Biomedical subjects

Xiangsheng Zheng

Publications and source records attributed to Xiangsheng Zheng.

4 recordsLinked to original sources

PubMed2005

Decrease in fluoroscopic cardiac silhouette excursion precedes hemodynamic compromise in intraprocedural tamponade.

BACKGROUND: Acute pericardial tamponade is a life-threatening complication of invasive cardiovascular procedures. Survival depends on early recognition and treatment. A diagnostic test to detect pericardial fluid accumulation before a significant fall in blood pressure and without contamination of the sterile field would be valuable. OBJECTIVE: We tested the hypothesis that fluoroscopic excursion of the cardiac silhouette decreases early in the course of acute pericardial tamponade and precedes hemodynamic compromise. METHODS: The pericardial space of seven pigs was accessed by a sub-xiphoid puncture. Tamponade was produced by intrapericardial saline infusion at 20-25 mL/minute until the pericardial pressure equalized with right ventricular end diastolic pressure or the systolic blood pressure reached 40 mmHg. Supine fluoroscopic images were obtained every 2 minutes in the left anterior oblique view with simultaneous echocardiography. The fluoroscopic heart silhouette was digitized, and the maximum excursion during the cardiac cycle was quantified by custom software. The qualitative excursion of the fluoroscopic heart silhouette on randomly selected video images was also graded by two independent observers who were blinded to the time course of the experiment and the hemodynamics. RESULTS: During progressive pericardial fluid accumulation, the cardiac silhouette excursion quantified by the custom software (p < 0.001) and by video rating (p < 0.0001) was significantly reduced within 2 minutes. A statistically significant fall in blood pressure compared with baseline did not occur until 6 minutes (89 +/- 21 vs. 121 +/- 15 mmHg, p < 0.001). The interobserver agreement was very close, with a kappa statistic of 0.78. The reduction in cardiac silhouette excursion was apparent as soon as the effusion was detected by echocardiography. CONCLUSION: Cardiac silhouette excursion becomes reduced early in the course of acute pericardial fluid accumulation. This fluoroscopic observation can be used to detect impending pericardial tamponade before hemodynamic collapse.

Acute Disease↗

PubMed2005

Evidence that activation following failed defibrillation is not caused by triggered activity.

BACKGROUND: Earliest postshock activation following failed defibrillation shocks slightly lower than the defibrillation threshold (DFT) in large animals appears to arise from a focus. We tested the hypothesis that these foci are caused by early or delayed afterdepolarizations (EADs or DADs) by performing epicardial electrical mapping and giving the EAD inhibitor pinacidil or the DAD inhibitor flunarizine to see if the foci were extinguished or altered in timing or location. METHODS AND RESULTS: A sock containing 504 electrodes was placed over the entire ventricular epicardium of 12 open-chested pigs. After the DFT was determined and additional shocks given, pinacidil was administered to 6 pigs and flunarizine to 6 pigs. Then, the DFT was again determined and additional shocks were given. Pinacidil significantly shortened the effective refractory period (ERP) (162 +/- 16 vs 130 +/- 28 msec) and action potential duration (APD(90)) (179 +/- 6 vs 149 +/- 19 msec) and significantly increased the peak frequency of the power spectrum of a left ventricle (LV) electrode during ventricular fibrillation (VF) (9.3 +/- 0.6 vs 10.5 +/- 1.0 Hz), while flunarizine did not significantly alter the ERP (162 +/- 8 vs 167 +/- 18 msec) or APD(90) (187 +/- 12 vs 191 +/- 20) but significantly reduced the peak frequency (9.2 +/- 0.5 vs 7.5 +/- 1.0 Hz). These findings suggest the drugs had their expected electrophysiological effects. However, the DFT was not significantly changed by either drug. Following the same strength shock 10% below the predrug DFT, earliest postshock activation arose in a focal epicardial pattern from the anterior-apical LV both before and after the drugs. The time from the shock until the appearance of this activation was not significantly different before and after either drug. CONCLUSION: The lack of change in DFT as well as the lack of change in the incidence, location, and timing of the postshock focus with sub-DFT strength shocks before and after pinacidil and flunarizine provide evidence that these foci are not caused by triggered activity.

Analysis of Variance↗

PubMed2004

Activation sequences following failed atrial defibrillation.

OBJECTIVES: The purposes of this study were to examine the first activations following atrial defibrillation shocks to help understand how and where atrial fibrillation (AF) relapsed following failed shocks and to assess the difference in postshock activation between failed and successful shocks. BACKGROUND: While many studies have investigated the mechanism of ventricular defibrillation, much less is known about the mechanisms of AF. METHODS: Sustained AF was induced electrically after pericardial infusion of methylcholine in 10 sheep. Biphasic subthreshold shocks were delivered to three configurations: right atrium to distal coronary sinus (RA-CS), sequential shocks with RA-CS as the first pathway followed by proximal CS to superior vena cava as the second pathway (Sequential), and right ventricle to superior vena cava plus can (V-triad). In eight sheep, global atrial mapping was performed with 504 electrodes spaced 3 to 4 mm apart. RESULTS: Earliest postshock activations mostly arose from the left atrium for V-triad but arose from either atrium for RA-CS and Sequential. Preshock AF cycle lengths were significantly shorter at the earliest activation sites than at seven of eight other sites globally distributed over both atria. In all type B successful episodes in which one or more rapid activations occurred after the shock and in 50 of the 72 failed episodes analyzed, activation fronts spread away from the earliest site in a focal pattern, and discrete nonfragmented activation complexes were present in the first derivatives of the electrograms. In the other 22 failed episodes, earliest activation fronts spread in a nonfocal pattern, and earliest postshock electrogram derivatives were fractionated. To better interpret the activation pattern in the fragmented regions, a 504 electrode plaque with 1.5-mm electrode spacing was placed on the right atrial appendage in two additional sheep. In 11 of 108 failed episodes, earliest postshock activation appeared inside the plaque and spread in a focal pattern with nonfragmented electrogram derivatives in 10 episodes and in a reentrant pattern with fragmented electrogram derivatives in the other. CONCLUSIONS: (1) The electrode configuration influenced the location of earliest postshock activation. (2) Earliest postshock activation occurred where the preshock AF cycle length was short. (3) Earliest activations following all type B successful and most failed episodes were not fragmented and spread in a focal pattern. (4) The region of earliest postshock activation in the failed episodes without a focal postshock activation pattern exhibited regions of fragmented electrogram derivatives that may represent conduction block and possibly reentry.

Animals↗

PubMed2002

Reduction of the internal atrial defibrillation threshold with balanced orthogonal sequential shocks.

INTRODUCTION: The aim of this study was to determine the atrial defibrillation threshold (ADFT) of a first shock across the standard right atrium (RA) to distal coronary sinus (dCS) configuration followed by a second shock along the atrial septum with a standard sequential waveform (the second shock leading edge equaled the first shock trailing edge) and a balanced sequential waveform (the leading edges of both shocks were equal). METHODS AND RESULTS: In nine sheep atrial fibrillation was induced with acetyl-beta-methylcholine and burst pacing. A catheter was placed with electrodes in the dCS, proximal coronary sinus (pCS), and RA. A J-shaped catheter was positioned with an electrode at Bachmann's bundle (BB) while another catheter was positioned with an electrode in the superior vena cava (SVC). The ADFTs of six single- and dual-pathway configurations were determined with single, standard sequential, or balanced sequential shocks. The ADFT of the RA-->dCS configuration (0.86 +/- 0.27 J, 159 +/- 29 V, 2.42 +/- 0.36 A) was significantly reduced when followed by an SVC-->pCS (0.58 +/- 0.17 J, 112 +/- 20 V, 1.64 +/- 0.39 A) or a BB-->pCS shock (0.64 +/- 0.16 J, 119 +/- 18 V, 1.81 +/- 0.38 A) with standard sequential shocks. With balanced sequential shocks, the peak voltage and current ADFTs were further significantly reduced (85 +/- 11 V and 1.24 +/- 0.21 A for second shock SVC-->pCS, and 93 +/- 13 V and 1.38 +/- 0.27 A for second shock BB-->pCS). CONCLUSION: The ADFT of the standard RA-->dCS shock is significantly reduced when followed by a second shock along the atrial septum delivered between electrodes in the pCS and either SVC or BB and ADFT is further reduced with balanced sequential shocks.

Animals↗