Rate Of Pressure Decay Research Articles

Characterization & Evaluation of Diastolic Heart Function Using the LabVIEW Signal Processing Environment

Advances in technology have enabled clinical engineers to greatly assist medical professionals in the performance of their clinical and research activities. Using the Langendorff isolated perfused rat heart preparation first discovered in 1895, heart performance can be evaluated using left ventricular pressure recordings. Although existing chart recordings are fairly useful in quantifying systolic indices such as dP/dtmax and dP/dtmin, they are largely unsuitable to assess diastolic indices, most notably the lusitropic time constant, x. This time constant is a measure of how well a heart relaxes, and it is estimated from the rate of pressure decay of the diastolic portion of the left ventricular pressure trace. The objective of this study was to develop a computerized laboratory system that would control, collect and analyze data from these experiments. Using the LabVIEW signal processing environment with a 12-bit data acquisition card, digital signal processing of left ventricular pressure data has made the difficult task of data collection and experimental control easy, and the next-to-impossible task of accurately estimating > from graphic left ventricular pressure tracings straightforward. Preliminary findings examining the effects of propofol on heart performance indicate that the curve fitting algorithm is excellent, achieving an average mean squared error of 0.81 mm Hg2 in 290 in 175 curve fitting experiments.

A New Pressure Probe Method to Determine the Average Volumetric Elastic Modulus of Cells in Plant Tissue.

A new in vivo method was used to determine an average volumetric elastic modulus ([epsilon]ave) for nongrowing cells in plant tissue. This method requires that both the relative transpiration rate, T, of the tissue and the average turgor pressure decay rate, (dP/dt)ave, of the cells are measured after the water source is removed from the plant tissue. Then [epsilon]ave is calculated from the equation [epsilon]ave = (-dP/dt)ave/T. This method was used to determine [epsilon]ave for cortical cells in stems of pea seedlings (Pisum sativum L.). The results demonstrate that [epsilon]ave increases from virtually zero at low P (approximately 0.01MPa) to approximately 10 MPa at high P (approximately 0.5 MPa). Analyses of the results indicate that the relationship between [epsilon]ave and P can be approximated by a linear function and more accurately approximated by a saturating exponential function: [epsilon]ave = [epsilon][infinity symbol][1 - exp {-k(P - Po)}], where Po is a plateau pressure (approximately 0.01 MPa), k is a rate constant (approximately 7 per MPa), and [epsilon][infinity symbol] (approximately 10 MPa) is the hypothetical maximum value of [epsilon]ave as P -> [infinity symbol]. Solutions for the turgor pressure decay (due to transpiration) as functions of time and symplasmic water mass (after the water source is removed) are derived.

Regional alternans in relaxation and the onset of pulsus alternans in the heart of the anaesthetized pig.

1. The factors leading to the alternation in myocardial contractility believed primarily responsible for pulsus alternans are not known. We examine regional and global contraction patterns in the in situ heart at stimulation rates just below the threshold for pulsus alternans to determine if events occurring in the transition to alternans can give clues to cellular mechanisms. 2. Twelve pigs were anaesthetized, the chest wall removed and regional contraction measured in three areas of the left ventricle using tripodal strain gauges. We analysed regional and global dynamics during right atrial pacing at cycle lengths 50-150 ms greater than the threshold for pulsus alternans. 3. At pacing cycle lengths 50 ms greater than that required to produce pulsus alternans seven of twelve pigs showed alternans in the maximum rate of ventricular pressure decay but none showed alternans in the maximum rate of pressure rise. Pigs showing alternans in global relaxation were more likely to show alternans in regional contracility (P < 0.05). 4. Twenty-six of the thirty-six areas sampled showed alternans in end-diastolic length at pacing rates below the threshold for pulsus alternans. In fifteen of these areas alternation in end-diastolic length occurred in the absence of alternans in measures of contractility. 5. Alternans in global measures of relaxation may simply be a manifestation of regional alternans in contractility. It is therefore not appropriate, from global haemodynamic data, to suppose that alternans in relaxation is the primary abnormality in the generation of pulsus alternans.(ABSTRACT TRUNCATED AT 250 WORDS)

Delineation of determinants of left ventricular early filling. Saline versus blood infusion.

Left atrial pressure (LAP) is often believed to play a dominant role in the determination of left ventricular (LV) early diastolic filling. In a previous study we found no significant relation between LAP and LV early filling velocity (E) but found instead a relation between E and two determinants of LV myocardial shortening (contractility and afterload). To determine if such disparate results may be related to the data ranges of the independent variables in a given population of animals, we took advantage of the differential hemodynamic effects of two modes of volume expansion: saline and whole blood. Eighteen closed-chest anesthetized dogs were instrumented with micromanometers for measurement of LV, left atrial, and aortic pressures. LV volumes were obtained with use of contrast ventriculography, pressures by micromanometry, and transmitral flow-velocity by Doppler echocardiography. After obtaining baseline measurements, group 1 (n = 9) received rapid infusion of 500 to 650 mL of saline over 10 minutes, and group 2 (n = 9) received the same volume infusion of whole blood. In terms of two known determinants of E, infusion of saline resulted in a significant increase in LAP at the moment of mitral valve opening (X1) (1.5 +/- 0.9 to 5.7 +/- 1.4 mm Hg; P < .05) and a moderate decrease in the pressure decay rate during isovolumic relaxation (tau 1/2) (22.9 +/- 2.4 to 26.3 +/- 3.5 milliseconds; P < .05). When these two factors were entered together into a multiple regression analysis with E as the dependent variable, the overall correlation was found to be significant (R = .722; P < .008), with both independent variables contributing significantly to the relation. When factors related to myocardial shortening (afterload and contractility) were added to this relation, they did not significantly improve the prediction of E. Like saline, whole blood infusion augmented X1 (1.6 +/- 2.4 to 8.8 +/- 3.2 mm Hg; P < .05) and tau 1/2 (21.5 +/- 2.6 to 32.0 +/- 6.3 milliseconds; P < .05) but also significantly increased LV afterload as measured by aortic diastolic pressure (91 +/- 10 to 110 +/- 12 mm Hg; P < .05). Multiple regression analysis of X1 and tau 1/2 with E again revealed a significant relation (R = .761; P < .002), with both independent variables contributing significantly to the relation. However, in this case, addition of contractility and afterload to the regression significantly improved the relation (R = .909; P < .001), with all four independent variables now contributing significantly to the prediction of E. Combined with our previous results, this study indicates the degree to which experimental methods can have an impact on the delineation of the determinants of a phenomenon as complex as LV early diastolic filling. Which independent variables emerge as primary determinants can be strongly influenced by the experimenter's choice of experimental design and manipulations. Specifically, experiments using volume infusion to delineate the responses of the cardiovascular system to variations in loading must allow for the hemodynamic changes that are inherent in the choice of infusate and infusion technique, especially when those interventions may significantly alter blood oxygen-carrying capacity and, in turn, differentially modify factors that affect the magnitude of the early diastolic transmitral pressure gradient.

Autogenous cardiac assist with chronic descending thoracic aortomyoplasty

Alternative surgical treatments to orthotopic cardiac transplantation are needed for patients with heart failure. We hypothesized that descending thoracic aortomyoplasty with conditioned (fatigue-resistant) latissimus dorsi muscle could provide diastolic augmentation that would improve left ventricular function. Six mongrel dogs were studied. The left latissimus dorsi muscle was wrapped clockwise around the descending thoracic aorta. Left ventricular volume was measured with a conductance catheter. Aortic and left ventricular pressures were measured with a micromanometer The following were measured after descending thoracic aortomyoplasty at baseline and with the descending thoracic aortomyoptasty stimulated 1:1 with the heart rate: stroke work, stroke volume, left ventricular peak pressure, maximum rate of increase of left ventricular pressure, diastolic relaxation time constant, peak rate of pressure decay, left ventricular end-diastolic pressure, endocardial viability ratio, mean diastolic aortic pressure, peak diastolic aortic pressure, and time-averaged aortic diastolic velocity. Before data collection, the latissimus dorsi was stimulated (5 pulses delivered at 33 Hz at a rate of 28 per minute for 4 weeks) with burst stimulation to induce fatigue resistance. Results (expressed as the mean ± the standard error of the mean) showed significant improvement in the indices of ventricular contractility (maximum rate of increase of left ventricular pressure, 1,217 ± 83 to 1,414 ± 91 mm Hg/s) and diastolc relaxation mechanics (peak rate of pressure decay, 1,152 ± 92 to 1,282 ± 79 mm Hg/s; diastolic relaxation time constant 43 ± 2 to 38 ± 2 ms). Significant differences were noted with stimulation at 1:1 in the endocardial viability ratio (0.90 ± 0.05 to 1.14 ± 0.04), an index of myocaidial oxygen supply. Systemic diastolic pressures (peak diastolic aortic pressure, 95 ± 6 to 107 ± 5 mm Hg; mean diastolic aortic pressure, 92 ± 6 to 102 ± 6 mm Hg) and the tune-averaged aortic diastolic velocity (1.5 ± 0.6 to 3.3 ± 1.0 m/s) increased significantly. We conclude that descending thoracic aortomyoplasty stimulation with conditioned latissimus dorsi muscle can improve indkes of ventricular contractility, diastolic relaxation mechanics, diastolic pressures, and diastolic aortic velocity in the nonfailed canine heart. Farther studies with the chronic failed heart model are required.

Reflections of Pressure Waves at Tunnel Portals

Reflections of plane waves from the open ends (portals) of axisymmetric pipes and plane two-dimensional (2-D) channels are investigated analytically, numerically and experimentally. An analytical approach developed by Rudinger [1] for pressure decay at an axisymmetric, flanged portal is extended to longer times, and equivalent analyses are developed for reflections from unflanged portals—both axisymmetric and plane 2-D. Predictions for the latter case are compared with numerical results from a computer program based on a 2-D method of bicharacteristics. The theoretical results are compared with measurements from a low pressure shock tube, which was used to investigate alternative end configurations including scarfed portals with and without flange plates. These confirm that the rate of pressure decay is much slower in the plane 2-D case and that flange plates further reduce the rate of decay, albeit slightly. Scarfed portals are shown to cause more uniform decay rates than 90° portals.

Efficacy of angiotensin-converting enzyme inhibition and AT1 receptor blockade on cardiac pump performance after myocardial infarction in rats.

To determine whether cardiac unloading by inhibition of angiotensin I (AI) to AII conversion by captopril or blockade of the AII receptor (AT1) by losartan was more effective in prevention of the detrimental hemodynamic consequences of myocardial infarction (MI), inhibition of metabolic production of AII by captopril was compared with blockade of AT1 with losartan in Sprague-Dawley rats with large MI. Infarcts were created by surgical occlusion of the left main coronary artery and oral drug therapy initiated immediately and continued until hemodynamic evaluation seven days later. Heart weight was unchanged in untreated infarcted animals, whereas captopril reduced heart weight in control animals and losartan increased heart weight in infarcted animals. Left ventricular (LV) peak systolic blood pressure (SBP) was lower in treated and untreated infarcted animals. Although captopril reduced end-diastolic pressure (EDP) to a greater degree than losartan, all infarcted group showed an increase in this parameter with respect to similarly treated controls. LV peak rates of pressure increase and decay in infarcted hearts were decreased significantly more by captopril than by losartan administration. Captopril also impaired right side cardiac function more than losartan when peak rate of pressure increase was evaluated. Thus, inhibition of the effects of AII during cardiac failure improved but did not normalize cardiac pump performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Time-course of left atrial performance during coronary artery occlusion followed by reperfusion in anesthetized dogs by densitometric analysis of digital atrioventriculographic images.

The left atrial (LA) function during coronary artery occlusion followed by reperfusion using densitometric analysis of digital atrioventriculographic images was evaluated. Eight anesthetized dogs underwent atrioventriculography at baseline, 10 and 60 min after left circumflex coronary artery (LCX) occlusion and 5, 30, 60, and 120 min of reperfusion. Time-density curves were obtained for LA and left ventricle (LV). The ratios of passive atrial video-densitometric change (VC) to total VC (Passive Ratio), and active VC to total VC (Active Ratio) were calculated. Left ventricular ejection fraction (LVEF), peak ejection rate (PER), and peak filling rate (PFR) were derived. Active Ratio, an index of atrial contraction, increased to 144%, and Passive Ratio decreased to 75% of baseline at 60 min of LCX occlusion. Two hours after reperfusion, both Active and Passive Ratios returned to control level. While LVEF reduced to 70%, PER to 67%, LV peak positive dP/dt to 88% of baseline at 60 min after occlusion, and remained depressed at 2 h after reperfusion. However, PFR, LV peak negative dP/dt and LV isovolumic pressure decay rate showed recovery at 2 h after reperfusion. There were significant correlations between PFR and Passive Ratio (r = 0.41), and between Active and Passive Ratios (r = 0.55). Thus, time-course of recovery of LV post-ischemic systolic and diastolic function was different. Return of LA function to control level during 2 h after reperfusion may be depend on recovery of LV diastolic function.

Dynamic cardiomyoplasty acutely impairs left ventricular diastolic function

In patients with congestive heart failure, medical treatment has a high rate of mortality and morbidity, and transplantation is limited by the availability of donor hearts. Dynamic cardiomyoplasty is being investigated as surgical therapy to improve left ventricular function in these patients. To evaluate the early postoperative effects of this procedure on left ventricular diastolic function, we studied seven dogs through the use of sonomicrometry and micromanometry in a canine model of dynamic cardiomyoplasty. Left ventricular diastolic parameters were determined before wrapping the latissimus dorsi muscle (baseline), after latissimus dorsi muscle wrap but without stimulation, and with synchronous left ventricular contraction-latissimus dorsi muscle stimulation. End-diastolic pressure was increased in both conditions after latissimus dorsi muscle wrap (without stimulation, 5 +/- 1; with stimulation, 6 +/- 2 mm Hg; p < 0.05) compared with baseline (3 +/- 2 mm Hg). The peak rate of diastolic pressure decay was greater at baseline (1560 +/- 370 mm Hg/sec) than after latissimus dorsi muscle wrap, both without (1260 +/- 330 mm Hg/sec, p < 0.01) and with (1120 +/- 420 mm Hg/sec, p < 0.01) stimulation. The constant of pressure decay was prolonged both without (53 +/- 10 seconds, p < 0.05) and with (62 +/- 11 seconds, p < 0.01) latissimus dorsi muscle stimulation compared with the baseline (38 +/- 5 seconds). Compared with baseline (0.2 +/- 0.2 cm-2), the constant of passive chamber stiffness increased after the latissimus dorsi muscle was wrapped around the heart (1.6 +/- 0.7 cm-2, p < 0.05) and with stimulation (2.1 +/- 1.0 cm-2, p < 0.01). The maximal diastolic filling rate (baseline, 18.1 +/- 6.7; without stimulation, 16.6 +/- 8.9; with stimulation, 16.6 +/- 4.1 cm2/sec, not significant) and end-diastolic short-axis area (baseline, 7.3 +/- 2.3; without stimulation, 7.4 +/- 2.1; with stimulation, 7.5 +/- 2.3 cm2, not significant) were similar among the three conditions. The latissimus dorsi muscle wrap prolonged relaxation and increased left ventricular passive stiffness. Synchronous latissimus dorsi muscle stimulation with left ventricular contraction did not improve diastolic function in this model. The results suggest that in the early postoperative period, dynamic cardiomyoplasty impairs diastolic function.

Hemodynamic and volume correlates of left ventricular diastolic relaxation and filling in patients with aortic stenosis

Objective. The aim of the present study was to evaluate the hemodynamic and volume correlates of early diastolic filling and isovolumetric relaxation in patients with aortic stenosis.Background. Left ventricular diastolic relaxation and filling have been found to be heterogeneous in patients with aortic stenosis. Potential mechanisms underlying this heterogeneity include individual differences in the severity of muscle hypertrophy or systolic dysfunction, or both, in the presence and severity of mitral regurgitation and in the level of left atrial pressure.Methods. Right (fluid-filled) and left (high fidelity micromanometer) ventricular pressures, left ventricular volumes (contrast angiography) and transmitral inflow dynamics (Doppler echocardiography) were measured in 17 patients with isolated severe aortic stenosis (valve area < 0.75 cm2). Measurements included left ventricular end-diastolic and end-systolic volumes, left ventricular ejection fraction, peak positive and negative first derivative of left ventricular pressure (dP/dt), the time constant of isovolumetric relaxation (tau), left ventricular end-diastolic pressure, left ventricular mass, left ventricular end-systolic stress, mean capillary wedge pressure and peak early (E) and late (A) transmitral filling velocities. Patients were subclassified according to left ventricular ejection performance at rest and mean capillary wedge pressure.Results. Patients with normal ejection performance and normal mean capillary wedge pressure had a normal rate of isovolumetric left ventricular pressure decay and an abnormal diastolic filling pattern, with diastolic filling occurring primarily during atrial systole. In contrast, in patients with systolic dysfunction and elevated mean capillary wedge pressure, isovolumetric pressure decay was prolonged and diastolic filling occurred essentially during the rapid filling period, with reduced atrial contribution to left ventricular filling and a short isovolumetric relaxation period. Stepwise multiple linear regression analysis identified two variables as independent predictors of transmitral velocity profile and three variables independently predictive of the rate of left ventricular pressure decay. The single most important predictor of transmitral filling pattern was the pulmonary capillary wedge pressure (p < 0.0001), followed by the left ventricular peak negative dP/dt (p = 0.002). The single most powerful predictor of the rate of reduction in left ventricular pressure was left ventricular mass index (p < 0.0001), followed by end-systolic volume index (p = 0.0002) and left ventricular peak negative dP/dt (p= 0.0029).Conclusions. In patients with aortic stenosis, left ventricular filling is essentially determined by left atrial pressure, whereas isovolumetric relaxation more closely depends on the severity of muscle hypertrophy and chamber dilation.

Chronic coronary arterial stenosis impairs alpha 1-adrenoreceptor signaling and cardiac performance in rats.

Coronary stenosis was induced in rats to determine whether chronic coronary artery constriction resulted in impairment of cardiac pump performance, alterations in alpha 1-adrenoreceptor signal transduction, and inadequate myocardial hypertrophy, and these parameters were examined 6 mo later. A 50% reduction in coronary diameter was associated with an elevation in left ventricular end-diastolic pressure, whereas left ventricular peak systolic pressure, rate of pressure rise and decay were reduced. The hypertrophic response was modest, since statistically significant increases of 11% and 23% in left and right ventricular weights were measured. Radioligand binding documented an 18% and a 38% statistically significant reduction in alpha 1-adrenoreceptor density of the left and right myocardium, respectively. ADP ribosylation of the 41-kDa substrate by pertussis toxin showed a 16% significant decrease of this parameter in the left myocardium. Moreover, a 29% decrease in norepinephrine stimulated phosphoinositol turnover was seen in myocytes, and this change was statistically significant. The depressed generation of intracellular second messengers linked to the alpha 1-adrenoreceptors was found in conjunction with a 19% significant reduction in myocardial norepinephrine content. In conclusion, the long-term effects of coronary stenosis involve impaired transduction of adrenergic signals, which, in combination with constraints on myocardial growth, may participate in the onset of ventricular dysfunction in this model.

The measurement of thermal stress distributions along the flow path in injection‐molded flat plates

AbstractInternal stresses in injection‐molded parts are the result of thermal, flow, and pressure histories. Internal stresses can be roughly divided into thermal and flow‐induced stresses. In this paper, a modified layer‐removal method is presented to determine thermal stress distributions in injection‐molded flat plates. With this method, the curvature of a rectangular specimen is determined after the removal of a layer from one surface. This curvature is converted into a stress via a mathematical relation, originally derived by Treuting and Read. By determining the local curvatures after successive layer removals, stress distributions along the flow path were obtained within a single specimen. Validation of this modified layer‐removal method is described. A good reproductibility was obtained. The method can be regarded as semi‐quantitative. Flat plates were injection‐molded from three amorphous polymers: polystyrene, polycarbonate, and a polyphenylene ether/high‐impact polystyrene blend. In general, the flat‐plate cross‐section shows a three‐region stress distribution with a tensile stress region both at the surface and in the core of the flat plate and an intermediate region with compressive stresses. The modified layer‐removal method was used to determine influences of mold temperature, annealing treatment, and pressure history on the thermal stress distributions. Increasing mold temperature results in a decreasing overall stress level, while the compressive stress region shifts to the surface. An annealing treatment significantly reduces the overall stress level, without affecting the stress pattern. Stress distributions along the flow path were influenced by the varying pressure histories from the entrance to the end of the mold cavity. The various features of the stress profiles are explained by the influence of the pressure decay rate in the injection‐molding process.

Myocardial mechanics predict hemodynamic performance during normal function and alcohol-induced dysfunction in rats

To determine whether mechanical evaluation of muscle tissue removed from the myocardium can be employed as a direct indicator of cardiac contractile performance in situ, isometric and isotonic parameters of muscle mechanics in vitro were correlated with in vivo global functional characteristics of the same heart. Twelve-month-old animals maintained on standard food and water were employed as representative of normal cardiac function. Animals of identical age with left ventricular (LV) dysfunction induced by oral alcohol (30%) ingestion from 4 to 12 mo were utilized to represent depressed cardiac performance. Accordingly, 24 h after the establishment of the hemodynamic profile for a control or experimental heart, the LV posterior papillary muscle was removed from the same heart and examined isometrically and isotonically. Least squares regression analysis was employed to establish a correlation coefficient and P values between various in vitro and in vivo parameters. Hemodynamic measurements were performed under chloral hydrate anesthesia and LV pump performance was evaluated with respect to aortic and ventricular pressures and the rates of rise and decay of the LV pressure trace. Papillary muscles were evaluated with respect to timing parameters of the isometric and isotonic twitch, the first derivative of isometric tension development, and the speed of muscle shortening at increasing physiologic loads. LV peak rate of pressure rise and decay were then correlated with the various isometric and isotonic properties. Myocardial mechanics and hemodynamics revealed depressed function in the papillary muscles and hearts from alcoholic rats. Moreover, significant correlations were found between the LV rate of pressure change (peak +dP/dt and -dP/dt) and both isometric and isotonic twitch measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

Some factors influencing air permeation measurements in cover concrete

The report concerns a method of measuring the apparent air permeability in cover concrete and the effects of air flow geometry, cracks and concrete moisture conditions. The method involved pressurizing a 20 mm diameter cavity cut 35 mm deep into the concrete and measuring the rate of pressure decay. A positive testing pressure coupled with the application of liquid soap solution permitted direct observation of air permeation as bubbles. The depth of the cavity was a critical factor and it was desirable to locate the cavity so that its centre-line was at least 40 mm from the nearest lateral surface. Cracks in the concrete increased the permeability and the variability of results. Pore water restricted air permeation through the cover concrete. Moisture conditions were conveniently monitored using a relative humidity probe in the cavity and by measuring weight losses during drying and wetting.

Leak detector for irregularly shaped containers — uses compressed air at regulated low pressure with timing and pneumatic valves measuring pressure decay rate : General Mills Inc US-395832; 4 September 1990

Leak detector for irregularly shaped containers — uses compressed air at regulated low pressure with timing and pneumatic valves measuring pressure decay rate : General Mills Inc US-395832; 4 September 1990

Left ventricular dysfunction induced by chronic alcohol ingestion in rats

To determine whether moderate ingestion of alcohol for protracted periods of time affects normal cardiac performance and produces myocyte damage, male Fischer 344 rats at 4 mo of age were given 30% ethanol in their drinking water every day for a period of 8 mo. Experimental animals and age-matched controls were examined hemodynamically and morphometrically at 12 mo of age. Body and cardiac growth were depressed in alcoholic animals by 15 and 12%, respectively. Although left ventricular (LV) weight was reduced by 14% in alcoholic rats, no difference in right ventricular (RV) weight was noted, and consequently the ratio of RV weight to body weight increased by 12%. Systemic arterial pressures as well as LV peak systolic pressure decreased in alcoholic rats despite an unchanged heart rate. Myocardial contractility in alcoholic rats was further depressed as revealed by a significant decrease in the peak rate of ventricular pressure decay. Importantly, end-diastolic pressure was elevated 5.2-fold in the left ventricle and 2.9-fold in the right ventricle after 8 mo of ethanol consumption. LV diastolic chamber volume increased through myocardial remodeling as the longitudinal axis and transverse diameters from the base to the apex increased in experimental animals while the thickness of the LV diminished. Structural and hemodynamic alterations resulted in a 571% increase in the volume of diastolic circumferential wall stress on the left ventricle. Damage to the myocardium was increased in alcoholic animals with the volume percent of myocardial lesions increasing 342% in the wall of the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Severe myocardial dysfunction induced by ventricular remodeling in aging rat hearts

To determine if aging engenders alterations in the functional properties of the myocardium and ventricular remodeling, the hemodynamic performance and structural characteristics of the left ventricle of male Fischer 344 rats at 4, 12, 20, and 29 mo of age were studied by quantitative physiology and morphology. In vivo assessment of cardiac pump function showed no change up to 20 mo, whereas left ventricular end-diastolic pressure was increased at 29 mo. Moreover, peak rates of pressure rise and decay, stroke volume, ejection fraction, and cardiac output were depressed at the later age interval, demonstrating the presence of ventricular failure at this time. The measurements of chamber size and wall thickness showed that ventricular end-diastolic and end-systolic volumes progressively increased with age with the greatest change occurring at 20-29 mo. Aging was also accompanied by a marked augmentation in the volume fraction of fibrotic areas in the ventricular myocardium that was due to an increase in their number and cross-sectional area with time. These architectural rearrangements, in combination with the abnormalities in ventricular function, resulted in an elevation in the volume of wall stress throughout the cardiac cycle. Wall stress increased by 64, 44, and 50% from 4 to 12, 12 to 20, and 20 to 29 mo of age. In conclusion, aging leads to a continuous rise in wall stress that is not normalized by ventricular remodeling. These two independent processes appear to be responsible for the onset of heart failure in the senescent rat.

Interpretation of shut-in pressure from the rate of pressure decay. Technical note : Tunbridge, L W Int J Rock Mech Min SciV26, N6, Dec 1989, P457–459

Interpretation of shut-in pressure from the rate of pressure decay. Technical note : Tunbridge, L W Int J Rock Mech Min SciV26, N6, Dec 1989, P457–459

Pulmonary venous flow determined by Doppler echocardiography in mitral stenosis

Recent studies have shown that pulmonary venous flow is normally biphasic. Both phases depend on changes in left atrial pressure that occur during the cardiac cycle. 1–3 The first phase corresponds to ventricular systole and is dependent on ventricular contraction and on a timed relaxation of the left atrium. The second phase occurs during diastole and follows the reduction in atrial pressure during the rapid transmitral flow and ventricular filling. In mitral stenosis (MS), flow rate across the mitral valve is reduced, as is the rate of left atrial pressure decay and left ventricular pressure rise. 4 These changes in left atrial hemodynamics may affect left atrial filling from the pulmonary veins. Moreover, many patients with MS have atrial fibrillation. This arrythmia results in a reduced systolic (J) phase of pulmonary venous flow. 1,5 The present study examines the pattern of pulmonary venous flow velocity in patients with MS.

Interpretation of the shut-in pressure from the rate of pressure decay

Interpretation of the shut-in pressure from the rate of pressure decay