03049nas a2200361 4500008004100000022001400041245008000055210006900135260001200204300001100216490000700227520206900234653001202303653002602315653001502341653002202356653001602378653002102394653001002415653002702425653001502452653002502467653001402492653001602506653002502522653001002547100001702557700001702574700001702591700001402608700001702622856004802639 2001 eng d a0006-349500aVisualizing excitation waves inside cardiac muscle using transillumination.0 aVisualizing excitation waves inside cardiac muscle using transil c01/2001 a516-300 v803 a

Voltage-sensitive fluorescent dyes have become powerful tools for the visualization of excitation propagation in the heart. However, until recently they were used exclusively for surface recordings. Here we demonstrate the possibility of visualizing the electrical activity from inside cardiac muscle via fluorescence measurements in the transillumination mode (in which the light source and photodetector are on opposite sides of the preparation). This mode enables the detection of light escaping from layers deep within the tissue. Experiments were conducted in perfused (8 mm thick) slabs of sheep right ventricular wall stained with the voltage-sensitive dye di-4-ANEPPS. Although the amplitude and signal-to-noise ratio recorded in the transillumination mode were significantly smaller than those recorded in the epi-illumination mode, they were sufficient to reliably determine the activation sequence. Penetration depths (spatial decay constants) derived from measurements of light attenuation in cardiac muscle were 0.8 mm for excitation (520 +/- 30 nm) and 1.3 mm for emission wavelengths (640 +/- 50 nm). Estimates of emitted fluorescence based on these attenuation values in 8-mm-thick tissue suggest that 90% of the transillumination signal originates from a 4-mm-thick layer near the illuminated surface. A 69% fraction of the recorded signal originates from > or =1 mm below the surface. Transillumination recordings may be combined with endocardial and epicardial surface recordings to obtain information about three-dimensional propagation in the thickness of the myocardial wall. We show an example in which transillumination reveals an intramural reentry, undetectable in surface recordings.

10aAnimals10aBiophysical Phenomena10aBiophysics10aElectrophysiology10aEndocardium10aFluorescent Dyes10aHeart10aModels, Cardiovascular10aMyocardium10aOptics and Photonics10aPerfusion10aPericardium10aPyridinium Compounds10aSheep1 aBaxter, Bill1 aMironov, S F1 aZaitsev, A V1 aJalife, J1 aPertsov, A V uhttp://www.ncbi.nlm.nih.gov/pubmed/1115942201811nas a2200373 4500008004100000022001400041245008700055210006900142260001200211300001200223490000700235520078300242653001201025653002601037653001501063653001801078653002401096653002501120653002101145653002201166653001001188653002701198653002701225653001501252653001001267653002001277100001201297700001701309700001901326700001701345700001401362700001401376856004701390 1996 eng d a0006-349500aVortex shedding as a precursor of turbulent electrical activity in cardiac muscle.0 aVortex shedding as a precursor of turbulent electrical activity  c03/1996 a1105-110 v703 a

In cardiac tissue, during partial blockade of the membrane sodium channels, or at high frequencies of excitation, inexcitable obstacles with sharp edges may destabilize the propagation of electrical excitation waves, causing the formation of self-sustained vortices and turbulent cardiac electrical activity. The formation of such vortices, which visually resembles vortex shedding in hydrodynamic turbulent flows, was observed in sheep epicardial tissue using voltage-sensitive dyes in combination with video-imaging techniques. Vortex shedding is a potential mechanism leading to the spontaneous initiation of uncontrolled high-frequency excitation of the heart.

10aAnimals10aBiophysical Phenomena10aBiophysics10aCell Membrane10aComputer Simulation10aElectric Stimulation10aElectrochemistry10aElectrophysiology10aHeart10aModels, Cardiovascular10aMyocardial Contraction10aMyocardium10aSheep10aSodium Channels1 aCabo, C1 aPertsov, A V1 aDavidenko, J M1 aBaxter, Bill1 aGray, R A1 aJalife, J uhttp://www.ncbi.nlm.nih.gov/pubmed/878527003364nas a2200289 4500008004100000022001400041245008700055210006900142260001300211300001100224490000700235520252500242653001202767653002402779653002702803653000902830653002202839653001002861653004802871653002402919100001702943700001902960700001702979700001702996700001403013856004703027 1993 eng d a0009-733000aSpiral waves of excitation underlie reentrant activity in isolated cardiac muscle.0 aSpiral waves of excitation underlie reentrant activity in isolat c03/1993  a631-500 v723 a

The mechanism of reentrant ventricular tachycardia was studied in computer simulations and in thin (approximately 20 x 20 x 0.5-mm) slices of dog and sheep ventricular epicardial muscle. A two-dimensional matrix consisting of 96 x 96 electrically coupled cells modeled by the FitzHugh-Nagumo equations was used to analyze the dynamics of self-sustaining reentrant activity in the form of elliptical spiral waves induced by premature stimulation. In homogeneous anisotropic media, spirals are stationary and may last indefinitely. However, the presence of small parameter gradients may lead to drifting and eventual termination of the spiral at the boundary of the medium. On the other hand, spirals may anchor and rotate around small discontinuities within the matrix. Similar results were obtained experimentally in 10 preparations whose electrical activity was monitored by means of a potentiometric dye and high-resolution optical mapping techniques; premature stimulation triggered reproducible episodes of sustained or nonsustained reentrant tachycardia in the form of spiral waves. As a rule, the spirals were elongated, with the major hemiaxis parallel to the longitudinal axis of the cells. The period of rotation (183 +/- 68 msec [mean +/- SD]) was longer than the refractory period (131 +/- 38 msec) and appeared to be determined by the size of the spiral's core, which was measured using a newly devised "frame-stack" plot. Drifting of spiral waves was also observed experimentally. Drift velocity was 9.8% of the velocity of wave propagation. In some cases, the core became stationary by anchoring to small arteries or other heterogeneities, and the spiral rotated rhythmically for prolonged periods of time. Yet, when drift occurred, spatiotemporal variations in the excitation period were manifested as a result of a Doppler effect, with the excitation period ahead of the core being 20 +/- 6% shorter than the excitation period behind the core. As a result of these coexisting frequencies, a pseudoelectrocardiogram of the activity in the presence of a drifting spiral wave exhibited "QRS complexes" with an undulating axis, which resembled those observed in patients with torsade de pointes. The overall results show that spiral wave activity is a property of cardiac muscle and suggest that such activity may be the common mechanism of a number of monomorphic and polymorphic tachycardias.

10aAnimals10aComputer Simulation10aDisease Models, Animal10aDogs10aElectrophysiology10aSheep10aTachycardia, Atrioventricular Nodal Reentry10aTorsades de Pointes1 aPertsov, A V1 aDavidenko, J M1 aSalomonsz, R1 aBaxter, Bill1 aJalife, J uhttp://www.ncbi.nlm.nih.gov/pubmed/8431989