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W L Maughan

Publications and source records attributed to W L Maughan.

At least 37 records · Page 2Linked to original sources
PubMed1989

Determinants of end-systolic pressure-volume relations during acute regional ischemia in situ.

The influence of extent and location of regional ischemia, baseline left ventricular systolic function, and autonomic reflexes on in situ left ventricular end-systolic pressure-volume relations (ESPVRs) during coronary occlusion were studied in 13 open-chest dogs. Circumflex or left anterior descending arteries were randomly occluded (at proximal or distal sites) for 3 minutes in reflex-blocked (n = 6, hexamethonium/vagotomy) and unblocked (n = 7) animals. Pressure-volume data were obtained by the conductance-catheter technique, with ESPVRs determined by transient inferior vena caval occlusion. Ischemic zone size was estimated for each occlusion by radiolabeled microspheres. The relative influence of each variable on ESPVR change with ischemia was determined by multiple regression analysis. As in previous studies, regional ischemia displaced ESPVRs to the right by an amount that varied directly with ischemic bed size (y = +0.48x, r = 0.76, p less than 0.001). However, in contrast to previous data, coronary occlusion also reduced the ESPVR slope (end-systolic elastance, Ees) in the majority of cases. The extent of slope change was primarily dependent on the baseline elastance (Eesbase), such that the higher the initial elastance, the larger its subsequent reduction for any amount of ischemia (delta Ees = -0.78Eesbase, r = 0.94, p less than 0.001). Active reflexes added an offset constant to this relation (+3.15 mm Hg/ml, p less than 0.001). In addition, Ees fell slightly more with larger ischemic regions. Thus, although previous studies have reported primarily rightward parallel shifts in ESPVR with regional ischemia, the present data also demonstrate that the slope of the relation is often reduced. Greater baseline elastances typical of in situ, as opposed to isolated, ventricles probably explain the differences in apparent responses.

Animals↗
PubMed1988

Use of a conductance (volume) catheter and transient inferior vena caval occlusion for rapid determination of pressure-volume relationships in man.

Determination of left ventricular pressure-volume relationships in situ ideally requires both a method for easy measurement of multiple pressure-volume loops and a rapid and reversible means of altering load. We report a technique, previously used in animals, that combines conductance catheter volumes and rapid inferior vena caval occlusion to permit routine measurement of calibrated P-V relationships in man for the first time. An 8F volume catheter with a 3F micromanometer tipped pressure catheter placed through its lumen was advanced to the left ventricular apex through a femoral artery. A thermodilution output catheter was placed through a 9F femoral venous sheath and later replaced with an IVC balloon occlusion catheter, through which a 2.5F bipolar wire was advanced for atrial pacing. A specialized data system facilitated collection, editing, and data analysis at the time of cardiac catheterization. Absolute volume calibration required cardiac output measurement and injection of hypertonic saline. IVC occlusion decreased peak left ventricular pressure by 42 +/- 17 (SD) (P less than .001) mm Hg in 15 patients. Endsystolic pressure-volume relationships (ESPVR) were determined with 5-8 cardiac cycles with an average of r2 of 0.94 +/- 0.05 and were generally reproducible. The slope of the ESPVR demonstrated consistency among a group of normal patients (n = 6), and was significantly lower than the slope derived from a group of patients with ventricular hypertrophy (n = 9). We conclude that left ventricular pressure-volume relationships can be easily and repeatedly determined as part of a routine cardiac catheterization in man.

Calibration↗
PubMed1988

Disproportionate epicardial dilation after transmural infarction of the canine left ventricle: acute and chronic differences.

The relation between acute disproportionate infarct dilation and late postinfarct left ventricular remodeling was examined by implanting multiple radiopaque epicardial markers in the left ventricle of eight dogs and determining regional surface deformation after acute and chronic transmural infarction. Transmural injury was produced by combining coronary ligation with distal embolization of a rubber polymer. Dogs were anesthetized and studied before and 1 h, 24 h and 1 week after infarction. Marker positions were recorded by rapid biplane cineradiography, and three-dimensional coordinates were reconstructed by a computer-assisted tracking system. Regional deformation was expressed by a local surface area equal to the sum of multiple (three to four) triangles generated by marker triplets. As early as 1 h after infarction, end-diastolic area in the infarct region increased by 20.3 +/- 3.1%, while that in the remote region increased by only 7.9 +/- 3.5%. Both changes and the difference between them were significant. At 24 h after infarction, both territories continued to undergo dilation, this time to a similar extent (additional +10.3% in the remote region and +10.1% in the infarct region), thus maintaining the significant disproportionate infarct dilation. At 1 week, however, the infarct territory remained dilated with a mean end-diastolic area 31.4 +/- 3.1% above control, while that in the remote region returned to a net mean 8.5 +/- 4.7% increase. Thus, the major extent of disproportionate infarct dilation occurs within 1 h after transmural injury and is accompanied by remote dilation as a compensatory response. The extent of further infarct dilation achieved by 24 h is maintained in the chronic infarct, and compensatory mechanisms enable noninjured myocardium to become less dilated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Influence of site of regional ischemia on LV cavity shape change in dogs.

We assessed whether altering the location of acute ischemia produced differing and consistent changes in cavity shape in the canine left ventricle. Twenty anesthetized open-chest dogs underwent transient occlusion of the left anterior descending (LAD) or circumflex (Circ) artery, and cavity shape change was recorded in two-dimensional short-axis echocardiograms. The extent of injury was assessed by radiolabeled microspheres. Shape was analyzed by converting digitized endocardial contours into polar form and expressing the result as a Fourier series. Series terms reflected specific shape deformations, i.e., 2nd term would equal "elongation," 3rd term would equal "triangular." During LAD occlusions, 32.5 +/- 3.0% of the ventricle was hypoperfused compared with 29.8 +/- 2.9% during Circ occlusions (NS). Normal ventricular shape became more circular during ejection indicated by a reduction in the power in nearly all of the Fourier spectra components. During Circ occlusion, the chamber became more elongated, seen in a 63 +/- 16% rise in the 2nd component, and overall shape significantly less circular at end systole than at end diastole. LAD occlusion produced an entirely different pattern, one with no significant elongation but the development of a more triangular shape (86 +/- 27% rise in the 3rd term) by end systole. We conclude that there are characteristic and contrasting shape deformations in LV short-axis contours that depend on the site of ischemic injury. These changes may relate to site-specific geometry and loading, and they point to potential limitations of left ventricular models that do not account for regional inhomogeneity.

Animals↗
PubMed1988

Effect of afterload resistance on end-systolic pressure-thickness relationship.

The influence of afterload resistance on the end-systolic pressure-thickness relationship (ESPTR) was assessed in six isolated canine left ventricles made to eject into a simulated arterial system. An increase of simulated peripheral resistance from 1.5 to 6.0 mmHg.s.ml-1 resulted in a modest but significant shift of the ESPTR upward and to the right, indicating augmented contractile performance. A relationship between the extent of systolic wall thickening and end-systolic performance was also observed: increased wall thickening impairing and decreased wall thickening enhancing end-systolic performance. The dependence of end-systolic performance on wall thickening history in this setting is consistent with shortening deactivation. This phenomenon appears to account at least in part for the observed shift in the ESPTR with altered afterload resistance.

Animals↗
PubMed1988

Abnormalities of dynamic ventricular shape change in patients with aortic and mitral valvular regurgitation: assessment by Fourier shape analysis and global geometric indexes.

The normal cardiac cycle is associated with dynamic changes in left ventricular shape, which can be disturbed in disease states. To assess the influences of diastolic volume, percent ejected volume, and abnormalities of acute or chronic systolic loading on general and detailed chamber geometry, we studied dynamic shape change recorded by x-ray contrast ventriculography in both normal patients and those with aortic (AR) or mitral (MR) valve regurgitation. While both lesions increased diastolic volume, the character of load throughout ejection differed markedly. Detailed cavity geometry was assessed by a Fourier analysis technique and general shape by eccentricity and circularity indexes. Normal hearts, showed increased systolic elongation by all indexes. AR patients displayed a similar rise in eccentricity during ejection; however, the extent of shape change when measured by Fourier and circular indexes was reduced. In contrast, MR patients displayed enhanced systolic shape change, particularly in chamber elongation. Neither simple eccentricity of circular indexes adequately differentiated these shape abnormalities, whereas detailed Fourier geometric analysis precisely characterized the abnormalities of shape change in these two diseases. Relations between the extent of shape change and ejected volume for each patient group revealed significantly more systolic deformation with a different shape versus volume relation for the MR hearts as compared with AR and controls. Thus, while dynamic left ventricular shape is certainly influenced by the extent of volume change, it also varies independently from volume related to the specific nature of loading during ejection.

Algorithms↗
PubMed1987

Extracardiac pressure changes do not alter contractile function of the isolated left ventricle.

To determine whether or not extracardiac pressure has an effect on left ventricular contractile function, we analyzed pressure-volume relationships of six isolated, perfused canine hearts in an air-tight chamber. The chamber pressure was set at -60, -30, 0, 30 and 60 mm Hg and left ventricular pressure-volume relationships studied. The slope (Ees) and volume axis intercept (Vo) of the transmural pressure-volume relationship were used to compare the pump functions of an individual heart at the different extracardiac pressures applied. No significant difference in either Ees or Vo was seen with different extracardiac pressures. During isovolumic ventricular contraction, developed left ventricular pressure did not change over the range of extracardiac pressures applied. The same was true during ejecting contraction; when the downstream pressure of the computer simulated afterload circuit and the venous filling pressure of the preload circuit were changed in parallel with the extracardiac pressure, pressure-volume loops remained identical throughout their course for all of the extracardiac pressures applied. We conclude that transmural pressure is the overwhelmingly dominant loading factor governing LV contraction, and myocardial contractile function is unaffected by the absolute value of extracardiac pressure.

Animals↗
PubMed1987

Quantitative comparison of canine right and left ventricular isovolumic pressure waves.

The mechanical properties of the right and left ventricles (RV and LV) have previously been studied separately. However, because of differences in RV and LV architecture, geometry, and muscle mass, it is not obvious how the properties of the two chambers would relate to each other. This study compared the time courses of RV and LV isovolumic pressure waves (LVP, RVP, respectively) measured simultaneously in the same heart. We compared RVP and LVP in each of five isolated, supported canine hearts after pentobarbital anesthesia. RV and LV volumes were varied independently so that on various beats peak LVP exceeded, equaled, or was less than peak RVP. There was a delay of approximately 35 ms between the onset of LV and RV pressure waves with atrial pacing, but only 5 ms with ventricular pacing. LVP and RVP were measured and digitized at a sampling rate of 200 Hz. Pressure waves were offset and rescaled by their respective amplitudes so that for each beat the pressure wave had a minimum value of 0% at end diastole and a maximum value of 100% at end systole. RVP was then shifted in time so that its upstroke was synchronous with that of the LVP at the point of 50% of maximal developed pressure. The rescaled, time-shifted RVP was plotted as a function of the rescaled LVP for each point of the cardiac cycle, and the relation between the two was quantified by their root mean square difference (Drms). Drms averaged 2.3 +/- 1.5% (SD) for the first half of contraction, 1.5 +/- 0.4% for the second half of contraction, and 4.6 +/- 1.6% during relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Ventricular systolic interdependence: volume elastance model in isolated canine hearts.

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

Algorithms↗
PubMed1987

Comparative influence of load versus inotropic states on indexes of ventricular contractility: experimental and theoretical analysis based on pressure-volume relationships.

We examined the quantitative influence of carefully controlled alterations in end-diastolic volume and afterload resistance on multiple simultaneously determined ejection and isovolumetric phase indexes of left ventricular contractile function in 23 isolated supported canine ventricles. The influence of load change on each index was compared with its sensitivity to inotropic stimulation, and this sensitivity was in turn contrasted to the response of the end-systolic pressure-volume relationship (ESPVR). Experimental data demonstrated various degrees of load sensitivity among the indexes, with a generally curvilinear relationship between load and index response for both preload and afterload alterations. The curvilinear nature of these relationships meant that over a select range of loading, many indexes demonstrated relative load independence. They also often displayed greater sensitivity to inotropic change than the ESPVR, and both factors help explain their enduring clinical utility. To further explore the influence of load and contractile state on several of the indexes, we developed a theoretical analysis, using variables common to pressure-volume relationships, in which these dependencies could be derived. The theoretical models fit very well with the experimental data, and reaffirmed the frequently curvilinear nature of the relationships. We conclude that while many clinical indexes of ventricular contractile function show significant load dependence, the information they provide can be reasonably interpreted within defined ranges of load and inotropic alteration. Any advantage of the ESPVR will derive not from the magnitude of its response to inotropic change, which is smaller than most other indexes, but from its relative insensitivity to load alteration over a wider range of load.

Animals↗
PubMed1986

Determination of left ventricular end-systolic pressure-volume relationships by the conductance (volume) catheter technique.

Using a multielectrode conductance catheter to estimate continuous left ventricular volume we determined the end-systolic pressure-volume relationship (ESPVR) in situ in open-chest anesthetized dogs. Dogs (n = 8) were studied in the control state and after pharmacologic sympathectomy (hexamethonium) and surgical vagotomy both before and after the administration of dobutamine. ESPVR was measured during brief (5 to 6 sec) preload reduction by balloon occlusion of the inferior vena cava (IVCBO). The relationship was highly reproducible. The slope (Ecs) and volume intercept (Vo) (mean +/- SD) in the control series were 5.8 +/- 3.6 mm Hg/ml and 6.5 +/- 12.5 ml, respectively. Upon release of the IVCBO (preload recovery), Ecs was 7.7 +/- 3.6 mm Hg/ml and Vo was 12.4 +/- 9.6 ml (p less than .01). Autonomic blockade produced a 50% reduction in Ecs and a concomitant decrease in Vo (p less than .01), and eliminated the difference between ESPVR generated by preload reduction (IVCBO) and preload recovery (IVCBO release). Subsequent dobutamine infusion increased Ecs to 6.1 +/- 3.5 mm Hg/ml and Vo to 4.1 +/- 6.9 ml, consistent with reported changes of the ESPVR with positive inotropic intervention. A small artifact of right ventricular filling was observed in the left ventricular volume catheter signal, but this did not appreciably alter the ESPVR. These results demonstrate the feasibility of the determination of ESPVR in situ by the conductance catheter and brief IVCBO and underline the importance of the use of rapid load changes to minimize reflex activation during the measurements.

Animals↗
PubMed1986

End-systolic measures of regional ventricular performance.

Dimension change measures of regional ventricular function, such as absolute or percent wall thickening (delta T or % delta T) or segmental shortening (delta L or % delta L), are highly load dependent. In 16 anesthetized mongrel dogs we assessed use of the end-systolic pressure-thickness and end-systolic pressure-length relationships (ESPTR, ESPLR) as more load-independent measures of regional function. We found that the ESPTR and ESPLR could be measured without detectable baroreceptor-mediated reflex changes in cardiac contractile state. Systemic administration of dobutamine shifted the ESPTR to the right and the ESPLR to the left of control, mainly due to a change in the slope (Ees) of the relationships. Both delta T, % delta T and delta L, % delta L failed to detect the positive inotropic effect of dobutamine because of an associated reduction in preload. With systemic administration of propranolol, ESPTR, ESPLR, delta T, % delta T, and delta L, % delta L detected the negative inotropic effect. Thus systemic propranolol shifted the ESPTR to the left and the ESPLR to the right of control, mainly due to a change in Ees. Regional administration of dobutamine shifted the ESPTR and the ESPLR in the direction of positive contractility in the region receiving the drug, whereas simple dimension change measures of regional function failed to detect the inotropic effect because preload fell and the timing of regional end-systole was altered. With regional propranolol both the ESPTR, ESPLR and simple dimension change measures detected the negative inotropic effect. Thus the ESPTR, ESPLR is a reliable measure of regional ventricular function and may be better than simple dimension change measures of regional function, particularly when loading conditions or the timing of regional systole is altered by an intervention.

Animals↗
PubMed1985

Stroke volume effect of changing arterial input impedance over selected frequency ranges.

We investigated the effect of changing arterial input impedance over three selected frequency ranges on stroke volume (SV) in nine isolated canine left ventricles. The input impedance was simulated with a three-element Windkessel model (i.e., resistance, characteristic impedance, and compliance) and was imposed on the ventricles with a servo-controlled loading system. Under a constant end-diastolic volume [33.1 +/- 1.5 (SE) ml], we changed the modulus of the afterloaded impedance over a low frequency range (below 0.13 Hz) by changing the resistance, over a transitional frequency range (in which the impedance modulus decreases from total resistance to characteristic impedance) by changing the compliance, and over a high frequency range (above 2.0 Hz) by changing the characteristic impedance. Each of the impedance components was changed from control to 50 and 200% of control. SV sensitively decreased from 16.1 +/- 0.7 to 7.4 +/- 0.5 ml in response to the increase in the low-frequency impedance modulus. SV was relatively insensitive, however, to the same percent increase in the impedance modulus over the transitional frequency range (from 11.2 +/- 0.6 to 12.3 +/- 0.7 ml) and over the high frequency range (from 11.9 +/- 0.6 to 11.6 +/- 0.7 ml). The average relative sensitivities of SV to the increase and decrease in impedance moduli in these frequency ranges were 1.2:0.12:0.04. We conclude that the modulus of impedance in the low frequency range is, by far, a more important determinant of SV than those in the transitional and high frequency ranges.

Animals↗
PubMed1985

Alternating contractility in pulsus alternans studied in the isolated canine heart.

We examined pulsus alternans in seven isolated, perfused canine left ventricles ejecting into a simulated arterial impedance. Left ventricular pressure-volume loops were measured during pulsus alternans while filing-source pressure was lowered. In all cases two distinct linear end-systolic pressure-volume relationships (ESPVRs) were noted for the strong and weak beats. The slopes of the ESPVRs of the strong beats were significantly greater than those of the weak beats (mean difference 0.9 +/- 0.6 mm Hg/ml, p less than .01), while the intercepts were not significantly different (mean difference 0.06 +/- 0.5 ml). Diastolic pressure-volume relationships for the strong and weak beats were not significantly different, excluding incomplete relaxation as a cause of pulsus alternans. Although the weak beats had both a smaller preceding end-diastolic volume and a larger end-systolic volume, the presence of two distinct ESPVRS for the strong and weak beats shows there is alternating ventricular chamber contractility in pulsus alternans that is not solely due to the Starling mechanism. The magnitude of alternation in pump function parameters such as pressure and stroke volume during pulsus alternans reflects the complex interactions of alternating contractile state with alternations in preload and afterload.

Animals↗
PubMed1985

Accuracy of volume measurement by conductance catheter in isolated, ejecting canine hearts.

We evaluated the accuracy of the recently reported technique of estimating intraventricular volume by measurement of intracavitary electrical conductance in six isolated, ejecting, canine left ventricles. Left ventricular volumes were measured directly by a previously validated servosystem that employed an electroconductive balloon placed in the left ventricular cavity. The volume measured continuously by the balloon method (Vbal) was compared with that estimated by the conductance method (Vcath). For this test, the hearts were made to eject and fill physiologically by the use of a previously described computer-simulated arterial loading system. Complex ejection and filling patterns were created by stimulating the atrium mechanically, which resulted in irregular arrhythmatic contractions spanning a wide range of volumes. We found that there was a highly linear relationship (r2 = .982 +/- .014) between Vbal and Vcath: Vcath = 0.82 (+/- .05) Vbal + 26.7 (+/- 11.8) ml. Despite the wide variation in the offset term of this relationship among the different hearts, the offset within a given heart was predicted within 3.5 ml by a previously detailed "dilution" method that is applicable to the heart in situ within a closed thorax. Thus, since the offset term is obtainable in situ, the conductance method provides a signal that is proportional to the actual volume. To determine whether right ventricular volume influenced the accuracy of left ventricular measurement, we compared the relationship between Vcath and Vbal obtained with right ventricular volumes of 0 and 30 ml. Increasing the right ventricular volume shifted the relationship upward by less than 3 ml in the working range.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effect of heart rate on the canine end-systolic pressure-volume relationship.

Although the rate dependence of isolated muscle contractility is well known, the ventricular end-systolic pressure-volume relationship (ESPVR) has been reported to be insensitive to heart rate. To resolve this contradiction, we used an isolated, ejecting canine heart preparation perfused at a constant coronary arterial pressure. Heart rate was changed from 60 to 200 beats/min in steps of 20 beats/min. At least 10 pressure-volume loops under different filling pressures were obtained at each heart rate in each of six hearts. Over a heart rate range from 60 to 120 beats/min, the slope of the ESPVR (Ees) increased significantly from 3.5 +/- 0.4 (SE) to 5.3 +/- 0.6 mm Hg/ml. In the range between 120 and 180 beats/min there was little change in Ees (5.3 +/- 0.6 to 5.4 +/- 0.6 mm Hg/ml), but at 200 beats/min Ees increased slightly to 5.7 +/- 0.5 mm Hg/ml. The volume axis intercept (V0) of the ESPVR changed little over the range of heart rate from 60 to 160 beats/min (10.2 +/- 2 ml to 9.4 +/- 1.3 ml) but increased to 15.2 +/- 1.2 ml at a rate of 200 beats/min. The change in ESPVR with increase in heart rate from 60 to 120 beats/min (i.e., increase in Ees without change in V0) is the same as those seen with a positive inotropic intervention with calcium or cathecholamines, whereas the V0 changes over the range from 160 to 200 beats/min is similar to those seen with regional ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Optimal arterial resistance for the maximal stroke work studied in isolated canine left ventricle.

In a previous analysis of ventricular arterial interaction (Sunagawa et al., 1983), we represented the left ventricle as an elastic chamber which periodically increases its volume elastance to a value equal to the slope of the linear end-systolic pressure-volume relationship. Similarly, the arterial load property was represented by an effective elastance which is the slope of the arterial end-systolic pressure-stroke volume relationship. Since the maximal transfer of potential energy from one elastic chamber to another occurs when they have equal elastance, we hypothesized that the left ventricle would do maximal external work if the ventricular elastance and the effective arterial elastance were equal. We tested this hypothesis in 10 isolated canine left ventricles, ejecting into a simulated arterial impedance, by extensively altering arterial resistance and finding the optimal resistance that maximized left ventricular stroke work under various combinations of end-diastolic volume, contractility, heart rate, and arterial compliance. Each of these parameters was set at one of three levels while others were at control. The optimal resistance varied only slightly with arterial compliance, whereas it varied widely with contractility and heart rate. We thus determined that the ratio of the optimal effective arterial elastance to the given ventricular elastance remained nearly unity. This result supports the hypothesis that the left ventricle does maximal external work to the arterial load when the ventricular and arterial elastances are equalized.

Animals↗