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ABSTRACT: To evaluate the value of double source multidetector computed tomography (MDCT) in visualization of cardiac veins in patients with chronic heart failure.
Thirty-five patients with chronic heart failure (aged 65.4 ± 8.8, 21 males and 14 females) were enrolled in the study. In Group A, MDCT and retrograde coronary venography (RCV) were performed consecutively; in Group B anterograde visualization of the coronary venous and RCV were performed.
Coronary sinus, GCV and MCV of all individuals were identified in MDCT. LVPV was observed in 65% patients of Group A, and 66.7% patients of Group B. The correlation coefficient between MDCT and RCV was 0.944, and that between CVG and RCV was 0.42.
Non-invasive evaluation of cardiac veins with double source CT is feasible and may be used in cardiac resynchronization therapy.
Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 11/2011; 40(6):663-6.
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ABSTRACT: To investigate the effects of metoprolol on electrophysiology of ischemic and anoxic myocardium in diabetic rats.
Forty Sprague-Dawley (SD) rats were divided into 4 groups: diabetes group; diabetes and ablation of left sympathetic nerve group; diabetes and metoprolol group and sham group. The diabetes model was induced by intraperitoneal injection of streptozotocin (STZ, 60 mg/kg). The ventricular diastolic effective threshold (DET), effective refractive period (ERP), and Ventricular fibrillation threshold (VFT) were measured. The serum concentration of nerve growth factor (NGF) was measured.
Metoprolol increased DET of ischemic and anoxic myocardium in diabetic rats. The ablation of the left sympathetic nerve increased VFT of diabetic rats. VFT in metoprolo group was significantly increased compared to diabetes group after ischemia. The concentrations of NGF in diabetic group and metoprolol group were higher than those in sham group. There were no difference in NGF levels between ablation of left sympathetic nerve group and sham group.
The remodeling of sympathetic nerve affects the electrophysiology of ischemic myocardium of diabetic rats. Metoprolol can increase the VFT and decrease the excitation threshold of the ischemic myocardium in diabetic rats.
Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 11/2011; 40(6):653-8.
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Yuan Yuan Chen,
Ning Ling Sun,
Wei Zhong Zhang,
Hai Ying Wu,
Lin Zhang,
Zhen Qiu Yu,
Fu Chun Zhang,
Xiao Ping Xiang,
Hui Liang Liu, Fa Rong Shen,
Jun Tao,
Jiu An Zhao
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ABSTRACT: To evaluate the efficacy, safety and tolerance of Felodipine controlled release tablets and Felodipine controlled release tablets associated combination each with Metoprolol, Lisinopril or Hydrochlorothiazide in the 12 weeks treatment of mild to moderate essential hypertension in China.
Multicenter, random samples, and open study have been processed.
(1)After 12 weeks associated combination treatment of antihypertension, the percentages of the persons who had attained the target were 80.2% of ITT group in Felodipine controlled release tablets associated combination with Hydrochlorothiazide, 74.1% of ITT group in with Metoprolol,and 80.5% of ITT group in with Lisinopril, respectively. (2)Mean reductions of systolic/diastolic blood pressure from baseline were 16.8/10.6 mm Hg in combination with Hydrochlorothiazide, 16.6/10.7 mm Hg in combination with Metoprolol,and 18.0/12.8 mm Hg in combination with Lisinopril each. There was no significant difference among these three groups (P>0.05). With the Felodipine controlled release tablets treatment alone, the mean reductions from baseline was 24.8/17.5 mm Hg. But in combination with Lisinopril, the blood pressure could lower more quickly, and then could reach the target more rapidly. (3)In the ITT group, the drug compliance with Felodipine controlled release tablets was 97.7%, with those in combination with Hydrochlorothiazide 89.8%, with those in combination with Metoprolol 100.0%, and with those in combination with Lisinopril 96.4%. The main adverse event related to Felodipine was headache, and to Lisinopril was cough.
Antihypertensive drug Felodipine controlled release tablets are good and effective. And Felodipine controlled release tablet associated combination each with Metoprolol, Lisinopril or Hydrochlorothiazide can make most patients reach the treatment target, with safety, good tolerance, and high compliance.
Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences 12/2007; 39(6):619-23.
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ABSTRACT: To investigate the effects of heme oxygenase 1 inducer hemin on protection of ischemia-reperfusion injury in rats and its mechanisms.
The Langendorff model of isolated rat heart was used; the left anterior descending coronary artery was occluded for 30 min and subsequently reperfused for 2 h. Then the ventricular function and infarct size were measured.
Hemin preconditioning prevented the increase in LVEDP, decrease in LVDP and +/- dp/dt(max) in the isolated ischemia-reperfusion rat hearts. The leakage of LDH and CK in the coronary effluent was significantly declined in hemin-treated rat hearts. And the infarct size was also reduced. Administration of a blocker of mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) 5-HD (5 mg/kg) before hemin preconditioning increased the LVEDP, and reduced the LVDP and +/- dp/dt(max). The leakage of LDH and CK in the coronary effluent and the infarct size were also increased compared with only hemin-treated rat hearts. Pretreatment of the rats with a blocker of sarcolemmal ATP-sensitive potassium channel (sarcK(ATP)) HMR-1098 (6 mg/kg) before hemin preconditioning also abolished the protective effect. Infusion of paxilline (1 micromol/L), a blocker of calcium activated potassium channel (K(Ca)) for 10 min before ischemia/reperfusion led to larger infarct size and poorer myocardial performance as compared with the hemin group. The leakage of LDH and CK in the coronary effluent was also increased.
Both mitoK(ATP)and sarcK(ATP)channels activation are required for the delayed cardioprotection induced by hemin. The opening of K(Ca) channels-dependent mechanism may be involved in the protection.
Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 02/2007; 36(1):7-12.
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ABSTRACT: To investigate whether cyclooxygenase-2 (COX-2) and heme oxygenase-1 (HO-1) are involved in the bradykinin-induced delayed protection.
Cardiac contractility, lactate dehydrogenase (LDH) and infarct area were analyzed in isolated rat hearts undergoing ischemia-reperfusion injury induced by Langendorff method.
Conscious rats received bradykinin (40 microg/kg), and the isolated hearts were subjected to 30 min of regional ischemia and 120 min of reperfusion 24 h later. Bradykinin pretreatment would improve post-ischemic performance, and reduced the release of LDH and infarct size. COX-2 inhibitor celecoxib (3 mg/kg) abolished bradykinin-induced protection, leading to poorer myocardial performance, release of more LDH and larger infarct sizes. Administration of HO-1 inhibitor ZnPP IX(20 microg/kg) before bradykinin partially abrogated the delayed protection. Pretreatment with the mitochondrial ATP sensitive potassium channel(mitoK(ATP) antagonist 5-HD before or 24 h after bradykinin administration also abolished the effect of protection.
The results indicate that activation of HO-1 and COX-2 might be involved in the delayed cardioprotection evoked by bradykinin, and mitoK(ATP) channel may serve as both a trigger and a mediator in the cardioprotection.
Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 02/2007; 36(1):13-20.
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Jian-hua Zhu,
Yuan-gang Qiu,
Jun-zhu Chen,
Fu-rong Zhang,
Guo-sheng Fu, Fa-rong Shen,
Wei-jian Huang,
Jian-an Wang,
Li-li Zhao,
Qian-min Tao,
Liang-rong Zheng
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ABSTRACT: The study was designed to compare the antithrombotic property and safety between nadroparin and unfractionated heparin during percutaneous coronary intervention (PCI).
A prospective, single blind, randomized study was performed. A total of 98 patients (aged 65.1 +/- 8.6 years, female, 28.6%, diabetes, 7.1%) undergoing selective PCI were randomized to be administered intravenously either nadroparin (0.075 ml/10 kg) or unfractionated heparin (100U/kg) for procedural anticoagulation, in whom stable angina was 42.9%, unstable angina, 27.6%, myocardial infarction, 29.6%, two or three-vessel disease, 23.5%, stent, 100%. Blood samples for anti-Xa level were assayed in the first 22 patients of the nadroparin group before and after administration at the following intervals: 8 min, 1 h, 2 h and 4 h. Bleeding complications were classified according to Thrombolysis In Myocardial Infarction (TIMI) criteria. The bleeding index (change in hemoglobin) was calculated. All patients were monitored for adverse clinical events (i.e. death, myocardial infarction, need for revascularization) during the period of 30 days after PCI.
(1) There were no significant differences in baseline characteristics between the two randomized groups. (2) Plasma anti-Xa activities were 0.10 +/- 0.00 IU/ml at the time just before the administration of nadroparin, 1.89 +/- 0.24 IU/ml, 0.96 +/- 0.24 IU/ml, 0.47 +/- 0.13 IU/ml, and 0.30 +/- 0.12 IU/ml at the time of 8 min, 1 h, 2 h and 4 h after the use of nadroparin (and the rate of > 0.5 IU/ml were 100%, 100%, 45% and 9% patients), respectively. (3) There were no significant differences in the mean bleeding index, post-PCI hemoglobin and hematocrit between nadroparin and unfractionated heparin group [(1.16 +/- 5.80) g/L vs (0.90 +/- 6.50) g/L, P = 0.858; (129.5 +/- 13.6) g/L vs (125.5 +/- 14.9) g/L, P = 0.175; (39.0 +/- 3.9)% vs (37.9 +/- 4.6)%, P = 0.205]. (4) None of the patients in two randomized groups were observed hemorrhagic events, which including TIMI major or minor bleeding complications, gross or microscopic hematuria, melena, positive stool occult blood. There were no blood transfusions and no hematoma at the vascular access site in either of the group. (5) No death, no recurrent angina pectoris, and no urgent revascularization occurred within 30 days in both groups. One patient in nadroparin group was observed "no reflow" phenomenon that was accompanied with an elevated ST segment and a risen serum level of cTnI. This patient was diagnosed as non-Q-wave myocardial infarction. Though no myocardial infarction was found in unfractionated heparin group, there was no significant difference in the rate of myocardial infarction between the two groups of the study (P = 0.970).
The administration of nadroparin before PCI seems effective and safe. Compared with unfractionated heparin, nadroparin was associated with neither an excess of bleeding nor an increase of clinical complications in this study.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 05/2005; 33(4):335-9.
