PubMed Health⌕ Search

Biomedical subjects

O Nwasokwa

Publications and source records attributed to O Nwasokwa.

6 recordsLinked to original sources
PubMed1998

Ventricular fibrillation: one spiral or many?

Ventricular fibrillation is the major cause of sudden cardiac death, the leading cause of death in the industrialized world; however, the mechanisms for its onset are not well understood. To further understand the dynamics of fibrillation at and near its onset, we compared spatial and temporal variability of mean interactivation intervals in a stable canine model for ventricular fibrillation. Temporal variability was very small, suggesting that the relevant physiological parameters remained constant during our experiments. Spatial variability was usually significantly larger and appeared incompatible with the dynamics of a single, meandering spiral wave. This confirmed recent results that a single spiral wave cannot generate ventricular fibrillation. Thus the onset of fibrillation is a multistage process, with spiral-wave breakdown providing a crucial step in the quasi-periodic route to fibrillation.

Analysis of Variance↗
PubMed1997

Quasiperiodicity and chaos in cardiac fibrillation.

In cardiac fibrillation, disorganized waves of electrical activity meander through the heart, and coherent contractile function is lost. We studied fibrillation in three stationary forms: in human chronic atrial fibrillation, in a stabilized form of canine ventricular fibrillation, and in fibrillation-like activity in thin sheets of canine and human ventricular tissue in vitro. We also created a computer model of fibrillation. In all four studies, evidence indicated that fibrillation arose through a quasiperiodic stage of period and amplitude modulation, thus exemplifying the "quasiperiodic transition to chaos" first suggested by Ruelle and Takens. This suggests that fibrillation is a form of spatio-temporal chaos, a finding that implies new therapeutic approaches.

Action Potentials↗
PubMed1996

Nonlinear dynamics in ventricular fibrillation.

Electrogram recordings of ventricular fibrillation appear complex and possibly chaotic. However, sequences of beat-to-beat intervals obtained from these recordings are generally short, making it difficult to explicitly demonstrate nonlinear dynamics. Motivated by the work of Sugihara on atmospheric dynamics and the Durbin-Watson test for nonlinearity, we introduce a new statistical test that recovers significant dynamical patterns from smoothed lag plots. This test is used to show highly significant nonlinear dynamics in a stable canine model of ventricular fibrillation.

Algorithms↗
PubMed1989

Differences in left ventricular adaptation to chronic mitral and aortic regurgitation.

For comparable volume load, impedance to ejection of the regurgitant volume in AR exceeds that in MR. To determine whether this load difference results in differences in PLVH and ejection performance, we studied consecutive, untreated, asymptomatic patients (11 in each group) by echocardiography and Doppler. Mean LVID, SBP, h, and FS were, respectively, in AR vs MR: 60.3 +/- 3.1 mm vs 62.0 +/- 2.3 mm (p = NS), 152 +/- 7.1 mm Hg vs 125 +/- 6.4 mm Hg (p less than 0.005), 12.1 +/- 0.4 mm vs 10.5 +/- 0.6 mm (p less than 0.04), and 0.38 +/- 0.02 vs 0.43 +/- 0.02 (p = NS). The h/R ratio reflects the PLVH-0.41 +/- 0.02 in AR and 0.34 +/- 0.02 in MR (p less than 0.02). The FS correlates positively with h/R in either lesion, but was higher in MR for any given h/R. The difference in loading conditions imposed by both lesions is associated with a difference in the PLVH as well as in ejection performance.

Adaptation, Physiological↗
PubMed1984

Short-term memory in the in situ canine myocardium.

We studied the effect of intracycle (short-term) mechanical history on canine myocardial performance. Intracycle muscle force and/or length history was varied, and the resultant changes in end-systolic force-length relationship were analyzed. Antecedent isotonic shortening impaired, whereas isometric force development enhanced end-systolic myocardial performance. A history of shortening concurrent with force development produced an intermediate effect. We conclude that decreasing force or length impairs whereas increasing length or force enhances performance in the same cycle. Different combinations of antecedent force and length changes affect end-systolic performance by algebraic summation (superposition) of their disparate effects. Time measurements established that 1) total systolic time varied little with altered history, 2) isotonic shortening took longer than isometric contraction in reaching a point P in the force-length plane, and 3) less time was therefore available for contraction after P with antecedent isotonic shortening than with antecedent isometric force development. This history-dependent time differential accounts for the corresponding differential in performance.

Animals↗