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Biomedical subjects

A Pasipoularides

Publications and source records attributed to A Pasipoularides.

At least 19 recordsLinked to original sources
PubMed1994

Effects of anaesthesia and recent surgery on diastolic function.

OBJECTIVE: The aims were to determine the effects and the extent to which halothane anaesthesia affects diastolic function both immediately after and remote from surgery and to investigate whether the effect is due to alterations in loading conditions. METHODS: Eight mongrel dogs were studied under halothane anaesthesia (0.5-1.5 end tidal vol%) with the chest closed, after acute instrumentation with left ventricular pressure transducers, left atrial and aortic catheters, and left ventricular diameter and wall thickness crystals. The same dogs were then studied in the fully conscious state, 2-3 weeks later. An additional four dogs were studied in the conscious state and then again under halothane anaesthesia remote from acute instrumentation. The left ventricular isovolumetric relaxation time constant, tau, as well as myocardial and chamber stiffness constants were used as indices of diastolic function. RESULTS: Following halothane anaesthesia and recent surgery, tau was prolonged significantly compared to the conscious state, at 30(SEM 1) v 22(1) ms (p < 0.01), but there were no changes in either myocardial or chamber stiffness. While tau remained sensitive to increased heart rate and enhanced contractility and was prolonged by increasing afterload in both the anaesthetised and conscious states, it was consistently prolonged following halothane anaesthesia and recent surgery even at matched levels of contractile states, heart rates and loading conditions, compared to the conscious state, at 26(1) v 19(1) ms (p < 0.01). When the effects of halothane anaesthesia were examined after full recovery from surgery, tau was still prolonged under halothane anaesthesia, at 29(2) v 20(1) ms (p < 0.01), compared to the conscious state, but in contrast to the findings following halothane anaesthesia and recent surgery, it was fully normalised [19(1) v 19(1) ms] when contractile state and loading conditions were matched. CONCLUSIONS: Left ventricular diastolic function is influenced markedly by halothane anaesthesia and recent surgery, and to a degree comparable to many pathological states. The effects of halothane anaesthesia and recent surgery appear to prolong the isovolumetric relaxation time constant independently of heart rate, contractility, and loading conditions and are most likely to be due to the combined direct effects of anaesthetics and acute instrumentation.

Anesthesia, Inhalation↗
PubMed1992

Cardiac mechanics: basic and clinical contemporary research.

This survey of cardiac hemodynamics updates evolving concepts of myocardial and ventricular systolic and diastolic loading and function. The pumping action of the heart and its interactions with arterial and venous systems in health and disease provide an extremely rich and challenging field of research, viewed from a fluid dynamic perspective. Many of the more important problems in this field, even if the fluid dynamics in them are considered in isolation, are found to raise questions which have not been asked in the history of fluid dynamics research. Biomedical engineering will increasingly contribute to their solution.

Animals↗
PubMed1992

Computational fluid dynamics of left ventricular ejection.

The present investigation addresses the effects of simple geometric variations on intraventricular ejection dynamics, by methods from computational fluid dynamics. It is an early step in incorporating more and more relevant characteristics of the ejection process, such as a continuously changing irregular geometry, in numerical simulations. We consider the effects of varying chamber eccentricities and outflow valve orifice-to-inner surface area ratios on instantaneous ejection gradients along the axis of symmetry of the left ventricle. The equation of motion for the streamfunction was discretized and solved iteratively with specified boundary conditions on a boundary-fitted adaptive grid, using an alternating-direction-implicit (ADI) algorithm. The unsteady aspects of the ejection process were subsequently introduced into the numerical simulation. It was shown that for given chamber volume and outflow orifice area, higher chamber eccentricities require higher ejection pressure gradients for the same velocity and local acceleration values at the aortic anulus than more spherical shapes. This finding is referable to the rise in local acceleration effects across the outflow axis. This is to be contrasted with the case of outflow orifice stenosis, in which it was shown that it is the convective acceleration effects that are intensified strongly.

Algorithms↗
PubMed1992

Alterations in left ventricular diastolic function in conscious dogs with pacing-induced heart failure.

We investigated in conscious dogs (a) the effects of heart failure induced by chronic rapid ventricular pacing on the sequence of development of left ventricular (LV) diastolic versus systolic dysfunction and (b) whether the changes were load dependent or secondary to alterations in structure. LV systolic and diastolic dysfunction were evident within 24 h after initiation of pacing and occurred in parallel over 3 wk. LV systolic function was reduced at 3 wk, i.e., peak LV dP/dt fell by -1,327 +/- 105 mmHg/s and ejection fraction by -22 +/- 2%. LV diastolic dysfunction also progressed over 3 wk of pacing, i.e., tau increased by +14.0 +/- 2.8 ms and the myocardial stiffness constant by +6.5 +/- 1.4, whereas LV chamber stiffness did not change. These alterations were associated with increases in LV end-systolic (+28.6 +/- 5.7 g/cm2) and LV end-diastolic stresses (+40.4 +/- 5.3 g/cm2). When stresses and heart rate were matched at the same levels in the control and failure states, the increases in tau and myocardial stiffness were no longer observed, whereas LV systolic function remained depressed. There were no increases in connective tissue content in heart failure. Thus, pacing-induced heart failure in conscious dogs is characterized by major alterations in diastolic function which are reversible with normalization of increased loading condition.

Animals↗
PubMed1991

Noninvasive assessment of intrinsic ventricular load dynamics in dilated cardiomyopathy.

On the basis of hemodynamic theory, a new noninvasive method is developed to provide improved insights into the significance of depressed Doppler left ventricular ejection variables in patients with dilated cardiomyopathy. The net force (F) associated with intraventricular flow throughout ejection can be written as: F = A.dv/dt + B.v2, where v is the ejection velocity and A and B are variables related to the geometry of the ventricle and its outflow tract. Instantaneous levels of this force were calculated in 9 normal subjects and 10 patients with dilated cardiomyopathy using Doppler, M-mode and two-dimensional echocardiography. The maximal ejection force (Fmax) was 47.5 +/- 8.5 kdyn in normal subjects and 25.5 +/- 6.2 kdyn in those with dilated cardiomyopathy (p = 0.0001). Peak local acceleration and outflow velocity were severely depressed in those with cardiomyopathy compared with normal subjects (1,260 +/- 129 versus 2,671 +/- 430 cm/s2 and 71 +/- 14 versus 109 +/- 7 cm/s, respectively; p = 0.0001). Maximal ejection force was attained very early in ejection. A significant linear correlation was found between peak outflow acceleration and maximal ejection force (n = 19; r = 0.91, p = 0.0001). At the time of peak ejection velocity, the net force had decreased to 64% of its peak value in those with cardiomyopathy, whereas in normal subjects, it had decreased to only 84% of its peak value (p = 0.008). In normal subjects, the ejection force was positive during the first 75% of ejection, but in those with cardiomyopathy, it was positive only during the first 54% (p = 0.0003). Once its peak value was attained, total left ventricular systolic wall stress declined rapidly during ejection in normal subjects (to 33% of its peak value by end-ejection), whereas it remained elevated throughout ejection in patients with cardiomyopathy (at 60% of its peak value by end-ejection, p = 0.0001 versus normal). The maximal ejection force corresponded to a calculated intraventricular peak pressure gradient of 9.8 +/- 1.6 mm Hg in normal subjects and 6 +/- 1.2 mm Hg in those with cardiomyopathy (p = 0.0001). The average contribution of the intrinsic component of the left ventricular systolic load (that is, wall stress associated with the ventricular to aortic pressure gradient) to the total myocardial load was 9.1% (range 7.3% to 11.2%) in normal subjects and 6.2% (range 3.9% to 7.5%) in those with cardiomyopathy (p = 0.0001).(ABSTRACT TRUNCATED AT 400 WORDS)

Blood Flow Velocity↗
PubMed1991

Changes in diastolic cardiac function in developing and stable perinephritic hypertension in conscious dogs.

The effects of developing perinephritic hypertension (2-3 weeks) and a more stable period of perinephritic hypertension (approximately 14 weeks) were examined on indexes of left ventricular (LV) diastolic function in conscious, chronically instrumented dogs. The complete period of diastole was studied using indexes of isovolumic relaxation (tau), early filling (LV +dD/dt), and stiffness (myocardial stiffness and chamber stress/diameter ratio). During developing hypertension, increased LV end-diastolic pressure, LV end-diastolic stress, peak filling rate, myocardial stiffness, and the stress/diameter ratio increased (p less than 0.05); the time constant tau was not changed. These changes were associated with preserved baseline levels of coronary blood flow (radioactive microspheres) but an impaired coronary vasodilator response to adenosine. Acute administration of phenylephrine in the normotensive dogs caused increases in systolic and diastolic stress and resulted in increases in myocardial stiffness and in the stress/diameter ratio similar to values observed in developing hypertension. During stable hypertension, LV end-diastolic stress, peak filling rate, and both parameters of late-diastolic function (myocardial stiffness and stress/diameter ratio) returned toward control values, but the isovolumic relaxation time constant was increased. Quantitative histological evaluation revealed no increase in stainable connective tissue in dogs with stable hypertension compared with control dogs, and hydroxyproline concentration was not increased in the subendomyocardium, midmyocardium, or subepimyocardium of the dogs with chronic perinephritic hypertension. Thus, in developing hypertension, major alterations in diastolic function were observed that were not structurally related, since these changes 1) could be induced in normal dogs by increasing preload and afterload acutely with phenylephrine and 2) were improved during the ensuing stable period of hypertension.

Adenosine↗
PubMed1990

Clinical assessment of ventricular ejection dynamics with and without outflow obstruction.

With the advent of multisensor micromanometric/velocimetric catheterization, digital angiography and Doppler and color echocardiography, extensive fluid dynamic quantitation is now possible in cardiology. Such high fidelity instantaneous measurements offer the clinician the prospect of identifying phasic changes in ventricular ejection dynamics that may disclose contraction abnormalities before overt muscle or pump failure is manifested. Accordingly, this review provides a basis for interpreting these measurements and a conceptual framework for understanding ventricular ejection dynamics with and without outflow obstruction. Necessary terminology and fluid dynamic background, including properties of flows generated by large transient forces, Euler and unsteady Bernoulli equations and local and convective acceleration gradients, are reviewed first. Physiologic aspects of ejection dynamics and transvalvular and intraventricular gradients without obstruction are discussed. Maximal outflow acceleration, rather than ejection velocity, coincides with the attainment of the early peak of the nonobstructive pressure gradients. These gradients are characteristically even more asymmetric than are the associated ejection velocity signals. Clinical correlations are introduced, beginning with obstructive transvalvular and subvalvular gradients in aortic stenosis and the phenomenon of recovery of pressure loss in the poststenotic dilation. The large obstructive gradients tend to be distinctively symmetric, as are the ejection waveforms, whose configuration they track more or less closely, depending on the degree of stenosis and relative preponderance of convective effects throughout ejection. Pitfalls in some unwarranted applications of the "simplified Bernoulli equation" are pointed out. Polymorphic gradients of hypertrophic cardiomyopathy, reflecting dynamically dissimilar intraventricular flow regimes in early, mid and late systole, are examined. Enormous late systolic gradients can be associated with progressive shrinkage of flow passage area and sharp increases in linear velocity while volumetric outflow is diminutive. The concept of ventriculoannular disproportion in dilated ventricles is defined and discussed. The implications of ejection fluid dynamics for systolic ventricular and myocardial loading are examined, and the concept of complementarity and competitiveness between intrinsic and extrinsic load components is introduced. Finally, critical research issues are identified and addressed. The primary emphasis is on using the basic principles of fluid dynamics to better understand ejection in the normal or abnormal human left ventricle and aortic root.(ABSTRACT TRUNCATED AT 400 WORDS)

Aortic Valve Stenosis↗
PubMed1989

Estimation of the ratio of pulmonary to systemic pressures by pulsed-wave Doppler echocardiography for assessment of pulmonary arterial pressures.

This study describes a method for estimation of the ratio of pulmonary to systemic pressures by pulsed-wave Doppler echocardiography. Sixty-eight patients ages 1 day to 68 years who underwent cardiac catheterization had Doppler studies of the right and left ventricular outflows. Preejection period (PEP), ejection time (ET) and mean acceleration to peak velocity (ACCm) were measured on each waveform. The expression: F = (PEP x ACCm)/ET was calculated for right and left ventricular outflows as an index of the effects that the interaction between ventricular contraction and afterload has on the shape of the Doppler waveforms generated in each outflow. The quotient of (F for the right outflow)/(F for the left outflow), or waveform contour ratio, was used to express the degree of pressure-dependent variability between each subject's right and left ventricular outflow tracings. The waveform contour ratio was strikingly similar to the ratio of systolic pulmonary to systemic pressures and also closely correlated to the ratio of mean pressures. The product of waveform contour ratio and arm systolic pressure gave a consistently accurate estimate of systolic pulmonary pressures. It is concluded that the present method can be used successfully for the noninvasive assessment of pulmonary arterial pressures.

Adolescent↗
PubMed1987

Hemodynamics of the Mueller maneuver in man: right and left heart micromanometry and Doppler echocardiography.

Ten subjects with normal hemodynamics were studied during elective cardiac catheterization with right and left heart multisensor micromanometry to assess hemodynamic responses to the Mueller maneuver. Simultaneous right and left circulatory hemodynamics and left ventricular, pulmonary arterial, and aortic pressures were recorded, in addition to pulmonary arterial and aortic flow velocities. Steady-state cardiac outputs were determined by thermal dilution. Aortic systolic and mean pressures were not significantly changed during the Mueller maneuver, in contrast to a lower diastolic (p = .019) and higher pulse pressure (p = .016). Mean right atrial pressure (+/- SE) decreased from 7 +/- 1 to -17 +/- 4 mm Hg (p = .0002) and the right atrial "x" descent was markedly accentuated. Left ventricular end-diastolic pressure decreased from 12 +/- 4 to -3 +/- 13 mm Hg (p = .0025). Systemic vascular resistance and left ventricular peak positive dP/dt were increased during the Mueller maneuver (p less than .02), cardiac output and stroke volume were reduced (p less than .05), and there was no significant change in heart rate. Right and left peak flow velocities showed a trend toward a bilateral decrease (right, p = .054; left, p greater than .1), and times to peak flow velocity were increased in the pulmonary artery (p = .007) and reduced in the aortic root (p = .03). Normal subjects were studied separately by pulsed Doppler echocardiography. During the sustained Mueller maneuver, the internal jugular and right ventricular dimensions decreased, and superior vena cava Doppler flow was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Nonobstructive left ventricular ejection pressure gradients in man.

Simultaneous intraventricular pressure gradients and ejection flow patterns were measured by a multisensor catheter in 6 patients with normal left ventricular function and no valve abnormalities, at rest and in exercise. Peak measured intraventricular pressure gradients were attained very early in ejection, amounted to 6.7 +/- 1.9 (SD) mm Hg at rest, and were intensified to 13.0 +/- 2.3 mm Hg during submaximal supine bicycle exercise. The augmentation of the gradients during exercise was associated with a pronounced accentuation of the flow acceleration and flow at the instant of peak gradient. A peak flow, the intraventricular gradients amounted to 5.4 +/- 1.7 mm Hg at rest and 10.0 +/- 1.8 mm Hg during submaximal exercise. The exercise-induced enhancement of the measured intraventricular pressure difference at the time of peak flow was underlain by an accentuation of the peak flow itself. A semiempirical fluid dynamic model for ejection was applied to the pressure gradient and simultaneous outflow rate and acceleration data to identify the contributions by local and convective acceleration effects to the instantaneous intraventricular gradient values. The peak intraventricular pressure gradient, which is attained very early in ejection, is mostly accounted for by local acceleration effects (85 +/- 5% of the total). Conversely, at peak flow only convective acceleration effects are responsible for the measured pressure gradient. Thus, when inertial effects are augmented, as in exercise and other hyperdynamic states, the intrinsic component of the total left ventricular systolic load can be substantial, even with no outflow tract or valve abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Myocardial relaxation and passive diastolic properties in man.

We have developed a model for assessing the influence of the decaying contractile systolic tension on diastolic wall dynamics and the passive properties of left ventricular muscle. Total measured left ventricular diastolic pressure and stress (sigma T) are determined by two overlapping processes: the decay of actively developed pressure and stress (sigma A) and the buildup of passive filling pressure and stress (sigma*). The decaying contractile stress sigma A is formulated in terms of a relaxation pressure with a time constant (T) assessed during the isovolumic relaxation interval. By subtracting the contribution of sigma A from sigma T we obtain sigma*. With micromanometry, echocardiography, and cineangiography, total and passive stress-strain relations and strain rates were evaluated over the entire filling period in six normal control subjects and in seven patients with aortic stenosis. Elastic stiffness constants (k), the slopes of the linear passive stiffness vs sigma* relations, did not differ in the two groups over a common lower stress range (6/6 normal, k = 9.37 +/- 1.23; 7/7 aortic stenosis, k = 9.34 +/- 1.08). Over a higher sigma* range, transition into a much steeper linear region occurred, and k values were much larger (4/7 aortic stenosis, k = 28.76 +/- 2.02). When diastolic stress levels are elevated, passive stiffness-stress relations can be better described as bilinear, with a much greater wall stiffness constant in the higher than in the lower stress range. Dynamic effects of decaying systolic contractile wall stress components are important in the rapid filling phase in normal hearts as well as in those with aortic stenosis.

Angiocardiography↗
PubMed1985

Different effects of two types of ischemia on myocardial systolic and diastolic function.

Acute increases in left ventricular (LV) diastolic pressure relative to volume occur during angina in humans and after pacing tachycardia in dogs with coronary stenoses. In this study we assessed myocardial function following pacing tachycardia in dogs with coronary stenoses and compared it with function of the same myocardial segment during coronary occlusion. Also we calculated regional wall stiffness following pacing tachycardia in dogs with coronary stenoses. In anesthetized dogs with two-vessel critical (90%) coronary stenoses, ultrasonic crystals were implanted subendocardially to measure either anterior wall (AW) and lateral wall (LW) segment lengths (SL; n = 14) or LV wall thickness (h; n = 7). LV pressure was measured using a high-fidelity micromanometer catheter. After pacing tachycardia in dogs with two-vessel coronary stenoses, there was a substantial rise in LV end-diastolic pressure (from 6 +/- 1 to 15 +/- 1 mmHg; P less than 0.001), a slight increase in end-diastolic segment length (AWEDSL from 15.6 +/- 1.0 to 16.4 +/- 1.0 mm; p less than 0.01; and LWEDSL from 13.8 +/- 1.4 to 14.3 +/- 1.4 mm; P greater than 0.01) and a reduction of percent systolic shortening of the ischemic segments. An upward shift of the diastolic pressure-SL relation was observed in the postpacing period. During coronary occlusion the diastolic pressure-SL relation of the same segment shifted rightward, or rightward and downward, and systolic shortening became holosystolic bulging. Ischemia due to coronary stenoses plus increased O2 demand had substantially different effects on regional wall motion and segmental diastolic mechanics than did ischemia due to coronary occlusion. Over the same range of residual transmural LV diastolic pressure, the radial stiffness modulus was higher after pacing tachycardia in the presence of coronary stenoses.

Animals↗
PubMed1985

Contribution of activation-inactivation dynamics to the impairment of relaxation in hypoxic cat papillary muscle.

Previous investigation of conventional isometric twitches of normothermic cat papillary muscle has shown that hypoxia prolongs relaxation, and this prolongation is actually accentuated during early reoxygenation. Our aim was to identify how hypoxia and reoxygenation affect the coupled processes of activation and inactivation that govern the time course of internally generated contractile tension (Ti). Activation and inactivation are modeled as first-order processes with rate constants ka and ki, respectively, and the overall isometric muscle as an underdamped second-order lag system driven by Ti. The analytical expression (To) for the externally recorded tension is dominated by two exponential terms incorporating ka and ki. Accurate least-squares fits of digitized twitches to To yielded estimates of ka and ki at 1- to 3-min intervals during control oxygenation, hypoxia, and early and late reoxygenation. Results follow. Compared with control, normothermic hypoxia prolonged activation [at 15 min ka decreased 61% from control, 35.5 +/- 6 (SE) s-1, P less than 0.05] and accelerated inactivation (at 15 min, ki increased 69% from control, 6.0 +/- 0.5 s-1, P less than 0.05). In early reoxygenation (1-3 min) activation remained impaired and inactivation returned to control levels (ki decreased 16% from control, NS). In late reoxygenation (15 min) both processes reverted to control. Thus inactivation kinetics can be dissociated from activation kinetics. Impaired relaxation in normothermic hypoxia is due to prolonged activation, whereas inactivation is actually accelerated. The further impairment of relaxation in early reoxygenation is due to rapid return of inactivation to control at a time when activation is still prolonged.

Animals↗
PubMed1984

Measurement of arterial pressure-dimension relationships in conscious animals.

Currently, considerable clinical interest exists in the vasoactivity of large coronary arteries due to the prevalence of coronary vasospasm in mediating angina pectoris and even myocardial infarction. Although arterial elastic properties have been studied extensively in acute, anesthetized animal experiments and in vitro preparations, few data are available on these properties in conscious, chronically instrumented animals, where the complicating influences of anesthesia, recent surgery, and acute manipulation of the vessel are minimized. To study vascular smooth muscle in the conscious animal we modified the transit-time dimension measurement technique by designing smaller, higher frequency (7 MHz) transducers, and introducing electronic refinements to accurately measure smaller dimensions (2 mm minimum). We applied this technique to the left circumflex coronary (LCC) artery, along with arterial pressure measurements from either chronically implantable strain-gauge manometers, or microtip catheter manometers, to study dynamic compliance and vascular control mechanisms of these arteries for periods of months in conscious, chronically instrumented animals. Infusion of an alpha-adrenergic vasoconstrictor, methoxamine (50 micrograms/kg/min), caused sustained reduction in LCC diameter (9% +/- 2%) at a time when mean arterial pressure rose by 65% +/- 5% and heart rate and mean coronary blood flow (electromagnetic flow probe) were returned to control levels. Methoxamine induced a marked leftward shift in the pressure-diameter and stress-radius relationships, reducing vascular caliber for any given stress and pressure level. Moreover, smooth-muscle activation raised the effective incremental modulus (Einc) of the coronary arterial wall when compared at similar radii, but it reduced Einc when compared at similar stress or pressure levels. Thus, for any given arterial pressure level the Einc of the LCC artery wall can be reduced considerably by the enhanced smooth-muscle activation elicited by methoxamine. Nitroglycerin (25 micrograms/kg) induced an initial decrease in LCC diameter as pressure fell and LCC blood flow rose. However, dimensions then increased, reaching a maximum 5 minutes later, when LCC blood flow was reduced, and heart rate and left ventricular dP/dt were at control levels. The calcium-channel antagonist, nifedipine, caused similar early changes, with the increase in LCC caliber persisting for 46 +/- 5 minutes while LCC blood flow returned to control in 15 +/- 3 minutes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1982

Fluid dynamics of aortic stenosis: subvalvular gradients without subvalvular obstruction.

Analysis of a tapering, pulsatile flow field predicts that substantial subvalvular pressure gradients exist in patients with valvular aortic stenosis (AS) without invoking a second anatomic site of obstruction. Using a catheter with two laterally mounted micromanometers, we examined the left ventricle in 11 patients with AS, mean age 64 +/- 11 years (+/- SD); the mean valve area was 1.0 +/- 0.3 cm2. Simultaneous measurements were made in (1) the left ventricular (LV) chamber and the LV outflow tract (LVOT) and (2) the LVOT and ascending aorta (AO). No patient had anatomic evidence of a subvalvular obstruction, but large subvalvular gradients were present in all. The average peak LV-LVOT and LV-AO gradients were 41 +/- 17 mm Hg and 58 +/- 23 mm Hg, respectively. Flow velocity was electromagnetically derived in two patients. The LV-LVOT gradient was associated with an increased flow velocity in the LVOT. This study suggests that large subvalvular gradients are present in AS and help overcome blood's inertia to convective and local accelerations in the tapering subvalvular flow field.

Adult↗