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Objective:To evaluate the value of adenosine triphophate (ATP)stress/rest nuclide myocardial perfusion imaging (MPI)in the diagnosis of female patients with coronary heart disease (CHD).Methods:The clinical materials of 47 female suspected CHD patients were retrospectively analyzed,aged from 39 to 74 years,and the average age was (53.7±6.3)years old.All patients were hospitalized and underwent two-day ATP stress and rest nuclide MPI and coronary angiography (CAG)in two weeks. The results and images of MPI and CAG were evaluated by more than 2 attending physicians. Using CAG as the “gold standard”, the diagnostic efficiency (sensitivity, specificity and accuracy) of MPI for CHD was evaluated. Results:Compared with CAG, the sensitivity,specificity and accuracy of ATP stress MPI in diagnosing the female CHD patients were 81.3% (13/16),77.4% (24/31)and 78.7% (37/47)individually;the positive predictive value and negative predictive value were 65.0% (13/20)and 88.9% (24/27).There were no severe adverse effects in the ATP stress test and the incidence of adverse effects was 85.1%.Conclusion:There is a highly diagnostic efficiency of ATP stress MPI in the CHD patients.It can be the first choice of examination methods for screening without injury and diagnosing the myocardial ischemia in the female patients.
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Objective To provide the new method for repairing degloving injury of the single finger.Methods From August 2007 to June 2010,eleven patients were repaired with the second free toe dorsal wrap around flap and fibula side flap of great toe.Patients including 9 men and 2 women.The mean age were 31 years(17-49 years).The finger including 6 index fingers,two middle fingers and 3 ring fingers,in which 4 patients were type I and 7 patients were type Ⅱ.All of them were emergency debridement VSD closed negative pressure attraction,surgical repair in 3-5 days after injury.The plantar digital nerve in the second free toe dorsal wrap around flap and fibula side flap of great toe with the digital nerve of the stump by end-to-end nerve anastomosis.The donor sites were covered with a free flap.Results All of 11 flaps survived,but 2 cases developed partial native second toe skin grafting necrosis,by dressing healed,one case of phalanges exposed through survival skin,the part of the exposed phalanx healed after surgical cut.All the 11 patients were followed up from 3 monthes to 3 years.The flaps survived completely with satisfactory cosmetic results and good sensibility.The sensation recovery was reached above S3.The great toe fibular flap for repair of finger pulp full,two-point discrimination was 6-9 mm,the mean was 7.0 mm.Finger flexion function by finger total activity (TAM) score assessment,excellent 9 cases,good 2 cases.Conclusion Transfer of the second free toe dorsal wrap around flap and fibula side flap of great toe to repair degloving injury of the single finger is an ideal method of treatment.
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Objective To dissect and observe the course of the deep branch of the ulnar nerve and its'distribution of the muscular branch,to provide imaging and anatomical basis for early diagnosis and treatment of the wrist deep branch of ulnar nerve injury in clinical. MethodsFrom October 2008 to August 2010,dissected 16 fresh and 4 antiseptic samples, with the most bump of the hook of the hamate bone as the origin O,set the axis over the O point.The distance from O to the intersection point of the X axis and the deep branch of ulnar nerve was OE ; the distance from O to the intersection point with the ulnaris of hook of hamate bone was OF; the distance from O to the proximal deep branch of ulnar nerve intersection point of the Y axis was OG; the distance from O to the distal deep branch of ulnar nerve respectively was OH.Named the head of the metacarpal bone and the palm side of the center of the basal of the 2nd to the 5th metacarpal bone, through these two points,the measure related data from the deep branch of the ulnar nerve and the metacarpal bone in the sagittal plane.Having a CT scan image data,the Barium Sulfate ( Ⅱ ) dry suspension was uniformly smeared onto the surface of the deep branch of ulnar nerve, the data obtained was analyzed using SPSS 13.0.ResultsThe length of OE was ( 4.96 ± 0.11 ) mm,CT result was (5.02 ± 0.12 ) mm; the length of OF was (3.69 ± 0.12 ) mm,CT result was(3.75 ± 0.12)mm; the length of OG was(10.55 ± 1.07)mm,CT result was(10.48 ± 0.84)mm;the length of OH was (7.23 ± 0.85)mm,CT result was (7.29 ± 0.84)mm; the length of EF was (1.27 ± 0.15 )mm,CT result was( 1.17 ± 0.16)mm.The measure related data from the deep branch of the ulnar nerve and the metacarpal bone in the sagittal plane. Each data set of the anatomical results and CT results had been tested by T,P values were more than 0.05. ConclusionsThere is no significant difference between anatomic and CT observations of deep branch of ulnar nerve, CT observations can be regarded as a clinical reference directly.Anatomic and CT observations can be seen as a guide for clinical work in the diagnosis and treatment of deep branch of ulnar nerve injury.
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Aim To observe the effects of simvastatin on PPARγ and p65 subunit of NF-κB and to invest the mechanism of simvastatin preventing hypertrophy and keeping cardiac function.Methods 24 rabbits were divided into 4 groups.Rabbits received sham operation as health control in group I. In other groups, aortic regurgitation and coarctation of ascending aorta were operated in rabbits.Rabbits received no drugs in Group Ⅱ. In group Ⅲ, rabbits were given simvastatin 5 mg·kg~(-1)·d~(-1) after the operation for 8 weeks. In group Ⅳ, rabbits were given simvastatin 5 mg·kg~(-1)·d~(-1) after 4 weeks of operation for 4 weeks. At the beginning and the end of the experiment, left ventricular end diastolic pressure (LVEDP) was measured with catheter. At the end of the experiment, heart weight (HW), left ventricular weight (LVW), body weight (BW), heart weight/body weight radio (HW/BW radio), left ventricular weight/body weight radio (LVW/BW radio) were measured.The PPARγ mRNA expression was analyzed by RT-PCR. PPARγ and p65 protein expression in cardiomyocyte nuclear were analyzed through Western blot. The activity of p65 was analyzed with EMSA.Results The HW, LVW, HW/BW were significantly decreased in the early and late treatment group than in CHF group(P<0.05,P<0.01). The LVW/BW was significantly decreased inearly treatment group than in CHF group, too (P<0.01). The LVEDP was significantly decreased in the early and late treatment group than in CHF group (P<0.01). The mRNA and protein of PPARγ significantly fell in CHF heart (P<0.01). The activity and protein expression of p65 were significantly increased in CHF heart (P<0.01). Simvastatin increased the mRNA and protein expression of PPARγ and decreased the activity and protein expression of p65 (P<0.01).Conclusions Simvastatin inhibits the cardiac hypertrophy and improves cardiac function. The mechanism of simvastatin on cardiac remodeling and function relates to the increase of PPARγ expression and preventing the NF-κB activation.
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Objective To evaluate the safety and efficacy of the temporary bedside cardiac pacing in controlling torsades de points (TdP) in patients with acquired long QT syndrome (LQTS). Methods Twelve patients with acquired LQTS were enrolled from April 2003 to August 2007 consecutively and their clinical data were analyzed. Bedside cardiac pacing was adopted when other methods couldn't terminate the repeated TdP. Results Twelve patients successfully experienced the temporary bedside cardiac pacing via femoral venous. The average time spent in bedside cardiac pacing was about (10.5±2.4) min. After cardiac pacing the interval of QT and QTc were shortened [ (0.42±0.03 ) svs (0.52±0.06) s, P < 0.05; (0.43± 0.04 ) s vs (0.53±0.05 ) s, P <0.05 ]. The TdP occurred (4.6±1.2 ) times per day before cardiac pacing and it didn't reoccur any more after bedside cardiac pacing. The average time for cardiac pacing was(3.8±1.4) d. When the patients were discharged, the interval of QT and QTe were (0.41±0.02) s and (0.42±0.05) s respectively, there were significant differences compared with that before cardiac pacing(P< 0.05). During 1 year follow-up, the patients didn't experience TdP any more, and the interval of QT and QTe were (0.41± 0.06) s and (0.42±0.05) s respectively. Conclusion The immediate bedside cardiac pacing is a safe and effective way to control the repeated TdP.
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Objective Clinical evidence has suggested that ATI receptor blocker (ARB) could prevent the development of heart failure. Decreased sareoplasmic reticulum(SR) Ca2+ content, which is due to reduced SR calcium reuptake by SERCA2a, is responsible for defective systolic function in failing heart. To better understand how ARB could improve cardiac systolic dysfunction, we studied the effects of Valsartan on calcium reuptake of SR and its regulatory proteins in heart failure rabbits. Methods Thirty rabbits were divided into three groups: sham rabbits(controls, n= 11), rabbits with heart failure treated with Valsartan (n= 11) and rabbits with heart failure but without Valsartan treatment (n=8).Rabbit heart failure model was established by volume plus pressure overload. Cardiac function was measured by echocardiography. SR calcium uptake was determined by measuring extra vesicular free [Ca2+] changes in a fluores-cence spectrophotometer. SERCA2a, Serl 6-phosphorylated phospholamban (p-PLB), PKA and PP1a protein abundance were deter-mined by use of Western blot analysis. Results Compared to control rabbits, the ejection fractions in the HF rabbits were significantly decreased (P<0.05), these changes could be significantly attenuated by Valsanan treatment (P<0.05).Calcium reuptake of SR, activity of SERCA2a and PKA decreased in heart failing myocytes (P<0.05), with down regulations of p-PLB, SERCA2a and PKA, but up regulation ofPP1αin ventricular samples from the failing rabbits (P<0.05). All of these changes were attenuated by Valsartan treatment (all P<0.05). Conclusion Valsartan improved cardiac function in volume plus pressure overload induced heart failure of rabbits possibly by restoring the SR calcium uptake resulted from attenuating the activities and expressions of SERCA2a and its regulatory proteins.
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Objective To compare the differences of cardiac function and interstitial remodeling between diastolic heart failure(DHF) and systolic heart failure(SHF) rabbit models. Methods To establish DHF model with abdo-mial aorta constriction and SHF model with abdomial aorta constriction plus aortic insufficiency. The cardiac func-tion was examined by UCG parameters and homodynamic parameters. The collagen content was measured through hydroxyproline colorimetric assay and shown as collagen area(CA), collagen volume fraction(CVF) and area ratio of Ⅰ to Ⅲ type collagen with PSR. Results Compared with control group, there were significantly increased thick-ness and stiffness of myocardium, impaired diastolic function but normal ejection fraction (EF), and significantly increased collagen content, CA, CVF and area ratio of Ⅰ to Ⅲ type collagen in DHF group; heart chamber was sig-nificantly enlarged, systolic function decreased, and collagen content, CA, CVF significantly increased, but ratio of Ⅰ to Ⅲ type collagen decreased in SHF group(P <0.05 or P <0.01). Conclusion DHF and SHF rabbit mod-els were established successfully, which can simulate clinical profiles and provide technical support to future re-search.
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Objective To analyze the effect of dominant accessory atrioventricular pathways (AP) on the end vector of ventricular depolarization. Methods All patients had single AP confirmed by radiofrequency cathteter abalation (RFCA) and were free from organic heart disease (including 102 cases of dominant accessory AP and 38 cases of concealed AP). The AP was divided into posterior septal(P3) ,mediate septal (MS) ,anterior septal (AS), left posterior free wall (LP), left anterior free wall (LA), right posterior free wall (RP) and right anterior free wall (RA). Results The end 40 ms vector of QRS wave changed in 102 patients with manifested AP and in 4 patients with concealed AP (P < 0. 05). Conclusion The end 40 ms vector of QRS wave of any site manifested AP can change and the changes have the specihty of leads.
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Objective To investigate the change in potassium channel in ventricular myocytes in vitro derived from diabetic rats and the effect of insulin and dichloroaectic acid(DCA). Methods The diabetic rat model was established by injection of streptozocin(STZ) peritoneally using male Sprague-Dawley rats with body weight 150-200 gram. Ventricular myocytes were isolated by enzymatic method and the whole-cell patch clamp technique was used to record the potassiumion currents. Results The I to density of ventricular myocytes in diabetic rats was significantly decreased compared with control rats[at+60 mV, 15.90?1.19 pA/pF (n=25) vs 28.55?0.97 pA/pF (n=12), P
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<p><b>OBJECTIVE</b>To explore the mechanism underlying the prolongation of action potential and delayed inactivation of the L-type Ca(2+) (I(Ca, L)) current in a feline model of left ventricular system hypertension and concomitant hypertrophy.</p><p><b>METHODS</b>Single Ca(2+) channel properties in myocytes isolated from normal and pressure overloaded cat left ventricles were studied, using patch-clamp techniques. Left ventricular pressure overload was induced by partial ligation of the ascending aorta for 4 - 6 weeks.</p><p><b>RESULTS</b>The amplitude of single Ca(2+) channel current evoked by depolarizing pulses from -40 mV to 0 mV was 1.02 +/- 0.03 pA in normal cells and 1.05 +/- 0.03 pA in hypertrophied cells, and there was no difference in single channel current-voltage relationships between the groups since slope conductance was 26.2 +/- 1.0 pS in normal and hypertrophied cells, respectively. Peak amplitudes of the ensemble-averaged single Ca(2+) channel currents were not different between the two groups of cells. However, the amplitude of this averaged current at the end of the clamp pulse was significantly larger in hypertrophied cells than in normal cells. Open-time histograms revealed that open-time distribution was fitted by a single exponential function in channels of normal cells and by a two exponential function in channels of hypertrophied cells. The number of long-lasting openings was increased in channels of hypertrophied cells, and therefore the calculated mean open time of the channel was significantly longer compared to normal controls.</p><p><b>CONCLUSION</b>Kinetic changes in the Ca(2+) channel may underlie both hypertrophy-associated delayed inactivation of the Ca(2+) current and, in part, the pressure overload-induced action potential lengthening in this cat model of ventricular left systolic hypertension and hypertrophy.</p>