Self-organization and the dynamical nature of ventricular fibrillation.

This article reviews recent data supporting the conjecture that, in the structurally and electrophysiologically normal heart, cardiac fibrillation is not a totally random phenomenon. Experimental and numerical studies based on the theory of excitable media suggest that fibrillation in the mammalian ventricles is the result of self-organized three-dimensional (3-D) electrical rotors giving rise to scroll waves that move continuously (i.e., drift) throughout the heart at varying speeds. A brief review of studies on the dynamics of rotors in two-dimensional (2-D) and 3-D excitable media is presented with emphasis on the experimental demonstration of such dynamics in cardiac muscle of various species. The discussion is centered on rotor dynamics in the presence and the absence of structural heterogeneities, and in the phenomena of drifting and anchoring, which in the electrocardiogram (ECG) may manifest as life-threatening cardiac rhythm disturbances. For instance, in the rabbit heart, a single electrical rotor that drifts rapidly throughout the ventricles gives rise to complex patterns of excitation. In the ECG such patterns are indistinguishable from ventricular fibrillation. On the other hand, a rotor that anchors to a discontinuity or defect in the muscle (e.g., a scar, a large artery or a bundle of connective tissue) may result in stationary rotating activity, which in the ECG is manifested as a form of so-called "monomorphic" ventricular tachycardia. More recent data show that ventricular fibrillation occurs in mammals irrespective of size or species. While in small hearts, such as those of mice and rabbits, a single drifting or meandering rotor can result in fibrillation, in larger hearts, such as the sheep and possibly the human, fibrillation occurs in the form of a relatively small number of coexisting but short-lived rotors. Overall, the work discussed here has paved the way for a better understanding of the mechanisms of fibrillation in the normal, as well as diseased human heart. (c) 1998 American Institute of Physics.

Electrical turbulence as a result of the critical curvature for propagation in cardiac tissue.

In cardiac tissue, the propagation of electrical excitation waves is dependent on the active properties of the cell membrane (ionic channels) and the passive electrical properties of cardiac tissue (passive membrane properties, distribution of gap junctions, and cell shapes). Initiation of cardiac arrhythmias is usually associated with heterogeneities in the active and/or passive properties of cardiac tissue. However, as a result of the effect of wave front geometry (curvature) on propagation of cardiac waves, inexcitable anatomical obstacles, like veins and arteries, may cause the formation of self-sustained vortices and uncontrolled high-frequency excitation in normal homogeneous myocardium. (c) 1998 American Institute of Physics.

Microvolt T-wave alternans and the risk of death or sustained ventricular arrhythmias in patients with left ventricular dysfunction.

OBJECTIVES: This study hypothesized that microvolt T-wave alternans (MTWA) improves selection of patients for implantable cardioverter-defibrillator (ICD) prophylaxis, especially by identifying patients who are not likely to benefit. BACKGROUND: Many patients with left ventricular dysfunction are now eligible for prophylactic ICDs, but most eligible patients do not benefit; MTWA testing has been proposed to improve patient selection. METHODS: Our study was conducted at 11 clinical centers in the U.S. Patients were eligible if they had a left ventricular ejection fraction (LVEF) < or =0.40 and lacked a history of sustained ventricular arrhythmias; patients were excluded for atrial fibrillation, unstable coronary artery disease, or New York Heart Association functional class IV heart failure. Participants underwent an MTWA test and then were followed for about two years. The primary outcome was all-cause mortality or non-fatal sustained ventricular arrhythmias. RESULTS: Ischemic heart disease was present in 49%, mean LVEF was 0.25, and 66% had an abnormal MTWA test. During 20 +/- 6 months of follow-up, 51 end points (40 deaths and 11 non-fatal sustained ventricular arrhythmias) occurred. Comparing patients with normal and abnormal MTWA tests, the hazard ratio for the primary end point was 6.5 at two years (95% confidence interval 2.4 to 18.1, p < 0.001). Survival of patients with normal MTWA tests was 97.5% at two years. The strong association between MTWA and the primary end point was similar in all subgroups tested. CONCLUSIONS: Among patients with heart disease and LVEF < or =0.40, MTWA can identify not only a high-risk group, but also a low-risk group unlikely to benefit from ICD prophylaxis.