2008 Vol. 5, No. 1
Background Patent foramen ovale (PFO)-related stroke is a possible and not easily manageable occurrence in 1.2 mm) probably imputable to hypertensive cardiomyopathy. Four patients developed atrial fibrillation during the first month post-implantation, all successfully treated with antiarrhythmic drugs. After a mean follow-up of 40±4.3 months left ventricle performance indices (ejection fraction and end-diastolic volume) and diastolic dysfunction parameters (E/A, deceleration time, diastolic dysfunction class) did not change significantly. Conclusion The present study suggests that PFO transcatheter closure may be safely performed in aged patients with diastolic dysfunction class 1-2.
Objective Aspirin has been used extensively in primary and secondary prevention of cardiovascular disease, particularly for subjects at high risk such as metabolic syndrome. However, the responsiveness to aspirin treatment may vary among individuals. The present study was conducted to investigate the profile and prevalence of aspirin resistance in patients with metabolic syndrome. Methods In 221 consecutive patients, platelet aggregation induced by arachidonic acid (0.5mg/ml) was assessed after 10 days of aspirin treatment (200mg/d). Aspirin resistance was defined as mean optical platelet aggregation =20%. Results Aspirin resistance occurred in 39 patients (17.6%). Serum fibrinogen level was higher in patients with than in those without aspirin resistance (2.6±0.4g/l vs 2.4±0.4g/L, P=0.017). The 2 groups, aspirin resistance group and no aspirin resistance group, did not differ significantly, with regard to gender, age, body mass index, waist-hip ratio, blood pressure level, serum cholesterol level and history of myocardial or cerebral infarction. Multivariate logistic regression analysis revealed that only serum fibrinogen level entered the model (odds ratio 2.973, p=0.023). Subgroup analysis further showed that aspirin resistance occurred more in male patients with myocardial infarction (50% vs14.5%, P=0.02) and in female patients with diastolic blood pressure=85mmHg (34% vs 15.5%, P=0.043). But after multifactor logistic regression, in women blood pressure=85mmHg was not a predictor any more. Conclusions In patients with metabolic syndrome, aspirin resistance is not uncommon, especially for men with history of myocardial infarction. Patients with aspirin resistance have an increased serum fibrinogen level.
Objective The effect of left atrial (LA) dimension on the occurrence of atrial fibrillation (AF) has been examined in some small studies. Less is known about the relationship of LA dimension, hemodynamic with AF during echocardiographic evaluation, especially, the flow dynamics in LA poorly described. The objective of this study was to investigate the relationship between LA dimension and the occurrence of AF. Methods Two hundred and forty-five consecutive patients with heart disease scheduled to undergo open heart surgery were prospectively enrolled in the study. Patients were divided into 2 groups according to atrial fibrillation: AF group (n=148, 99 men and 49 women, with a mean age 59.3±8.4 years), and no-AF group (n= 97, 60 men and 37 womem). Echocardiography was performed before surgery. All measurements were performed following the American Society of Echocardiography recommendations. Results There were more patients with congestive heart failure in AF group than in no-AF group (45.9% vs 39.1%, P <0.05). The mean LA volume was 49.2±12.2 ml/m2 in AF group and 33.1±10.8 ml/m2 in no-AF group. There were also significant differences between two groups in left atrial end systolic dimension (LAESD) (50±13mm vs 27±14mm), left atrial end diastolic dimension (LAEDD ) (79±17mm vs 53±13mm), PA pressure ( 41.3±11.6 mmHg vs 37.5±10.4 mmHg), and ratio of mitral E velocity and septal mitral annulus motion velocity ( E/E’) .The percentage of abnormal diastolic function grades (DGF) was also higher in AF than in no-AF group (89.9% versus 59.8% );. Conclusion Atrial fibrillation is associated more frequently with an increased LA dimension and more severe atrial hemodynamics disorder.
Objective To assess the predictive value of serum uric acid levels for cardiovascular and all-cause mortality in a large prospective population based study. Methods The study was based on 3648 participants in Shanghai and Beijing, who were inpatients with high cardiovascular(CV) risk at baseline (2004 .7 to 2005.1), and blood was taken. Follow-up for death from cardiovascular disease and any cause was complete until January 1, 2006. Results The mean follow-up was 1 years. There were 303 deaths during follow-up, of which 121 were cardiovascular. Crude mortality rates were 8.3 % for all patients, 6.8% for female patients (116/1715), and 9.7% (187/1933) for male patients. Among men, patients in the lower and higher uric acid groups had increased cardiac and overall mortality risks compared with patients in the normal uric acid groups. Similar relation was found in women but not statistically significant. After adjusting for other conventional risk factors (age, diabetes, hypertension, diuretic use and smoking), baseline uric acid level was still associated with increased risk for death from cardiovascular disease (P=0.005), or death from all causes (P=0.014) Conclusion Our data suggest that abnormal serum uric acid levels are independently and significantly associated with risk of cardiovascular and all-cause mortality.
Background Interleukin-18(IL-18) plays a key role in the development, progression and outcome of coronary artery disease and its complications. However, its variability relation to the characterization of atherosclerotic plaque and percutaneous coronary intervention are still unknown. Methods Fifty four patients with coronary artery disease [22 patients with stable angina (SA) and 32 patients with acute coronary syndrome (ACS)] were enrolled in this study. All patients underwent percutaneous coronary intervention (PCI). The stability of the plaques at the criminal vessels was assessed with analogical IVUS. Serum IL-18 levels were measured at the time points of 5 min before PCI, and 0h, 6h, 24h and 1month after PCI in all patients. Results ACS group consisted mainly of lipidic unstable plaques while SA group of fibrous stable plaques. Moreover, compared with those in SA group, eccentricity index (EI) and remodeling index (RI) were significantly higher in ACS group. Positive remodeling was seen in ACS group while negative or no remodeling in SA group. Further, serum IL-18 levels were significantly elevated in patients with ACS than those in SA group before PCI, increased at 0h, 6h, 24h after PCI (P<0.05)and were not significant different at 1 month after PCI from those before PCI. Conclusions There is significant difference in the composition and structural characteristics of atherosclerotic plaques between ACS and UA groups. PCI triggersd and enhances the inflammatory response in a short time. Serum levels of IL-18 are the predictors of progression of unstable plaque in atherosclerosis. Post-operative complications of PCI might be reduced by inhibiting IL-18.
Objective The present study was designed to investigate changes in serum or plasma concentrations of nitric oxide and its derivatives in diabetic patients. Methods Serum nitrate concentration of 84 diabetic patients was measured by using an enzyme kinetic method, and the plasma S-nitrosothiols concentration of 10 cases was measured by using HPLC technique. Results Serum nitrate concentration and plasma S-nitrosothiols concentration in the diabetics were significantly higher than in control group (P<0.01 and P<0.05, respectively). The serum nitrate concentration in diabetics also had a significant positive correlation with the serum glucose concentration (R=0.7256, P<0.05), but this correlation was not found in control group. Conclusion These data showed that NO and its derivatives are overproduced in the diabetic patients.
Objective Mechanisms of pulmonary vein isolation (PVI) for atrial fibrillation remain controversy. This study aimed to investigate the impact of PVI on vagal modulation to atria. Methods Eighteen adult mongrel dogs under general anesthesia were randomly divided into two groups. Bilateral cervical sympathovagal trunks were decentralized and sympathetic effects was blocked by metoprolol administration. Atrial electrical remodeling (AER) was established by rapid right atrial pacing at the rate of 600 bpm for 30 minutes. PVI was performed in group A. Atrial effective refractory period (ERP), vulnerability window (VW) of atrial fibrillation, and sinus rhythm cycle length (SCL) were measured at baseline and during vagal stimulation before and after atrial rapid pacing with and without PVI at right atrial appendage (RAA), left atrial appendage (LAA), distal coronary sinus (CSd) and proximal coronary sinus (CSp). Results (1) Effects of PVI on vagal modulation: Shortening of SCL during vagal stimulation decreased significantly after PVI compared with that before PVI in group A (P<0.001). Shortening of ERP during vagal stimulation decreaseed significantly after PVI compared with that before PVI (P<0.05). VW of atrial fibrillation during vagal stimulation decreased significantly after PVI compared with that before PVI (P<0.05). (2) Effects of PVI on AER: shortening of ERP before and after atrial rapid pacing increased significantly at baseline and vagal stimulation in group B compared with that in group A (P<0.05). VW during vagal stimulation increased significantly after atrial rapid pacing in group B (P<0.05). Conclusion PVI attenuates the vagal modulation to the atria, thereby decreases the susceptibility to atrial fibrillation mediated by vagal activity. PVI releases AER, which maybe contributes to the vagal denervation. Our study indicates that PVI not only can eradicate triggered foci but also modify substrates for AF.
Objective To study the protective effect of fluvastatin, one of the HMG-CoA reductase inhibitors (statins), against oxygen radical-induced oxidative damages in human aortic endothelial cell, and the role of Bcl-2 in this protection. Methods Human aortic endothelial cells with or without Bcl-2 siRNA transfection were subjected to 1-100 nM of fluvastatin and 100 |ìhydrogen peroxide for 24 hours. Bcl-2 mRNA and protein expression were measured by Taqman quantitative PCR and Western blotting. Cell apoptosis was measured by normal and fluorescent microscopy and Cell Death Detection ELISA. Results In the Bcl-2-expressed cells, fluvastatin significantly reversed hydrogen peroxide-induced microscopic apoptosis and apoptotic DNA fragmentation, which were accompanied by a markedly upregulation of Bcl-2 expression by fluvastatin. However, the endothelial protection by fluvastatin was completely lost in Bcl-2 siRNA transfected cells. Conclusion Fluvastatin protects human endothelial cells against oxygen radical-induced cell apoptosis in vitro, and this protection seemed to be mediated in a Bcl-2 dependent pathway.
Objective To study the effect of ivabradine on hyperpolarization activated cation current in canine pulmonary vein(PY) sleeve cardiomyocytes with atrial fibrillation. Methods Dissociation of PVs yielded single cardiomyocytes from a Landengorff column without or with pacemaker activity from long-term rapidly atrial pacing (RAP) canines. If current was measured with the whole-cell patch-clamp technique. Results Compared with the control group, the rapidly atrial pacing canine PV cardiomyocytes had spontaneous diastolic depolarization and had larger If densities. Ivabradine (Iva,1|ìM), a selective inhibitor of the If current, markedly reduced If currents in the RAP from -2.66±0.4 pA/pF to -1.58±0.1 pA/pF at the test potential of -120 mV (P<0.01,n=12). Inhibition effect of Iva of If current showed concentration-dependent range from 0.1 to 10.0 |ìM, with IC50 of 2.2 |ìM ( 1.8–2.9 |ìM, 95% CL). Furthermore, V1/2 of steady-state activated curve was shifted from -84.3±4.9 mV to -106.9±3.4 mV and k value of steady-state activated curve was changed from 12.1±2.6 mV to 9.9±3.4 mV by the application of. 1.0 |ìM Iva ( P<0.01, n=12). Conclusions Our study revealed that Ivarbadine may significantly decrease If of rapidly atrial pacing pulmonary vein sleeve cells with atrial fibrillation.
Objective To describe changes that occur in stent morphology and structure after its implantation in coronary bifurcation. Side branch (SB) compromise after stenting of main vessel in coronary bifurcation is a major intraprocedural problem and for the long term, as a place of restenosis. Methods We created an elastic wall model (parent vessel diameter 3.5mm, daughter branches 3.5mm and 2.75mm) with 30, 45 and 60 degree distal angulation between branches. After stent implantation, struts to the side branch were opened with 2.0mm and consequently 3.0mm diameter balloons. Subsequent balloon redilatations and kissing balloon inflations (KBI) were performed. All stages of the procedure were photographed with magnification up to 100 times. Results We found that the leading mechanism for side branch compromise was carina displacement, and discovered theoretical description for expected ostial stenosis severity. Based on our model we found that displacement of bifurcation flow divider cause SB stenosis with almost perfect coincidence with our theoretical predictions. Opening of stent cells through the proximal and distal stent struts always increased interstrut distance, but never achieved good apposition to the wall. Balloon diameter increase didn’t give proportional enlargement in stent cell diameters. KBI leads to some small better stent positioning, correcting main vessel strut dislodgment from wall, but never gave full strut-wall contact. Distance between struts and wall was minimal only when the stent cell perfectly faced ostium of SB. This was also our observation that the shape of ostium of SB becomed elliptically-bean shaped after stent implantation and generally kept that shape during consequent stages of experiment. Measured diameter and area stenosis were perfectly fitted and theoretically predicted from our concept. Conclusion We have described stent-wall deformations in stent-balloon technique for treatment of coronary bifurcation demonstrating carina displacement as possibly main mechanism of side branch compromise after main vessel stenting. We have shown that KBI could not give full strut-wall contact if there is no perfect facing of stent cell and SB ostium.
Left ventricular hypertrophy (LVH) is one of the vicious organ damages of essential hypertension. It contributes a lot to high mortality of essential hypertension due to sudden cardiac death, ventricular arrhythmia and heart failure. Many factors involve in the pathogenesis of hypertension-induced LVH including inherited variants as well as environmental factors. For the genic influence, nucleus’ involvement has been discussed for years. However, much fewer interest has been put in the other inherited system—mitochondrion. To make clear the relationship of mitochondria and LVH, we try to illustrate the clinical and pathological characteristics of LVH, the structure and function of mitochondria and mitochondrial role in LVH as follows
Essential hypertension (EH) is an escalating problem for developed and developing countries. It is currently seen as a ‘complex’ genetic trait caused by multiple susceptibility genes which are modulated by gene-environment and gene-gene interactions. Over the past 10 years, mitochondrial defects have been implicated in a wide variety of degenerative diseases, aging, and cancer. Recently several studies showed that human essential hypertension has excess maternal transmission which suggests a possible mitochondrial involvement. However, the exact pathophysiology of mitochondrial DNA mutation (mtDNA) in essential hypertension still remains perplexing. With the application of a variety of imaging approaches and successive mouse model of mitochondrial diseases we convince that these problems will be resolved in the near future.