Hemodynamic Benefits of Atrio-Biventricular Pacing in Open Chest Dogs

BACKGROUND AND OBJECTIVES: The ventricular pacing electrodes are customarily placed into the right ventricular muscle because there is easily accessible. However detailed physiologic studies have shown that the single stimulation of right ventricular sites causes dysynchronous ventricular contraction due to early depolarization of the right ventricle and delayed depolarization of the left ventricle. In contrast, normal human ventricular activation, which is conducted by the Purkinje system, spreads transmurally from the endocardium to multiple paraseptal epicardial regions and results in more synchronous contraction of the ventricle. Therefore, the hypothesis that producing biventricular activation by simultaneously pacing ventricles across the septum might confer hemodynamic benefits over those of conventional right ventricular pacing. The purpose of this study was to evaluate the acute hemodynamic changes of different pacing modes (right ventricular : RV, biventricular : BV, atrio-right ventricular : A-RV, and atrio-biventricular : A-BV pacing). MATERIALS AND METHOD: In 9 open chest dogs anesthetized with alpha-chloralose, sinus node crushing was done, and then hemodynamic data (QRS width, femoral arterial pressure : FAP, pulmonary arterial pressure : PAP, and Cardiac output : CO) were acquired after 5 minutes of pacing at a fixed rate during each pacing mode. RESULTS: Results were as follow : 1. BV pacing significantly increased cardiac output compared with RV pacing (P<0.01). BV pacing significantly shortened QRS width compared with RV pacing (P<0.01). 2. A-BV pacing significantly increased cardiac output compared with A-RV pacing (P<0.01). A-BV pacing significantly shortened QRS width compared with A-RV pacing (P<0.01). 3. A-RV pacing significantly increased systolic pulmonary arterial pressure and cardiac output compared with BV pacing (P<0.01). CONCULSION: These results support the use of atrio-biventricular pacing to improve acute hemodynamic performance.

The Inhibition of Neointimal Hyperplasia by Combination of External Radiation and Paclitaxel in A Rat Carotid Injury Model

BACKGROUND AND OBJECTIVES: Radiation therapy is one of the promising new treatment for restenosis, which is a major problem for the long-term success after angioplasty. We compared radiation therapy only and combined therapy of paclitaxel and radiation on neointimal hyperplasia after injury of rat carotid artery to see whether we can reduce the effective dosage of radiation and thus diminish untoward consequence of radiation if paclitaxel could function as a cell-cycle selective radiosensitizer. MATERIAL AND METHODS: A standardized carotid balloon catheter arterial injury was produced in 65 rats. First group was composed of a single dose of paclitaxel 1 mg/kg body weight, 2 mg/kg or 4 mg/kg, which was administrated intraperitoneally at 2 hours after injury. Second group received external radiation at doses of 2.5 or 5 Gy at 24 hours after injury. Third group was treated with combined paclitaxel-radiation: paclitaxel was injected at 2 hours after injury and then external radiation was delivered 24 hours later. At 21 days after injury, the cross-sectional area of neointima and the ratio of intima/medial area were determined from axial sections using image analysis. RESULTS: Single dose of paclitaxel had no effect in reducing smooth muscle cell proliferation. Minimum effective single dose to inhibit neointimal hyperplasia was 5 Gy. Combined paclitaxel-radiation group except subgroup with paclitaxel 1 mg/kg and 2.5 Gy radiation showed significant reduction of neointimal area compared to group with 2.5 Gy radiation. CONCLUSION: Low-dose external radiation combined with paclitaxel can more effectively inhibit smooth muscle cell pro-liferation and neointimal hyperplasia than radiation only in the rat carotid injury model.

Inhibition of Neointimal Hyperplasia by External Radiation in Rat Carotid Injury Model-The Possible Role of Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1-

BACKGROUND AND OBJECTIVES: Despite significant improvement in the field of angioplasty, restenosis remains a major obstacle to the long-term success of the procedure. Radiation can effectively inhibit neointimal hyperplasia by causing the arrest of mitosis during cell division and limiting proliferation by reducing the number of regenerating clonal progenitors. Balloon injury could induce the cell adhesion molecule, ICAM-1 and VCAM-1, on SMCs and regenerating endothelial cells (ECs). ICAM-1 and/or VCAM-1 may play a role in the progression of neointimal hyperplasia induced by balloon injury and external radiation may effectively inhibit neointimal hyperplasia by attenuating their expression. The purpose of this study was to examine the effect of external radiation against ICAM-1 and VCAM-1 on neointimal hyperplasia after balloon injury in rat carotid arteries. MATERIAL AND METHODS: A standardized carotid balloon catheter arterial injury was produced in 51 rats and external beam radiation with doses from 5-20 Gy were delivered in 28 rats (radiation treated group) at 24 hours after injury. To investigate the effect of the external radiation on neointimal hyperplasia, the intima area and the intima/medial area of arteries were measured at day 14 after injury. The expressions of ICAM-1 and VCAM-1 at day 2, day 7, and day 10 after injury were studied in control group and radiation treated group by immunohistochemistry. RESULTS: Means of intimal area and intima/medial ratio in radiation treated group were significantly lower than those in control group and significantly reduced with increasing radiation dosage. At day 2 after injury, medial SMCs of injury group extensively expressed ICAM-1, while it was focally expressed with 10 Gy radiation treated group. At day 7 and day 10 after injury, ICAM-1 expression on medial SMCs was attenuated and neointimal ICAM-1 expression was increased. As compared with control group, ICAM-1 expression after radiation was weak and focal just around the internal elastic lamina. At 2 days after injury, medial SMCs moderately expressed VCAM-1, which was weakly and focally expressed with 10 Gy radiation treated group. At day 7 and day 10 after injury, focal expression of VCAM-1 was noted around the internal elastic lamina, but there was no VCAM-1 expression on neointima with radiation. CONCLUSION: External radiation after carotid arterial injury may potentially inhibit SMC proliferation and neointimal hyperplasia, and balloon injury-induced or upregulated expressions of ICAM-1 and VCAM-1 may be attenuated with external radiation.

Echocardiographic Measurement of Systolic Time Intervals in Normal Adults and the Patients with Dilated Cardiomyopathy

The systolic time intervals were measured in 25 normal controls and 23 patients with dilated cardiomyopathy by simultaneous recording of the aortic valve echocardiogram and ECG. These values were compared to corresponding ones obtained from the method using simultaneously recorded phonocardiogram, ECG, and indirect carotid pulse tracings. And we assessed left ventricular function by systolic time intervals in dilated cardiomyopathy. The results were as followings. 1) High degree of correlation(r> or =0.94) was found between the two methods for each intervals, EMS, LVET, PEP, PEP/LVET. 2) In normal controls, PEP/LVET obtained from echocardiographic measurement was 0.31+/-0.02. 3) In the patients with dilated cardiomyopathy, PEP/LVET(0.59+/-0.13) was significantly higher(p<0.001), PEP index was longer(p<0.05), LVET index was shorter(p<0.05) than in normal controls.