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At least 1,063 records · Page 59Linked to original sources
PubMed1993

Experimental basis of determining maximum coronary, myocardial, and collateral blood flow by pressure measurements for assessing functional stenosis severity before and after percutaneous transluminal coronary angioplasty.

BACKGROUND: Severity of coronary artery stenosis has been defined in terms of geometric dimensions, pressure gradient-flow relations, resistance to flow and coronary flow reserve, or maximum flow capacity after maximum arteriolar vasodilation. A direct relation between coronary pressure and flow, however, may only be presumed if the resistances in the coronary circulation are constant (and minimal) as theoretically is the case during maximum arteriolar vasodilation. In that case, pressure measurements theoretically can be used to predict maximum flow and assess functional stenosis severity. METHODS AND RESULTS: A theoretical model was developed for the different components of the coronary circulation, and a set of equations was derived by which the relative maximum flow or fractional flow reserve in both the stenotic epicardial artery and the myocardial vascular bed and the proportional contribution of coronary arterial and collateral flow to myocardial blood flow are calculated from measurements of arterial, distal coronary, and central venous pressures during maximum arteriolar vasodilation. To test this model, five dogs were acutely instrumented with an epicardial, coronary Doppler flow velocity transducer. Distal coronary pressures were measured by an ultrathin pressure-monitoring guide wire (0.015 in.) with minimal influence on transstenotic pressure gradient. Fractional flow reserve was calculated from the pressure measurements and compared with relative maximum coronary artery flow measured directly by the Doppler flowmeter at three different levels of arterial pressure for each of 12 different severities of stenosis at each pressure level. Relative maximum blood flow through the stenotic artery (Qs) measured directly by the Doppler flowmeter showed an excellent correlation with the pressure-derived values of Qs (r = 0.98 +/- 0.01, intercept = 0.02 +/- 0.03, slope = 0.98 +/- 0.04), of the relative maximum myocardial flow (r = 0.98 +/- 0.02, intercept = 0.26 +/- 0.07, slope = 0.73 +/- 0.08), and of the collateral blood flow (r = 0.96 +/- 0.04, intercept = 0.24 +/- 0.07, slope = -0.24 +/- 0.06). Moreover, the theoretically predicted constant relation between mean arterial pressure and coronary wedge pressure, both corrected for venous pressure, was confirmed experimentally (r = 0.97 +/- 0.03, intercept = 9.5 +/- 13.3, slope = 4.4 +/- 1.2). CONCLUSIONS: These results provide the experimental basis for determining relative maximum flow or fractional flow reserve of both the epicardial coronary artery and the myocardium, including collateral flow, from pressure measurements during maximum arteriolar vasodilation. With a suitable guide wire for reliably measuring distal coronary pressure clinically, this method may have potential applications during percutaneous transluminal coronary angioplasty for assessing changes in the functional severity of coronary artery stenoses and for estimating collateral flow achievable during occlusion of the coronary artery.

Angioplasty, Balloon, Coronary↗
PubMed1993

Application of color Doppler flow mapping to calculate effective regurgitant orifice area. An in vitro study and initial clinical observations.

BACKGROUND: Analogous to stenotic valve area in the assessment of valvular stenosis, regurgitant orifice area (ROA) represents a fundamental parameter to assess valvular insufficiency. However, this parameter has not been routinely available up to now. In this study, we introduce the concept and provide the methodology to calculate regurgitant orifice area noninvasively, based on the analysis of the proximal flow convergence zone. METHODS AND RESULTS: In an in vitro study, we showed the feasibility and the accuracy of calculating effective ROA by the proximal flow convergence method throughout a range of driving pressures. The calculated and true ROA showed an excellent correlation with r = .992, delta ROA = -1.4 +/- 2.9 mm2. We then applied this concept clinically in 77 patients with mitral regurgitation and showed a very good correlation between effective ROA calculated by the proximal flow convergence method and calculated by the Doppler echocardiographic method: r = .95, delta ROA = -0.2 +/- 3.9 mm2. The ROA also correlated very well with Doppler echocardiographic-derived regurgitant stroke volume (r = .93) and regurgitant fraction (r = .82). In a subgroup of 20 patients who underwent invasive evaluation, the calculated effective ROA also correlated well with the angiographic grade of mitral regurgitation (rho = .81). CONCLUSIONS: We conclude that effective ROA represents unique information on the severity of a regurgitant lesion and can easily be calculated by the proximal flow convergence method. This new parameter should enhance our understanding and improve the serial assessment of valvular regurgitation.

Blood Flow Velocity↗
PubMed1993

Ionic mechanisms of electronic inhibition and concealed conduction in rabbit atrioventricular nodal myocytes.

BACKGROUND: The term "concealed conduction" is used in electrocardiography when a proximal (atrial or ventricular) impulse penetrates the atrioventricular (AV) node but fails to traverse it completely. Its penetration into the node is inferred by its after effects on the propagation of succeeding impulses. Concealed AV nodal conduction is a well-established phenomenon, but its precise cellular and subcellular mechanisms are unknown. It has been suggested that concealed conduction results from a transient impairment of excitability caused by the subthreshold depolarization (ie, electrotonic inhibition) that is elicited downstream of the site of block. METHODS AND RESULTS: We studied the ionic mechanism of electrotonic inhibition and concealed conduction in single myocytes isolated from the rabbit AV node. Cells were paced using just-threshold current pulses delivered at a constant (basic) cycle length of 1 second. Appropriately timed interpolation of a conditioning pulse of depolarizing but subthreshold current led to failure of the subsequent, previously successful activation. The ability of the subthreshold response to inhibit subsequent excitation was increased when the interval between the conditioning and succeeding pulses was shortened, when the amplitude of the conditioning pulse was increased, or when the inward sodium current was blocked by superfusion with tetrodotoxin (30 microM). Voltage clamp analysis demonstrated that electrotonic inhibition results from partial inactivation of the transient calcium current (ICa.T). Similar results were obtained using a mathematical model (Hodgkin-Huxley type) of the AV nodal myocyte. Additional simulations in a linear array of AV nodal cells showed that when a premature impulse fails to traverse the AV node, the subthreshold depolarization elicited downstream of the site of block may lead to a transient reduction of excitability with consequent delay or block of the succeeding impulse. CONCLUSIONS: The overall data strongly suggest that some of the electrocardiographic manifestations of concealed AV conduction are the result of electrotonic inhibition of excitability secondary to a transient decrease in ICa.T.

Animals↗
PubMed1993

Determination of the most appropriate velocity threshold for applying hemispheric flow convergence equations to calculate flow rate: selected according to the transorifice pressure gradient. Digital computer analysis of the Doppler color flow convergence region.

BACKGROUND: While flow convergence methods have been promising for calculating volume flows from color Doppler images, it appears that the velocity threshold used and the transorifice pressure gradient dramatically influence the accuracy of application of the simple hemispheric flow convergence equation for calculation of flow rate. The present in vitro study was performed to determine whether the value of velocity threshold at which the shape of proximal isovelocity surface best fits given shape assumptions with different orifice sizes and flow rates is predictable as a function independent of orifice size from clinically measurable peak velocity or transorifice pressure gradient information. METHODS AND RESULTS: In an in vitro model built to facilitate ultrasound imaging, steady flow was driven through circular discrete orifices with diameters of 3.8, 5.5, and 10 mm. Flow rates ranged from 2.88 to 8.28 L/min with corresponding driving pressure gradients from 14 to 263 mm Hg. At each flow rate, Doppler color-encoded M-mode images through the center of the flow convergence region were obtained and transferred into the microcomputer (Macintosh IIci) in their original digital format. Then, the continuous wave Doppler traces of maximal velocity through the orifice were derived for the calculation of driving pressure gradient. Direct numerical spatial velocity measurements were obtained from the digital color encoded M-mode velocities with computer software. For each flow rate, we could calculate flow volume from any number of velocity distance combinations with a number of assumptions and use the results to assess expected flow convergence shape based on a priori knowledge of the progression from oblate hemispheroid to hemisphere to prolate hemispheroid changes observed previously. Our results showed that for a given ratio of calculated flow rate to actual flow rate (0.7 and 1), the velocity threshold that could be used for the calculation of flow rate with a hemispheric flow convergence equation correlated well with the pressure gradient for a given orifice size, and the differences in velocity threshold that could be used this way among different orifice sizes once they were adjusted for the covariate pressure gradients were not statistically significant (P = .79 for ratio = 0.7, and P = .81 for ratio = 1). CONCLUSIONS: Our present study provides an orifice size-independent quantitative method that can be used to select the most suitable velocity threshold for applying a simple hemispheric flow convergence equation based on clinically predictable pressure gradients ranging from 40 to 200 mm Hg, and it offers a correction factor that can be applied to the hemispheric flow convergence equation when the pressure gradient is less than 40 mm Hg.

Blood Flow Velocity↗
PubMed1993

Accuracy of electronic digital calipers compared with quantitative angiography in measuring coronary arterial diameter.

BACKGROUND: Quantitative angiography is the accepted method for measuring coronary luminal diameter. Electronic digital calipers have been used to assess arterial diameters in vasomotor function studies and after interventional procedures. However, careful validation of calipers against quantitative angiography has not been described. METHODS AND RESULTS: We used digital calipers and quantitative angiography to measure 517 arterial diameters (88 nonstenotic segments) in 24 transplant patients undergoing vasomotor function studies with acetylcholine and nitroglycerin, 20 stenoses in 14 patients with coronary artery disease, and 15 stenoses in 15 patients before and after excimer laser-facilitated coronary angioplasty and at 6 months' follow-up. In nonstenotic arterial segments ranging in size from 0.6 to 3.5 mm, calipers overestimated diameters measured by quantitative angiography by 0.29 +/- 0.21 mm (mean +/- SD) (limits of agreement, -0.13 to 0.71 mm). However, when the vasomotor responses were expressed as percent diameter change, the two methods did not differ significantly (-1 +/- 10%; limits of agreement, -21% to 19%). In the 35 stenoses measured before intervention and 30 stenoses measured after intervention, calipers and quantitative angiography differed by 3 +/- 9% (limits of agreement, -15% to 21%) across a range of stenosis severity (11% to 80%). Repeat caliper measurements by the same observer of the percent diameter change in the transplant patients and the percent stenosis in the coronary artery disease patients led to standard deviations of the differences of 9.3% and 7.6%, respectively. Two different observers recorded percent diameter change and percent stenosis that differed with standard deviations of 9.6% and 7.8%, respectively. CONCLUSIONS: Quantitative angiography and electronic digital calipers produce similar relative changes in arterial diameters and percent stenosis in a broad range of severities. Digital calipers thus are a rapid and convenient alternative to computerized quantitative angiography in certain research studies and clinical practice of assessing stenosis severity.

Coronary Angiography↗
PubMed1995

Comparison of valvular resistance, stroke work loss, and Gorlin valve area for quantification of aortic stenosis. An in vitro study in a pulsatile aortic flow model.

BACKGROUND: Valvular resistance and stroke work loss have been proposed as alternative measures of stenotic valvular lesions that may be less flow dependent and, thus, superior over valve area calculations for the quantification of aortic stenosis. The present in vitro study was designed to compare the impacts of valvular resistance, stroke work loss, and Gorlin valve area as hemodynamic indexes of aortic stenosis. METHODS AND RESULTS: In a pulsatile aortic flow model, rigid stenotic orifices in varying sizes (0.5, 1.0, 1.5 and 2.0 cm2) and geometry were studied under different hemodynamic conditions. Ventricular and aortic pressures were measured to determine the mean systolic ventricular pressure (LVSPm) and the transstenotic pressure gradient (delta Pm). Transvalvular flow (Fm) was assessed with an electromagnetic flowmeter. Valvular resistance [VR = 1333.(delta Pm/Fm)] and stroke work loss [SWL = 100.(delta Pm/LVSPm)] were calculated and compared with aortic valve area [AVA = Fm/(50 square root of delta Pm)]. The measurements were performed for a large range of transvalvular flows. At low-flow states, flow augmentation (100-->200 mL/s) increased calculated valvular resistance between 21% (2.0 cm2 orifice) and 66% (0.5-cm2 orifice). Stroke work loss demonstrated an increase from 43% (2.0 cm2) to 100% (1.0 cm2). In contrast, Gorlin valve area revealed only a moderate change from 29% (2.0 cm2) to 5% (0.5 cm2). At physiological flow rates, increase in transvalvular flow (200-->300 mL/s) did not alter calculated Gorlin valve area, whereas valvular resistance and stroke work loss demonstrated a continuing increase. Our experimental results were adopted to interpret the results of three clinical studies in aortic stenosis. The flow-dependent increase of Gorlin valve area, which was found in the cited clinical studies, can be elucidated as true further opening of the stenotic valve but not as a calculation error due to the Gorlin formula. CONCLUSIONS: Within the physiological range of flow, calculated aortic valve area was less dependent on hemodynamic conditions than were valvular resistance and stroke work loss, which varied as a function of flow. Thus, for the assessment of the severity of aortic stenosis, the Gorlin valve area is superior over valvular resistance and stroke work loss, which must be indexed for flow to adequately quantify the hemodynamic severity of the obstruction.

Aortic Valve↗
PubMed1995

Comparative validation of quantitative coronary angiography systems. Results and implications from a multicenter study using a standardized approach.

BACKGROUND: Computerized quantitative coronary angiography (QCA) has fundamentally altered our approach to the assessment of coronary interventional techniques and strategies aimed at the prevention of recurrence and progression of stenosis. It is essential, therefore, that the performance of QCA systems, upon which much of our scientific understanding has become integrally dependent, is evaluated in an objective and uniform manner. METHODS AND RESULTS: We validated 10 QCA systems at core laboratories in North America and Europe. Cine films were made of phantom stenoses of known diameter (0.5 to 1.9 mm) under four experimental conditions: in vivo (coronary arteries of pigs) calibrated at the isocenter or by use of the catheter as a scaling device and in vitro with 50% contrast and 100% contrast. The cine films were analyzed by each automated QCA system without observer interaction. Accuracy and precision were taken as the mean and SD of the signed differences between the phantom stenoses, and the measured minimal luminal diameters and the correlation coefficient (r), the SEE, the y intercept, and the slope were derived by their linear regression. Performance of the 10 QCA systems ranged widely: accuracy, +0.07 to +0.31 mm; precision, +/- 0.14 to +/- 0.24 mm; correlation (r), .96 to .89; SEE, +/- 0.11 to +/- 0.16 mm; intercept, +0.08 to +0.31 mm; and slope, 0.86 to 0.64. CONCLUSIONS: There is a marked variability in performance between systems when assessed over the range of 0.5 to 1.9 mm. The range of accuracy, intercept, and slope values of this report indicates that absolute measurements of luminal diameter from different multicenter angiographic trials may not be directly comparable and additionally suggests that such absolute measurements may not be directly applicable to clinical practice using an on-line QCA system with a different edge detection algorithm. Power calculations and study design of angiographic trials should be adjusted for the precision of the QCA system used to avoid the risk of failing to detect small differences in patient populations. This study may guide the fine-tuning of algorithms incorporated within each system and facilitate the maintenance of high standards of QCA for scientific studies.

Algorithms↗
PubMed1995

Effects of anterior communicating artery diameter on cerebral hemodynamics in internal carotid artery disease. A model study.

BACKGROUND: Collateral circulatory pathways are considered the primary determinant of cerebral hemodynamics in patients with obstructive lesions of the internal carotid arteries (ICaAs). However, the hemodynamic effects of the diameter of the anterior communicating artery (ACoA) have never been assessed quantitatively in humans. METHODS AND RESULTS: Two different mathematical models were used to simulate changes affecting blood pressures and flows in cerebral arteries as a function of ACoA diameter and ICaA stenoses or occlusions. Small changes in ACoA diameter were found to have marked hemodynamic effects when they occurred within the range of 0.4 to 1.6 mm, a situation observed in 80% of the cases. Outside this range, changes in ACoA diameter had no effect. Simulated pressure drops through a stenotic ICaA were consistent with those observed. They were found to depend on the degrees of the stenoses in both ICaAs and on ACoA diameter according to a simple equation. Pressure reserve in the middle and anterior cerebral arteries decreased to below the lower limit of autoregulation, despite a normal mean arterial blood pressure, when the arteries were distal to a unique 70% ICaA stenosis associated with a small-diameter ACoA or to a 50% ICaA stenosis associated with a contralateral ICaA occlusion and a large-diameter ACoA. Above these thresholds, the circle of Willis allowed for an almost complete global cerebral blood flow compensation that involved all the afferent and communicating vessels. CONCLUSIONS: ACoA diameter strongly modulates the effects of ICaA lesions on cerebral hemodynamics. Some proposals for endarterectomy indications can be derived from our study.

Blood Flow Velocity↗
PubMed2002

Ionic current basis of electrocardiographic waveforms: a model study.

Body surface electrocardiograms and electrograms recorded from the surfaces of the heart are the basis for diagnosis and treatment of cardiac electrophysiological disorders and arrhythmias. Given recent advances in understanding the molecular mechanisms of arrhythmia, it is important to relate these electrocardiographic waveforms to cellular electrophysiological processes. This modeling study establishes the following principles: (1) voltage gradients created by heterogeneities of the slow-delayed rectifier (I(Ks)) and transient outward (I(to)) potassium current inscribe the T wave and J wave, respectively; T-wave polarity and width are strongly influenced by the degree of intercellular coupling through gap-junctions. (2) Changes in [K+]o modulate the T wave through their effect on the rapid-delayed rectifier, I(Kr). (3) Alterations of I(Ks), I(Kr), and I(Na) (fast sodium current) in long-QT syndrome (LQT1, LQT2, and LQT3, respectively) are reflected in characteristic QT-interval and T-wave changes; LQT1 prolongs QT without widening the T wave. (4) Accelerated inactivation of I(Na) on the background of large epicardial I(to) results in ST elevation (Brugada phenotype) that reflects the degree of severity. (5) Activation of the ATP-sensitive potassium current, I(K(ATP)), is sufficient to cause ST elevation during acute ischemia. These principles provide a mechanistic cellular basis for interpretation of electrocardiographic waveforms.

Action Potentials↗
PubMed2004

Vanilloid receptor TRPV1, sensory C-fibers, and vascular autoregulation: a novel mechanism involved in myogenic constriction.

Myogenic constriction describes the innate ability of resistance arteries to constrict in response to elevations in intraluminal pressure and is a fundamental determinant of peripheral resistance and, hence, organ perfusion and systemic blood pressure. However, the receptor/cell-type that senses changes in pressure on the blood vessel wall and the pathway that couples this to constriction of vascular smooth muscle remain unclear. In this study, we show that elevation of intraluminal transmural pressure of mesenteric small arteries in vitro results in a myogenic response that is profoundly suppressed following ablation of sensory C-fiber activity (using in vitro capsaicin desensitization resulted in 72.8+/-10.3% inhibition, n=8; P<0.05). Activation of C-fiber nerve endings by pressure was attributable to stimulation of neuronal vanilloid receptor, TRPV1, because blockers of this channel, capsazepine (71.9+/-11.1% inhibition, n=9; P<0.001) and ruthenium red (46.1+/-11.7% inhibition, n=4; P<0.05), suppressed the myogenic constriction. In addition, this C-fiber dependency is likely related to neuropeptide substance P release and activity because blockade of tachykinin NK1 receptors (66.3+/-13.7% inhibition, n=6; P<0.001), and not NK2 receptors (n=4, NS), almost abolished the myogenic response. Previous studies support a role for 20-hydroxyeicosatetraenoic acid (20-HETE) in myogenic constriction responses; herein, we show that 20-HETE-induced constriction of mesenteric resistance arteries is blocked by capsazepine. Together, these results suggest that elevation of intraluminal pressure is associated with generation of 20-HETE that, in turn, activates TRPV1 on C-fiber nerve endings resulting in depolarization of nerves and consequent vasoactive neuropeptide release. These findings identify a novel mechanism contributing to Bayliss' myogenic constriction and highlights an alternative pathway that may be targeted in the therapeutics of vascular disease, such as hypertension, where enhanced myogenic constriction plays a role in the pathogenesis.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2004

Proarrhythmic consequences of a KCNQ1 AKAP-binding domain mutation: computational models of whole cells and heterogeneous tissue.

The KCNQ1-G589D gene mutation, associated with a long-QT syndrome, has been shown to disrupt yotiao-mediated targeting of protein kinase A and protein phosphatase-1 to the I(Ks) channel. To investigate how this defect may lead to ventricular arrhythmia during sympathetic stimulation, we use integrative computational models of beta-adrenergic signaling, myocyte excitation-contraction coupling, and action potential propagation in a rabbit ventricular wedge. Paradoxically, we find that the KCNQ1-G589D mutation alone does not prolong the QT interval. But when coupled with beta-adrenergic stimulation in a whole-cell model, the KCNQ1-G589D mutation induced QT prolongation and transient afterdepolarizations, known cellular mechanisms for arrhythmogenesis. These cellular mechanisms amplified tissue heterogeneities in a three-dimensional rabbit ventricular wedge model, elevating transmural dispersion of repolarization and creating other T-wave abnormalities on simulated electrocardiograms. Increasing heart rate protected both single myocyte and the coupled myocardium models from arrhythmic consequences. These findings suggest that the KCNQ1-G589D mutation disrupts a critical link between beta-adrenergic signaling and myocyte electrophysiology, creating both triggers of cardiac arrhythmia and a myocardial substrate vulnerable to such electrical disturbances.

Action Potentials↗
PubMed1989

Estimating cardiac transmembrane activation and recovery times from unipolar and bipolar extracellular electrograms: a simulation study.

A model of one-dimensional action potential propagation was used to compare activation times and recovery times measured from simulated unipolar and bipolar electrograms with the activation and recovery times measured from simulated transmembrane action potentials. Theory predicts that the intrinsic deflection--the time of the maximum negative slope of the unipolar electrogram QRS complex--corresponds to the time of maximum positive slope of action potential depolarization. Similarly, the time of the maximum positive slope of the unipolar electrogram T wave corresponds to the time of maximum negative slope of action potential repolarization. This study showed that the difference between the unipolar electrogram activation time and the action potential activation time and the difference between the unipolar electrogram recovery time and the action potential recovery time were small during ideal conditions of uniform propagation in a long cable. Nonideal conditions, however, were associated with activation time differences in excess of 1.8 msec and recovery time differences in excess of 30 msec (243 msec in certain conditions). Nonideal conditions that had a major influence were changes in activation sequence, propagation in a short cable, and propagation through regions of nonuniform coupling resistance and/or nonuniform membrane properties. Nonideal conditions that had a smaller influence were variations in distance from the measurement site to the simulated tissue surface, nonzero reference potentials, and the addition of distant events. Recovery time differences were more sensitive to the nonideal conditions than were activation time differences, and both depended on the action potential shape. When distant events significantly contributed to the unipolar electrogram waveform, the time differences when bipolar electrograms were used were less than those when unipolar electrograms were used; however, under other conditions, the time differences were comparable. Results showed that activation times and especially recovery times measured from electrograms can be greatly affected by conditions independent of changes in the underlying action potential waveforms.

Action Potentials↗
PubMed1989

Constitutive relations and finite deformations of passive cardiac tissue II: stress analysis in the left ventricle.

We present a new approach for estimation of transmural distributions of stress and strain in the equatorial region of a passive left ventricle. We employ a thick-walled cylindrical geometry, assume that myocardium is incompressible, and use a three-dimensional constitutive relation that yields a material symmetry consistent with observed transmural variations in muscle fiber orientations. Moreover, we consider finite deformations including inflation, extension, twist, and transmural shearing and suggest a new method for determination of the requisite deformation parameters directly from experimental strain data. We show representative transmural distributions of stress and strain, and perform a parametric study to illustrate differing predictions of stress induced by varying boundary conditions, muscle fiber orientations, or modes of deformation. Our analysis can be used to guide and check future predictions of cardiac stresses, and to guide experimentalists by suggesting the accuracy of measurements essential for stress analysis in the heart.

Animals↗
PubMed1991

Directional characteristics of action potential propagation in cardiac muscle. A model study.

Propagation of an elliptic excitation wave front was studied in a two-dimensional model of a thin sheet of cardiac muscle. The sheet model of 2.5 x 10 mm consisted of a set of 100 parallel cables coupled through a regular array of identical transverse resistors. The membrane dynamics was represented by a modified Beeler-Reuter model. We defined the charging factor (CF) to represent by a single number the proportion of input current used to charge the membrane locally below threshold and showed that CF is inversely correlated with the time constant of the foot of the action potential (tau foot) during propagation on a cable. A safety factor of propagation (SF) was also defined for the upstroke of the action potential, with SF directly correlated with the maximum rate of depolarization (Vmax) and, for cablelike propagation, with propagation velocity. Propagation along the principal longitudinal axis of the elliptic wave front is cablelike but, in comparison with a flat wave front, transverse current flow provides a drag effect that somewhat reduces the propagation velocity, Vmax, SF, and CF. With a longitudinal-to-transverse velocity ratio of 3:1 or more, the wave front propagating along the principal transverse axis is essentially flat and is characterized by multiple collisions between successive pairs of input junctions on a given cable; Vmax, SF, and CF are larger than for longitudinal propagation, but CF is no longer correlated with tau foot. There are transient increases in propagation velocity and Vmax with distance from the stimulation site along both principal axes until stablized values are achieved, and a similar transient decrease in tau foot. Away from the principal axes, the action potential characteristics change progressively along the elliptic wave front.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1991

Cooperative effects due to calcium binding by troponin and their consequences for contraction and relaxation of cardiac muscle under various conditions of mechanical loading.

A mathematical model for the regulation of mechanical activity in cardiac muscle has been developed based on a three-element rheological model of this muscle. The contractile element has been modeled taking into account the results of extensive mechanical tests that involved the recording of length-force and force-velocity relations and muscle responses to short-time deformations during various phases of the contraction-relaxation cycle. The best agreement between the experimental and the mathematical modeling results was obtained when a postulate stating two types of cooperativity to regulate the calcium binding by troponin was introduced into the model. Cooperativity of the first type is due to the dependence of the affinity of troponin C for Ca2+ on the concentration of myosin crossbridges in the vicinity of a given troponin C. Cooperativity of the second type assumes an increase in the affinity of a given troponin C for Ca2+ when the latter is bound by molecules neighboring troponin.

Animals↗
PubMed1995

Transverse shear along myocardial cleavage planes provides a mechanism for normal systolic wall thickening.

Recent studies in humans and other species show that there is substantial transverse shear strain in the left ventricular myocardium, and others have shown transverse myocardial laminae separated by cleavage planes. We proposed that cellular rearrangement based on shearing along myocardial cleavage planes could account for > 50% of normal systolic wall thickening, since < 50% can be explained by increases in myocyte diameter. To test this hypothesis, we measured strains at two sites with different cleavage-plane anatomy in eight open-chest dogs. Columns of radiopaque markers were implanted in the left ventricular anterior free wall and septum. Markers were tracked with biplane cineradiography, and strains were quantified by using finite deformation techniques. Hearts were perfusion-fixed with glutaraldehyde, and cleavage-plane orientations at the bead sites were measured in three orthogonal planes. At subendocardial sites of the anterior left ventricular wall, where the cleavage planes approach the endocardium obliquely from the apical side of the surface normal in the longitudinal-radial plane (-67 +/- 11 degrees), systolic longitudinal-radial transverse shear (E23) was positive (0.14 +/- 0.08). At the septal sites where the subendocardial cleavage planes approach the endocardium obliquely from above the surface normal (44 +/- 12 degrees), E23 was negative (-0.12 +/- 0.08). The differences in cleavage-plane angle and E23 at the two sites were each highly significant (P < .0005). At both sites, the transverse shear strain accompanied substantial systolic wall thickening at the subendocardium (anterior, E33 = 0.44 +/- 0.16; septum, E33 = 0.22 +/- 0.14). These data are not representative of the behavior in midwall and outer wall sites, where cleavage-plane orientation was not consistently different between anterior left ventricle and septum. Our data indicate that rearrangement of myocytes by slippage along myocardial cleavage planes is in the correct direction and of sufficient magnitude in the subendocardium (inner third) to account for a substantial proportion (> 50%) of systolic wall thickening. Furthermore, three-dimensional reconstruction of the myocardial laminae and local comparison with maximum strain vectors indicate that for the inner third of the ventricular wall the maximum shear deformation is a result of relative sliding between myocardial laminae.

Animals↗