This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Valderrábano, M. Articles by Chen, P.-S. Search for Related Content PubMed PubMed Citation Articles by Valderrábano, M. Articles by Chen, P.-S.

EXPERIMENTAL STUDY

Obstacle-induced transition from ventricular fibrillation to tachycardia in isolated swine right ventricles

Insights into the transition dynamics and implications for the critical mass

^a Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, and UCLA School of Medicine, Los Angeles, California, USA

Manuscript received September 16, 1999; revised manuscript received May 12, 2000, accepted July 12, 2000.

Reprint requests and correspondence: Dr. Peng-Sheng Chen, Room 5342, CSMC, 8700 Beverly Blvd., Los Angeles, California 90048-1865
chenp{at}csmc.edu

OBJECTIVES

The study was done to test the hypothesis that an artificial anatomical obstacle prevents the maintenance of ventricular fibrillation (VF) by stabilizing reentrant wavefronts (RWF) and increases the critical mass (CM) of myocardium required to sustain VF.

BACKGROUND

Artificial obstacles can anchor RWF in simulated models of VF. Whether an artificial obstacle affects multiple-wavelet VF in real tissue is unclear.

METHODS

The endocardial surfaces of seven isolated, perfused swine right ventricles were mapped using a plaque of 477 bipolar electrodes with 1.6-mm resolution. An 8-mm hole was punched in the tissue. The CM was reached by tissue mass reductions, at which VF converted to periodic activity (ventricular tachycardia, VT).

RESULTS

After the creation of the obstacle, the VF cycle length increased from 71.6 ± 18.4 ms to 87.5 ± 13.0 ms (p < 0.05). The obstacle, together with the papillary muscle, facilitated the transition from VF to VT by serving as attachment sites for the RWF. When one RWF attaches to the obstacle and another attaches to the papillary muscle, it may result in stable VT with figure-eight patterns. The CM for VF in the presence of an 8-mm hole (28.7 ± 3.8 g) was higher than in the control group (swine right ventricles without holes, 24.0 ± 3.4 g, p < 0.05).

CONCLUSIONS

An artificial anatomical obstacle induces slowing and regularization of VF, impairs the persistence of VF as judged by an increase of the CM, and can convert VF to VT by serving as an attachment site to reentrant excitation.

Abbreviations and Acronyms   CL = cycle length   CM = critical mass   pECG = pseudoelectrocardiogram   PM = papillary muscle   RWF = reentrant wavefront   SD = standard deviation   2D = two-dimensional   VF = ventricular fibrillation   VT = ventricular tachycardia

This article has been cited by other articles:

				L. Tang, G.-S. Hwang, H. Hayashi, J. Song, M. Ogawa, K. Kobayashi, B. Joung, H. S. Karagueuzian, P.-S. Chen, and S.-F. Lin Intracellular calcium dynamics at the core of endocardial stationary spiral waves in Langendorff-perfused rabbit hearts Am J Physiol Heart Circ Physiol, July 1, 2008; 295(1): H297 - H304. [Abstract] [Full Text] [PDF]

				T. Ohara, Z. Qu, M.-H. Lee, K. Ohara, C. Omichi, W. J. Mandel, P.-S. Chen, and H. S. Karagueuzian Increased vulnerability to inducible atrial fibrillation caused by partial cellular uncoupling with heptanol Am J Physiol Heart Circ Physiol, September 1, 2002; 283(3): H1116 - H1122. [Abstract] [Full Text] [PDF]

				M. Valderrabano, M.-H. Lee, T. Ohara, A. C. Lai, M. C. Fishbein, S.-F. Lin, H. S. Karagueuzian, and P.-S. Chen Dynamics of Intramural and Transmural Reentry During Ventricular Fibrillation in Isolated Swine Ventricles Circ. Res., April 27, 2001; 88(8): 839 - 848. [Abstract] [Full Text] [PDF]