Effects of Isoprenaline，Phenylephrine on Heart and Influence of Nifedipine on These Effects

In a perfused isovolumetrically contracting rat heart model, the effects of isoprenaline(IPN) and phenylephrine (PE) on myocardial contraction and relaxation were investigated,and the influence of nifedipine on these effects was studied. Both IPN and PE increased the myocardial contraction and improved its relaxation, but some differences existed.Nifedipine (10 nmol/L)substantially inhibited the PE-mediated inotropic effect, but in case of IPN-mediated inotropic ones, it did not.It was assumed that there may be various types of slow channels, one was activated by IPN,and the other, by PE.

Coronary microembolization induced myocardial contractile dysfunction and tumor necrosis factor-α mRNA expression partly inhibited by SB203580 through a p38 mitogen-activated protein kinase pathway

Background The microemboli produced during spontaneous plaque rupture and ulceration and during coronary intervention will reduce coronary reserve and cause cardiac dysfunction. It is though that inflammation caused by the microinfarction induced by the microembolization may play an essential role. It is known that the activation of p38 mitogen-activated protein kinases （MAPK） in both infected and non-infected inflammation in myocardium may cause a contractile dysfunction. But the relation between the activation of p38 MAPK and microembolization is still unknown. Methods Sprague-Dawley rats were randomly divided into three groups： Sham group, coronary microembolization （CME） group and SB203580 group （n=-10 per group）. CME rats were produced by injection of 42 pm microspheres into the left ventricle with occlusion of the ascending aorta. SB203580, a p38 MAPK inhibitor, was injected into the femoral vein after the injection of microspheres to make the SB203580 group. Left ventricular ejection fraction （LVEF） was determined by echocardiography. The protein concentration of P38 MAPK in the myocardium was assessed by Western blotting. The relative expression of mRNA for tumor necrosis factor （TNF）-a was assessed by the technique of semi-quantitative polymerase chain reaction amplification. Results LVEF was depressed at three hours up to 12 hours in the CME group. Increased p38 MAPK activity and TNF-a mRNA expression were observed in the CME group. The administration of SB203580 partly inhibited p38 MAPK activity, but did not fully depress the TNF-α expression, and partly preserved cardiac contractile function. Conclusions p38 MAPK is significantly activated by CME and the inhibition of p38 MAPK can partly depress the TNF-a expression and preserve cardiac contractile function.

Anteroapical aneurysm plication improves mechanical intraventricular dyssynchrony in patients with anterior myocardial infarction

Background Left ventricular （LV） dyssynchrony has been described to occur in patients with myocardial infarction. Dyssynchrony of left ventricular mechanical contraction produces adverse hemodynamic consequences. This study aimed to test the capacity of geometric rebuilding by aneurysm plication to restore a more synchronous contractile pattern after a mechanical, rather than electrical, intervention. Methods A total of sixty patients with anterior myocardial infarction, QRS duration 〈120 ms, electively undergoing operation between January 2008 and January 2010 were included for analysis. Real-time 3-dimensional echocardiography was performed to assess LV function, LV systolic and diastolic dyssynchrony by measuring ejection fraction （EF）, peak ejection rate （PER）, peak filling rate （PFR） and LV dyssynchrony. LV dyssynchrony was defined as the systolic dyssynchrony of the time to reach the minimum systolic volume for 16 LV segments, expressed in percent cardiac cycle, systolic dyssynchrony index （SDI）. We compared changes of LV dyssynchrony at different interval times. Results LV contraction was significantly asynchronous because preoperative SDI was higher, EF, PER and PFR were lowered. Compared with function after operation, LV mechanical intraventricular resynchronization was improved with decreased SDI （（8.7_＋0.5） % vs. （14.3_＋1.6） %, P=0.01）; LV function was improved with EF increasing （（43_＋9）% vs. （37_＋7）%, P=0.001）, and LV systolic and diastolic dyssynchrony was improved with more rapid PFR （199.4_＋15.6 vs. 148.4_＋21.2, P=0.002） and PER （212.4_＋14.5 vs. 156.3_＋_26.2, P=0.001）. Conclusions Systolic and diastolic dyssynchrony was highly prevalent in patients with aneurysm, irrespective of QRS duration. Aneurvsm olication oroduces a mechanical intrave.ntricular rP.~vnc.hrnniTation.

Assessment of left ventricular systolic synchronicity by real-time three-dimensional echocardiography in patients with dilated cardiomyopathy

Background Recent advances in real-time three-dimensional echocardiography （RT3DE） offer the potential to assess the left ventricular （LV） dyssynchrony simultaneously by analyzing the 17 segments time-volume curves. The purpose of this study was to test the feasibility and accuracy of RT3DE for quantitative evaluation of left ventricular systolic synchronicity. Methods Twenty-four patients with dilated cardiomyopathy （DCM） and twenty-ftve healthy volunteers were enrolled in this study. Full volume RT3DE was performed by using Philips IE33 with X3-1 probe. The global and 17-segmental time-volume curves were obtained by the on-line Qlab software （version 4.2）. The time to minimal systolic volume in each segment （Tmsv） was taken to derive the following indexes of systolic asynchrony： Tmsv 16-SD, Tmsv 16-Dif, Tmsv 12-SD, Tmsv 12-Dif, Tmsv 6-SD and Tmsv 6-Dif, which meant the standard deviation or the maximal difference of Tmsv among the 16, 12 and 6 segments of the left ventricle respectively. The software also provided with each of the above parameters as a percentage of the cardiac cycle. Results Tmsv 16-SD, Tmsv 12-SD and Tmsv 6-SD were all significantly larger in the DCM group than those of the control group [Tmsv 16-SD： （52.9±40.6） ms vs （8.8±6.2） ms; Tmsv 12-SD： （29.5＋30.8） ms vs （6.9±4.0） ms; Tmsv 6-SD： （28.9±34.6） ms vs （7.0±4.7）ms, all P≤0.001]. Tmsv 16-Dif, Tmsv 12-Dif and Tmsv 6-Dif were also significantly larger in the DCM group. There were close negative relations between the LVEF determined by RT3DE and each of the indexes of systolic asynchrony, among which the indexes of Tmsv-16-SD% and Tmsv-16-Dif% correlated most closely （r=-0.703 and r=-0.701, respectively）. The DCM patients had significantly larger EDV and ESV, with significantly reduced LVEF compared with the healthy subjects. Conclusion RT3DE provides a simple, useful and unique approach to assess the systolic synchronicity of all the left ventricular segments simultaneously.

Cardiac conductive system excitation maps using intracardiac tissue Doppler imaging

OBJECTIVE: To precisely visualize cardiac anatomic structures and simultaneously depict electro-mechanical events for the purpose of precise underblood intervention. METHODS: Intracardiac high-resolution tissue Doppler imaging was used to map real time myocardial contractions in response to electrical activation within the anatomic structure of the cardiac conductive system using a canine open-chest model. RESULTS: The detailed inner anatomic structure of the cardiac conductive system at different sites (i.e., sino-atrial, atrial wall, atrial-ventricular node and ventricular wall) with the inside onset and propagation of myocardial velocity and acceleration induced by electrical activation was clearly visualized and quantitatively evaluated. CONCLUSION: The simultaneous single modality visualization of the anatomy, function and electrical events of the cardiac conductive system will foster target pacing and precision ablation.