Atorvastatin use and coronary flow reserve in patients with coronary slow flow / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the impact of statin use on coronary flow reserve (CFR) in patients with slow coronary flow.</p><p><b>METHODS</b>A total of 91 patients with chest pain and coronary slow flow but normal coronary angiography were included in this study, patients were divided into statin group (atorvastatin 20 mg/d for 8 weeks, n = 51) and non-statin group (n = 40), 26 healthy subjects with normal angiography and negative exercise ECG test served as normal controls. Blood cholesterol was measured. Doppler coronary flow velocity and Doppler reserve measurement of distal left anterior descending were recorded at rest and adenosine infusion (140 microgxkg(-1)xmin(-1)) induced hyperemia state, CFR was calculated by the ratio of maximal hyperemia and baseline peak diastolic coronary flow velocity (hCFV and bCFV) before and after atorvastatin treatment.</p><p><b>RESULTS</b>(1) Eight weeks later, total cholesterol and LDL-C levels were significantly lower in statin group than in non-statin group and control group [TC (3.83 +/- 0.80) mmol/L vs. (5.30 +/- 1.18) mmol/L vs. (5.32 +/- 1.17) mmol/L, P < 0.05; LDL-C (2.26 +/- 0.64) mmol/L vs. (3.28 +/- 0.85) mmol/L vs. (3.30 +/- 0.82) mmol/L, P < 0.05]. (2)Baseline CFR levels were significantly lower in statin group and non-statin group than that in control group (2.32 +/- 0.30 vs. 2.25 +/- 0.33 vs. 3.15 +/- 0.34, P < 0.05). Compared with non-statin group and statin group before treatment, 8 weeks statin treatment was associated with reduced bCFV [(26.06 +/- 3.22) cm/s vs. (29.02 +/- 3.36) cm/s and (26.06 +/- 3.22) cm/s vs. (28.43 +/- 3.40) cm/s, P < 0.05], increased hCFV [(77.63 +/- 8.96) cm/s vs. (65.17 +/- 7.22) cm/s and (77.63 +/- 8.96) cm/s vs. (64.58 +/- 6.26) cm/s, P < 0.05] and increased CFR (3.07 +/- 0.29 vs. 2.28 +/- 0.35 and 3.07 +/- 0.29 vs. 2.32 +/- 0.30, P < 0.05). bCFV, hCFV and CFR of statin group post treatment were similar to those of controls (P > 0.05).</p><p><b>CONCLUSION</b>Patients with coronary slow flow were associated with lower CFR which could be significantly improved by statin therapy.</p>

Causes of death analysis in 133 congestive heart failure patients / 中华心血管病杂志

<p><b>OBJECTIVE</b>To analyze the causes of death in patients with heart failure.</p><p><b>METHODS</b>A total of 133 heart failure patients died during hospitalization in our hospital between January 2005 and December 2008 were enrolled in this study. Patients were divided to two groups: sudden death (group A, n = 73, 54.9%), chronic end-stage pump failure (group B, n = 55, 41.4%). The remaining 5 cases died of other causes were excluded from the final analysis. Clinical data (medical history, blood pressure, clinical manifestation, NYHA cardiac function class, left ventricular diameter of diastole, left ventricular ejection fraction, ventricular arrhythmias, drug therapy) of group A and B were analyzed.</p><p><b>RESULTS</b>There were no significant differences in terms of medical history (including hypertension and diabetes), blood pressure, heart rate and the incidence of ventricular arrhythmia between the two groups. In group A, the NYHA functional class was mostly II or III grade, and LVEF value was significantly higher than that of group B. The incidence of angina pectoris was significantly higher in group A compared to group B. beta-blocker and angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker use was also significantly higher in group A than in group B, however, the treatment dose was significantly lower and therapy duration was significantly shorter in group A than in group B. There were significantly less patients received statins and anti-platelet aggregation drugs in group A compared to group B.</p><p><b>CONCLUSION</b>In our patient cohort, sudden cardiac death often occurred in heart failure patients with NYHA cardiac function II to III grade, angina pectoris, probably due to the unstable coronary plaque and less statins and anti-platelet drug use in these patients.</p>

On angiotensin II receptor distribution after myocardial infarction in dogs / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effects of valsartan on expression of angiotensin II receptors in different regions of heart after myocardial infarction (MI).</p><p><b>METHODS</b>Canines were divided into sham-operated control group (n=7), infarction group (n=7) and Valsartan group (10 mg x kg(-1) x day(-1) for 4 weeks after MI operation, n=7). Four weeks after operation, Doppler tissue imaging (DTI) was used to evaluate regional ventricular function in the noninfarcted myocardium (apical and basal near to the infarction region). The mRNA and protein expressions of angiotensin II type 1 receptor (AT1-R) and angiotensin II type 2 receptor (AT2-R) on the corresponding regions were detected by competitive reverse-transcriptase polymerase chain reaction technique and immunohistochemical technique respectively. Results The protein and mRNA expressions of AT1-R were significantly increased in both apical and basal regions near to the infarction in dogs with MI compared with those in control group (P < 0.05) which could be downregulated by valsartan (P < 0.05). AT2-R expressions were significantly upregulated in infarction group in both apical and basal regions compared with those in control group and valsartan further increased AT2-R expressions in both areas (P < 0.05). Myocardial peak systolic velocity (Sm), myocardial peak early diastolic velocity (Em) and myocardial peak late diastolic velocity (Am) at both apical and basal regions near to the infarction regions were significantly lower in MI group than those in the control group which could be significantly improved by valsartan.</p><p><b>CONCLUSION</b>Both mRNA and protein expressions of AT1-R and AT2-R are upregulated in noninfarcted regions near MI, valsartan improved myocardial function via inhibiting AT1-R upregulation and enhancing AT2-R upregulation.</p>

Pathologic observation on ventricu lar myocardium of epicardium and focus underneath atrioventricularring produced by microwave catheter ablation / 中国地方病学杂志

Objective To observe the variation of enzymatic activity and areas and bulk of focus of heart injuries by using controllable catheter to ablate epicardial tmsue of rabbits and focus underneath atrioventrieular ring narcosis with 20% urethane(4 ml/kg)and divided into three groups.Each group included 7 rabbits.Anterior wallepieardium of left ventricle was ablated thirty seconds in each group(10,20 and 30 W)with self-made ablationspheroid microwave antenna,refilling with high pressure normal saline at same time.Then all of the rabbits were sacrificed respectively and their ventricular myocardium were taken out to undergo immunohistochemistry in order to display suceinate dehydrogenase(SDH).Also amplitude Wag measured in order to calculate areas of heart injuries.(8F)wag delivered to the pre-selected sites around atrioventricular ring of thirty-two healthy dogs,which had beenin intravenous narcosis with pentobarbital sodium(30 mg/kg).The dogs were divided into four groups(40,50,60 and 80 w) and two time points(60 and 120 s),by the combined method of X-ray and endocardial electrocardiograph,the microwave antenna could be confirmed to be located at the accurate position between anterior and posterior wall close to septum of left/right ventricle.After ventricular myocardium had been taken out,amplitude were measuredin order to calculate bulk of heart injuries by 1/6×3.14 x long×wide×deep.In addition.the histological changesand transmural injury were examined by optic microscope.Results In each group,the centre of injuries wagenzyme deficiency locus.The diameter and areag of heart injuries enlarged significantly(3.99.±0.41),(5.20±0.25),(6.31±0.37)mm and(12.53±2.56),(21.19±3.14),(30.96±3.76)mm2 with the increased microwave power level(10、20、30 W).Group comparison had statisficM significance(F＝76.8,58.5;P＜0.01 or ＜0.05).A total of 116points were ablated.The myocardial lesion showed ellipse in shape,and continuous symmetrical coagulationnecrosis under microscopic examination.There was a clear demarcated line around tlle myocardial tissue and fewparietal thmmbus.There were 16 transmura]injuries and five-with lung damage.The bulk of lesion aroundatrioventrieular ring hag been significantly enlarged(46.7±2.5),(51.1±2.7),(133.2±3.4),(141.8±3.9),(248.5±6.2),(260.3±6.5),(313.7±9.5),(327.4±10.5)with the increased microwave power level(40,50,60and 80 W)and/or distance of microwave ablation(60 and 120 s).Groups comparison had statistical significance(F＝31.16,27.85;all P＜0.01).In each time point,the lesion bulks had conspicuous distinction of statistics.In the same microwave power,the time wag longer,the bulk was larger(P＜0.01).Conclusions The more the microwave power level and time,the severe the heart injuries is.It is possible to use the microwave energy to ablate the deep focus under endocardium around atrioventricular ring.

Study on the pathological change and the expression of neuron specific enolase in the hippocampus dentategyrus granular cell layer of epilepsy patients / 中国地方病学杂志

Objective To find out pathologieal change and the expression of neuron specific enolage (NSE)in the hippocampus dentate gyrus granular cell layer of epilepsy patients,to investigate the relationship between the pathological change and the cause of the epilepsy.Methods The specimens of hippocampus were from 9 epilepsy patients and 20 normal persons and the pathological change were investigated under the staining of the hematoxylin and eosin staining.The expression of NSE in the hippocampns denmte gyrus granular cell layer of epilepsy patients was detected by immunohistochemistry(IHC)with specific antibody,and the rate of NSE positive nenrons was evaluated.Results The nuclear pyknosis was observed in all of hippocampus from the epilepsy patients and some neurons were swelling.The positive of NSE was showed to have yellow granule;the rate of NSE positive was 28.66%.The expression of NSE of the neurons in the hippocampus dentate gyrus granular cell layer was.significantly reduced in epilepsy patients(7.9±5.6)%.The normal neuron nuclear was big and round in the middle of the cell and the nucleolus could be seen easily.The expression of NSE of the neurons in the hippocampus dentate gyrus granular cell layer was(39.0±17.4)%.Compared with normal group,the number of neurons with yellow granule was reduced.The difference of the NSE expression rate between the two group was statistically significant(t＝-5.13,P＜0.01).Conclusions The result suggests that the pathological abnormality and the reduced expression of NSE on the hippocampus dentate gyrus granular cell layer neurons could be one of the main reasons of the occurring of epilepsy.

Arsenic trioxide eluting stents to prevent restenosis of injured iliac arteries in rabbits / 中华心血管病杂志

<p><b>OBJECTIVE</b>To assess the efficiency of eluting stent coated with arsenic trioxide (As(2)O(3)) suspended in poly-L-lactic acid (PLLA) to prevent in-stent restenosis in rabbits.</p><p><b>METHODS</b>Forty-five male New Zealand white rabbits were assigned to three groups (n = 15 for each group) at random: uncoated stents, stents coated with PLLA or stents coated with As(2)O(3) in PLLA. Animals were euthanized 28 days after stent implantation into the iliac arteries of rabbits. Neointimal thicknesses and apoptosis of vascular smooth muscle cell (VSMC) were measured. Stents coated with As(2)O(3) in PLLA were implanted in another 48 male New Zealand white rabbits, As(2)O(3) concentrations in serum and arterial tissue at implantation site were measured at 2 h and 1, 3, 7, 14, 28 days after As(2)O(3) eluting stent implantation (n = 8 for each time point).</p><p><b>RESULTS</b>Neointimal hyperplasia was significantly reduced 51% and 31% and apoptosis significantly increased (21.0 +/- 3.3; 6.2 +/- 1.9(*); 5.3 +/- 2.1(*), (*)P < 0.01 vs. As(2)O(3) eluting stent) with As(2)O(3) eluting stent, versus PLLA-coated stents and uncoated stents. As(2)O(3) concentrations in arterial tissue at implantation site were 18.6 +/- 9.1 (ng/mg) at 1 day and 0.3 +/- 0.1 (ng/mg) at 28 days after stent implantation.</p><p><b>CONCLUSIONS</b>As(2)O(3) coated stents released As(2)O(3) to local tissue for at least 28 days, suppressed neointimal hyperplasia in rabbit iliac arteries and increased local VSMC apoptosis might be one of the mechanisms for inhibiting restenosis by As(2)O(3) coated stents.</p>

Effect of Cilazapril on endothelial cell function and fibrinolysis system in the canine atrial fibrillation models / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effect of cilazapril on endothelial cell function and fibrinolysis system in the canine atrial fibrillation (AF) models.</p><p><b>METHODS</b>All canines were divided into three groups: (1) Control group, without atrial pacing; (2) Atrial pacing group, in which atrial fibrillation was established by rapid atrial pacing at 400 bpm for 6 weeks; (3) Atrial pacing together with cilazapril group, in which cilazapril was given before and after atrial pacing. Nitric oxide (NO) of atrial endocardium was measured with NO-specific microelectrode. The expression of plasminogen activator inhibitor-1 (PAI-1) and tissue-type plasminogen activator (tPA) protein in atrium was determined by Western Blot analysis and immunohistochemical staining. Plasma levels of von Willebrand Factor (vWF), PAI-1 and tPA were analyzed by enzyme-linked immunoadsorbent assay.</p><p><b>RESULTS</b>NO production from atrial endocardium was significantly increased in atrial pacing together with cilazapril group than atrial pacing group [(42.6 +/- 9.9) nmol/L vs (23.4 +/- 5.8) nmol/L, P < 0.05], whereas the plasma levels of vWF were decreased [(75.4 +/- 12.8)% vs (125.9 +/- 20.6)%, P < 0.05]. Compared to controls, the expression of atrium tPA protein in atrial pacing together with cilazapril group was significantly upregulated (4052 +/- 857 vs 1936 +/- 421, P < 0.05) and PAI-1 protein was downregulated (2487 +/- 542 vs 3164 +/- 827, P < 0.05). Cilazapril also significantly increased tPA antigen and decreased PAI-1 antigen in plasma.</p><p><b>CONCLUSION</b>Cilazapril can favorably improve endothelial function and resume the balance of fibrinolysis system in AF, which might be of beneficial to hypercoagulated state in AF.</p>

The experimental study on changes of endothelial nitric oxide synthase and plasminogen activator inhibitor-1 protein in the canine atrial fibrillation model / 中华心血管病杂志

<p><b>OBJECTIVE</b>To evaluate the changes in the expressions of endothelial nitric oxide synthase (eNOS) and plasminogen activator inhibitor-1 (PAI-1) and the alterations of nitric oxide (NO) concentration in atrial endocardium in atrial fibrillation (AF) in order to investigate the mechanisms that contribute to thrombosis.</p><p><b>METHODS</b>In canine AF was produced with rapid atrial pacing at 400 bpm for 6 weeks, whereas the controls had no atrial pacing. NO production was measured by NO-specific microelectrode. The expression of endocardial eNOS and PAI-1 protein were determined by Western blot analysis and immunohistochemical Staining. Plasma levels of PAI-1 were analysed by Enzyme-linked immunoadsorbent assay.</p><p><b>RESULTS</b>Left atrial NO concentration was decreased in AF than that in controls [(23.4 +/- 5.8)nmol/L vs (63.8 +/- 16.1)nmol/L, P < 0.01]. Endocardial eNOS expression was also significantly decreased (855 +/- 217 vs 2320 +/- 694, P < 0.05), whereas the expression of the PAI-1 was increased (3164 +/- 827 vs 1371 +/- 352, P < 0.01). Neither NO concentration, nor PAI-1, eNOS expression were altered in the right atria at the same time. A significant increase for plasma levels of PAI-1 was also detected in AF group. No correlation was found between eNOS and PAI-1 protein expression (r = 0.217, P > 0.05).</p><p><b>CONCLUSION</b>In the canine model AF was associated with a marked decrease in endocardial NOS expression and NO concentration and with an increase in PAI-1 expression in the left atrium, which may contribute to the thrombosis in AF.</p>