, leading to the disassembly of the AJ. Therefore, inhibitors of PKC-alpha/-epsilon and Src family kinase are potential candidates as cardioprotection agents against OA-induced heart injury during ischemia-reperfusion.

Joint effects of N-terminal pro-B-type-natriuretic peptide and C-reactive protein vs angiographic severity in predicting major adverse cardiovascular events and clinical restenosis after coronary angioplasty in patients with stable coronary artery disease.

BACKGROUND: This study was designed to evaluate the joint effects of plasma C-reactive protein (CRP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) vs coronary angiographic severity on cardiovascular risk stratification. METHODS AND RESULTS: A total of 345 patients with stable coronary artery disease (CAD) were recruited after successful percutaneous coronary intervention (PCI). Endpoints were major adverse cardiovascular events (MACE) and cumulative clinical restenosis rate after 18-36-month follow-up. Plasma NT-proBNP and CRP levels were among the strongest predictors of MACE. Adjusted hazard ratios of MACE according to combined biomarkers were 2.4 (p=0.05) for elevated CRP only, 5.22 (p<0.001) for elevated NT-proBNP only, and 7.04 (p<0.001) for elevation of both. The differential capacity using both plasma CRP and NT-proBNP in a receiver-operating-characteristics curve analysis (area under curve, AUC: 0.82) was significantly higher than using either biomarker alone or conventional risk factors (AUC: 0.67). Significant predictors of clinical restenosis were plasma NT-proBNP and the Gensini score. The combination of NT-proBNP and the Gensini score was the strongest predictor (AUC: 0.77) for clinical restenosis. CONCLUSIONS: Plasma NT-proBNP, CRP, and the Gensini score are complementary in risk stratification. Combined use of these biomarkers has provided substantial extra information to conventional risk factors in stable CAD patients.

Revision in reference ranges of peripheral total leukocyte count and differential leukocyte percentages based on a normal serum C-reactive protein level.

BACKGROUND/PURPOSE: A higher total leukocyte count is a predictor of all-cause mortality and cardiovascular morbidity. The currently used reference range for peripheral total leukocyte count is wide (4.5-11.0 x 10(9)/L) and is associated with a low sensitivity in identifying non-infectious chronic diseases. We attempt to revise it based on a normal serum C-reactive protein (CRP) level. METHODS: Study subjects were participants in a health check program at our hospital between 2000 and 2002. Those whose leukocyte analysis had been checked with the Sysmex Cell Counter NE-9000 were enrolled. RESULTS: Significantly positive relationships between CRP level and total leukocyte count, neutrophil percentage, and monocyte percentage were found in all subjects (n = 14,114; p < 0.0001). In contrast, CRP level had a significantly inverse correlation with lymphocyte percentage (p < 0.0001). A proposed new reference range for total leukocyte count was estimated based on the data in the normal CRP level group (CRP < 0.1 mg/dL; n = 4839). To rest on the essence of statistics that the range of [mean +/- 2 standard deviations] contains approximately the middle 95% of observations in a sampled population, a new reference range for total leukocyte count was accordingly estimated to be 3.11-8.83 x 10(9)/L. CONCLUSION: In view of the abundant evidence showing that a higher peripheral total leukocyte count is harmful to health, a down-correction of its upper reference range from the currently used 11.0 x 10(9)/L to the proposed 8.83 x 10(9)/L, based on a normal CRP level, should allow more abnormal health conditions to be identified and promote the usefulness of peripheral leukocyte analysis.

Usefulness of drug eluting stent in percutaneous coronary intervention--a single center experience in Taiwan.

BACKGROUND/PURPOSE: Drug eluting stents (DES) have been shown to reduce in-stent restenosis rate and target vessel revascularization in large clinical trials. However, the safety and efficacy of DES use in the Taiwanese population has not been reported. We designed this trial to analyze the clinical results in patients using DES in a single tertiary center. METHODS: We retrospectively analyzed the clinical data of all patients treated at National Taiwan University Hospital, Taipei, Taiwan, with sirolimus- or paclitaxel-eluting stents between September 2003 and January 2005. RESULTS: A total of 585 patients (466 men, 119 women; mean age, 64.5 +/- 11.2 years) were enrolled. Meanwhile, 205 sirolimus- and 717 paclitaxel-eluting stents were implanted, with a mean of 1.6 stents per patient. Half (50.2%) of the stents were placed in the left anterior descending artery. Among the enrolled patients, 41.8% had diabetes mellitus, 25% had a diagnosis of acute coronary syndrome, and 10.7% was treated with primary percutaneous coronary intervention for ST-segment elevation myocardial infarction. Overall 8-month target vessel revascularization, major adverse cardiac event rate, and cardiac death rate were 8.8%, 9.7% and 2.5%, respectively. There was no difference in clinical events between sirolimus- and paclitaxel-eluting stents. The overall subacute stent thrombosis rate was 1.36%, significantly lower than that in patients who presented with acute coronary syndrome (4%). CONCLUSION: The use of DES in the Taiwanese population yielded comparable results as those in large clinical trials. Subacute stent thrombosis rate was higher in acute coronary syndrome. The safety of DES in these situations should be further clarified.

Human C-reactive protein (CRP) gene 1059G>C polymorphism is associated with plasma CRP concentration in patients receiving coronary angiography.

BACKGROUND/PURPOSE: Elevation of C-reactive protein (CRP) level is associated with increased risk of cardiovascular events. The 1059 G>C polymorphism in exon 2 of the CRP gene has been shown to affect plasma concentration of CRP. We want to elucidate the effect of this polymorphism on the development of coronary artery disease (CAD) among the Chinese population in Taiwan. METHODS: We scrutinized 536 patients undergoing coronary angiography (365 patients with CAD and 171 controls with patent coronaries) and evaluated the association of CRP gene 1059 G>C polymorphism with CAD. Genotyping of the polymorphism was performed by polymerase chain reaction and MaeIII restriction enzyme digestion. RESULTS: The CC genotype was associated with lower plasma CRP concentration (GG, 6.5+/-5.8; GC, 3.3+/-4.4; CC, 2.3+/-3.1 mg/L; p=0.02). Subjects with CAD or myocardial infarction (MI) had significantly higher plasma CRP concentration than that in controls (CAD vs. controls, 8.9+/-18.9 vs. 3.3+/-7.2 mg/L; p<0.001), while patients with MI showed higher CRP when compared to those with chronic stable angina (13.5+/-22.9 vs. 5.2+/-14.1 mg/L; p<0.001). However, this polymorphism was not associated with CAD in our population. CONCLUSION: Our data suggest that human CRP gene 1059 G>C polymorphism is associated with plasma CRP concentration among Chinese in Taiwan receiving coronary angiography.

Mechanism of oleic acid-induced myofibril disassembly in rat cardiomyocytes.

This study investigated the mechanism of oleic acid (OA)-induced disassembly of myofibrils in cardiomyocytes. OA treatment disrupted myofibrils, as revealed by the disorganization of several sarcomeric proteins. Since focal adhesions (FAs) are implicated in myofibril assembly, we examined structural changes in FAs after OA treatment. Immunofluorescence studies with antibodies against FA proteins (vinculin, integrin beta1D, and paxillin) showed that FAs and costameres disintegrated or disappeared after OA treatment and that the changes in FA proteins occurred prior to myofibril disassembly. The effects of OA on FAs and myofibrils were reversed after removal of OA. OA decreased expression of integrin beta1D, paxillin, vinculin, and actin, and induced tyrosine dephosphorylation of FA kinase (FAK) and paxillin. These effects were blocked by pretreatment with sodium orthovanadate, a protein tyrosine phosphatase (PTP) inhibitor. This inhibitor also prevented OA-induced myofibril disassembly, indicating the involvement of PTP in myofibril disassembly. Furthermore, OA increased protein levels of PTP-PEST. The upregulation of this phosphatase correlated with the tyrosine dephosphorylation of paxillin and FAK, which are targets for PTP-PEST. In addition, OA decreased RhoA activity and the phosphorylation of cofilin, a downstream target of RhoA. Cofilin dephosphorylation increased its actin-severing activity and led to the depolymerization of F-actin, which might provide another potential mechanism for OA-induced myofibril disassembly.