Left Ventricular Cavity Area Research Articles

Acetaminophen and Myocardial Stunning after Transient Ischemia in Rabbit Hearts

Myocardial stunning is a lingering contractile dysfunction that occurs after brief ischemia, even in the absence of necrosis. Recent studies have shown that acetaminophen may have some benefit on the return of left ventricular function after brief global ischemia in an in vitro model. This study was conducted to determine whether treatment with acetaminophen results in enhanced myocardial tolerance to transient ischemia-reperfusion by improving left ventricular function and decreasing stunning in an in vivo model. Anesthetized, open-chest rabbits were randomized to receive acetaminophen (37 mg/kg, n = 13) or saline (n = 11) 15 minutes before a series of transient coronary artery occlusions followed by reperfusion (three 10-minute periods of ischemia with 5 minutes reperfusion between). Hemodynamics and maximal and minimal values of developed pressure velocity (dP/dt) were measured at baseline, during ischemia, and throughout 2 hours of reperfusion. To assess myocardial stunning, echocardiography was used to determine regional systolic wall thickening fractions and global indices of function such as LV cavity dimensions and ejection fraction. Hemodynamic variables, including left ventricular systolic pressure and positive and negative dP/dt, were similar in both groups throughout the study. Left ventricular end-diastolic pressure was significantly lower in the acetaminophen group during occlusion and early reperfusion. The repeated short periods of ischemia in the free wall of the heart caused myocardial stunning in both groups. During ischemia, contractile function in the free wall was severely reduced, and although it improved during reperfusion, dysfunction persisted in the postischemic free wall after 2 hours of reflow, recovering to less than 52% of preischemic values (P < .01). The degree of dysfunction was similar in both groups. During ischemia, the end-diastolic left ventricular cavity area increased from 1.14 +/- 0.05 cm2 at baseline to 1.33 +/- 0.08 cm2 (P < .05) in controls, but had recovered after 2 hours of reflow. The end-diastolic area in acetaminophen-treated hearts increased from 1.13 +/- 0.08 cm2 at baseline to 1.35 +/- 0.08 cm2 during ischemia and also recovered 2 hours later. No significant differences in LV cavity areas were noted between the groups. Acetaminophen had no effect on changes in ejection fraction, which decreased similarly in both groups during ischemia to approximately 75% of baseline values. Although ejection fraction improved, it remained depressed at the end of reflow in both groups. Data from this study show that in a rabbit model of myocardial stunning, acetaminophen has a neutral effect on hemodynamics, recovery of fractional thickening, and on indices of global recovery such as left ventricular cavity dimensions or ejection fraction. Thus in the setting of experimental myocardial stunning, treatment with acetaminophen was safe but not cardioprotective.

Effects of Postischemic Regional Left Ventricular Diastolic Wall Motion Abnormalities or Delayed Relaxation Following Coronary Vasospasm on Global Diastolic Function

Regional left ventricular (LV) diastolic wall motion abnormalities detected by color kinesis (CK), an echocardiographic technique, may be a more sensitive measure to postischemic damage following coronary spasm than parameters of global diastolic function. Regional LV diastolic wall motion was evaluated by using CK in 18 patients with variant angina on the day following coronary spasm, which was induced by intracoronary acetylcholine. Fractional regional LV cavity area expansion in the short-axis view during the first 30% of the LV filling time, was used to identify postischemic asynchronous diastolic wall motion. Regional delayed relaxation was observed in any of the LV regions in all the patients, who were divided into 2 groups (Group S: 7 patients with single-vessel spasm with regional delayed relaxation in one area. Group M: 11 patients with multivessel spasm or spasm of the proximal left anterior descending branch with regional delayed relaxation in multiple areas). In Group S, no abnormality (0%) was noted in any of the indexes of global diastolic function including the isovolumic relaxation time, the ratio of peak rapid filling to peak atrial filling velocities and the deceleration time. In contrast, in 5 (45%) of the Group M patients, abnormalities were noted in all of those indexes. Postischemic regional LV-delayed relaxation following coronary vasospasm was detected sensitively by analysis of CK images. The indexes of global LV diastolic function are insensitive to postischemic damage following single vessel spasm, although they are somewhat sensitive following multivessel spasm.

Effect of antecedent systemic hypertension on subsequent left ventricular dilation after acute myocardial infarction (from the Survival and Ventricular Enlargement trial)

Whether antecedent systemic hypertension influences the risk of subsequent left ventricular (LV) dilation in patients after an acute myocardial infarction with LV systolic dysfunction is unclear. We assessed echocardiographic evidence of ventricular remodeling from baseline (mean ± SD 11 ± 3 days) to 2 years after an acute myocardial infarction in 122 hypertensive (defined as a history of treated hypertension, baseline systolic blood pressure ≥140 or baseline diastolic blood pressure ≥90 mm Hg) and 334 nonhypertensive patients in the Survival and Ventricular Enlargement echocardiographic substudy. Compared with nonhypertensives, baseline heart size, defined as the sum of the average short- and long-axis LV cavity areas, was similar (70.1 ± 11.9 vs 68.8 ± 11.2 cm 2, p = 0.33 at end-diastole; 50.1 ± 11.3 vs 48.8 ± 10.8 cm 2, p = 0.31 at end-systole), but short-axis LV myocardial area (24.7 ± 4.3 vs 25.7 ± 5.0 cm 2, p = 0.043) and wall thickness (1.15 ± 0.16 vs 1.21 ± 0.17 cm, p = 0.004) at end-diastole were greater among hypertensives. The myocardial infarct segment lengths were similar in the 2 groups (p = 0.22). Although LV cavity areas increased significantly in the 2 groups from baseline to 2 years (p ≤0.001), the increase was significantly greater in hypertensives than in nonhypertensives (+5.6 ± 11.5 vs +2.2 ± 10.7 cm 2, p = 0.005 at end-diastole; +6.23 ± 12.75 vs +2.94 ± 11.4 cm 2, p = 0.012 at end-systole). There was no concomitant difference in the change in LV myocardial area or LV wall thickness between the 2 groups (p >0.30). After adjusting for known confounders, antecedent hypertension was associated with a doubling of the risk of LV dilation (50.8% vs 37.7%, odds ratio 2.09, 95% confidence interval 1.27 to 3.45, p = 0.004). This association was not modified by diabetes mellitus, myocardial infarct segment length, or captopril use (all p values for interaction >0.10). We conclude that antecedent hypertension is associated with subsequent LV dilation in patients after acute myocardial infarction with LV systolic dysfunction.

Cardiac ventricular performance in the appropriate‐ for‐gestational age and small‐for‐gestational age fetus: relation to regional cardiac non‐uniformity and peripheral resistance

To investigate the relationship between parameters of diastolic function, loading conditions and remodeling of the left ventricle in the appropriate-for-gestational age and small-for-gestational age fetus. Two-dimensional echocardiographic left ventricular images were digitized in 24 appropriate-for-gestational age and 14 small-for-gestational age fetuses. The maximal short axis and long axis were measured. The left ventricular contour was divided into 12 segments. The changes in whole left ventricular cavity area were calculated for ventricular global area change assessment. The coefficient of variation for segmental fractional area change was calculated for the evaluation of left ventricular regional wall motion non-uniformity. Mean left ventricular long axis/short axis ratio in the small-for-gestational age fetus (1.11 +/- 0.08) was smaller (P < 0.01) than in the appropriate-for-gestational age fetus (1.75 +/- 0.26). Mean fractional area change in the small-for-gestational age fetus was larger (P < 0.01) than in the appropriate-for-gestational age fetus (37.8 +/- 17.6% vs. 21.1 +/- 9.9%). Mean left ventricular global area change in the small-for-gestational age fetus was smaller (P < 0.05) than in the appropriate-for-gestational age fetus (53.2 +/- 7.4% vs. 61.5 +/- 10.3%). Mean ventricular isovolumic relaxation time in the appropriate-for-gestational age fetus was shorter (P = 0.03) than in the small-for-gestational age fetus (37 +/- 6 ms vs. 57 +/- 9 ms). Mean transmitral E-wave/A-wave ratio in the small-for-gestational age fetus was smaller (P < 0.01) than in the appropriate-for-gestational age fetus (0.69 +/- 0.08 vs. 0.80 +/- 0.08). A negative correlation (P < 0.05) was demonstrated between: (i) fractional area change and global area change in both small-for-gestational age (r = -0.62) and appropriate-for-gestational age fetuses (r = -0.58); (ii) umbilical artery systolic/diastolic ratio and transmitral E-wave/A-wave ratio in both appropriate-for-gestational age (r =-0.58) and small-for-gestational age (r = -0.60) fetuses. A positive correlation existed between fractional area change and isovolumic relaxation time in the small-for-gestational age fetus (r = +0.72; P < 0.01). The changes in ventricular shape, wall motion, spatial non-uniformity and diastolic function in the small-for-gestational age fetus could be considered as adaptive changes, known as ventricular remodeling. It is proposed that the leading cause of ventricular remodeling in the small-for-gestational age fetus is chronic pressure overload due to increased placental vascular resistance.

Improvement of left ventricular remodeling and function by hydroxymethylglutaryl coenzyme a reductase inhibition with cerivastatin in rats with heart failure after myocardial infarction.

Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) attenuate angiotensin II-induced cellular signaling. Because angiotensin II is involved in left ventricular (LV) remodeling after myocardial infarction (MI), we examined the effects of statin treatment in an experimental model of chronic heart failure after MI. Rats with extensive MI were treated with placebo or cerivastatin (0.3 mg/kg per day) as a dietary supplement or via gavage for 11 weeks starting on the 7th postoperative day. Infarct size and cholesterol levels were similar among all groups. LV cavity area, an index of LV dilatation, was reduced in MI rats on cerivastatin compared with placebo. LV end-diastolic pressure was increased in MI rats on placebo (24.1+/-4.1 mm Hg versus sham: 5.1+/-0.3 mm Hg; P<0.01), and it was significantly reduced by cerivastatin treatment (13.7+/-2.7 mm Hg; P<0.05 versus placebo). Cerivastatin partially normalized LV dP/dt(max) and dP/dt(min), indices of LV systolic and diastolic function, which were significantly reduced in MI rats on placebo. Improvement of LV function by cerivastatin was accompanied by a reduced expression of collagen type I and beta-myosin heavy chain. LV endothelial nitric oxide synthase was increased, whereas the nitrotyrosine protein level was decreased in MI rats by cerivastatin treatment. Cerivastatin improved LV remodeling and function in rats with heart failure. This effect was associated with an attenuated LV expression of fetal myosin heavy chain isoenzymes and collagen I. Statin treatment may retard the progression of chronic heart failure.

Defibrillation and the geometry of the heart: a novel measurement with implications fordefibrillation mechanisms

We present a novel measurement for studying defibrillation mechanisms:the time course of changes in the size of the left ventricular (LV) cavitywithin 500 ms following defibrillation. Mechanical changes can be linked toelectrical mechanisms via an understanding of excitation-contraction coupling.Eight mongrel dogs were internally defibrillated 5-50 seconds (includingbackup shocks) after the onset of 20 ventricular fibrillation (VF) episodesper animal. Two dimensional, short axis, LV cavity, ultrasound images wererecorded at 30 frames per second just prior to inducing VF, duringdefibrillation and following the shock. Each frame was individually analysedto yield the LV cavity area as a function of time. Defibrillation shocks werefollowed by a highly reproducible phenomenon: (1) a dramatic and rapidincrease in LV area, (2) a more or less prominent LV area plateau and (3) adecrease in the LV area. The peak fractional area increase ranged from 1.65 to4.64 times larger than the baseline (LV area just prior to defibrillation),averaging 2.18±0.686. Successful shocks took significantly longer (p < 0.01)to return to 1.3 times the baseline (407±209 ms) than unsuccessful shocks(296±130 ms). Extrapolating to electrical mechanisms, our novelmeasurement demonstrates that defibrillation causes immediate relaxation andtherefore suggests a significant role for de-excitation in defibrillation.

Coronary Artery Disease Modifies Left Ventricular Remodelling due to Heavy Alcohol Consumption

Coronary artery disease (CAD) and excessive alcohol use can both damage the myocardium. Their combined effect on the heart muscle has not been characterized. We set out to assess whether the presence of CAD modifies the effects of chronic alcohol consumption on the left ventricular (LV) structure in middle-aged men. A postmortem examination was performed on 700 Finnish men (age range, 33-70 years) who experienced a sudden, nonhospital death. A coronary arteriography and measurement of the LV wall thickness, cavity area, and ratio by planimetry of transversal ventricular slices were done at the autopsy. The men were grouped by the most severe coronary artery diameter stenosis (<30%, 30-60%, >60%) and by daily alcohol dose (<12 g, 12-72 g, 72-180 g, >180 g) estimated by a structured interview of their lifetime partner. Analysis by ANCOVA, adjusted for age, body size, smoking, hypertension, and diabetes, showed a statistically significant interaction between the effects of coronary artery stenosis and daily alcohol dose on the LV cavity area (p = 0.037) and on the LV wall thickness/cavity area ratio (p = 0.018). In the group with <30% stenosis, the LV wall thickness/cavity area ratio (mean +/- SEM) increased from 1.6 +/- 0.2 mm/cm2 in men drinking <12 g/day to 6.2 +/- 1.4 mm/cm2 in men drinking 72-180 g/day (p = 0.021). A similar trend was seen in men with 30-60% coronary stenosis (p = 0.32). By contrast, in men with >60% coronary stenosis, the LV wall thickness/cavity area ratio decreased with increasing daily alcohol use from 2.2 +/- 0.3 to 1.4 +/- 0.1 mm/cm2 (p = 0.27). CAD modulates the effects of alcohol on the heart muscle. Heavy drinking results in concentric LV remodelling in men with no or only mild coronary artery stenoses whereas an opposite trend is seen in men with severe coronary artery obstructions. The mechanism of the interaction remains unknown.

Effect of transmyocardial laser revascularization on chronic ischemic hearts in sheep.

We investigated the effect of transmyocardial laser revascularization (TMR) on myocardial function and regional blood flow in an animal model of ischemic heart disease. Chronic ischemia was induced in 11 sheep by the application of coronary stenosis on the left anterior descending (LAD) and circumflex coronary artery (LCX). Ten weeks later, in six of them, transmyocardial channels were created in the anterior free wall and in the posterior wall of the left ventricle. Five animals served as controls. The myocardial function was assessed by echocardiography taken at baseline and every 2 weeks after coronary stenosis and after TMR. Myocardial perfusion was measured by colored microspheres, injected at baseline, immediately after coronary stenosis, before and after TMR, and at 20 weeks after coronary stenosis. The hearts were retrieved at 20 weeks for light microscopic examination. The left ventricular end-diastolic and end-systolic cavity area was elevated 20 weeks after coronary stenosis in the control and TMR groups. There was no difference between groups (analysis of variance; ANOVA, non-significant). The wall thickening fraction (WTF) decreased progressively and significantly after coronary stenosis in both groups. The WTF was further acutely reduced by TMR, and recovered gradually to the pre-TMR level. No significant difference in WTF was observed between the TMR and control groups. The resting myocardial blood flow was significantly increased by TMR at 20 weeks (P=0.03). Light microscopic examination revealed channel patency in 49% of the laser scars at 10 weeks post-TMR. A dense capillary network was observed at the edges of the surrounding scar. In an experimental model of ischemic heart disease, TMR developed angiogenesis in the lased channels, but, however, failed to improve myocardial function.

Nicardipine Intravenous Bolus Dosing for Acutely Decreasing Arterial Blood Pressure During General Anesthesia for Cardiac Operations: Pharmacokinetics, Pharmacodynamics, and Associated Effects on Left Ventricular Function

The objective of this study was to evaluate the efficacy of nicardipine, a dihydropyridine calcium channel antagonist, administered as an IV bolus dose to acutely decrease arterial pressure in anesthetized cardiac surgical patients. We performed a double-blind, randomized, self-controlled, dose-ranging study in 40 adult cardiac surgical patients to determine the pharmacokinetics and pharmacodynamics of nicardipine 0.25 mg, 0.50 mg, 1.00 mg, and 2.00 mg administered as an IV bolus. Transesophageal echocardiography was used to assess left ventricular preload, afterload, and global systolic function. Plasma nicardipine concentration was measured using high-performance liquid chromatography. Nicardipine selectively decreased arterial pressure in a dose-dependent manner with a maximum response within 100 s and recovery to half the maximum response within 3-7 min without associated changes in heart rate. The decreases in arterial pressure were associated with only small decreases in left ventricular end-systolic wall stress and small increases in global left ventricular systolic function without changes in left ventricular end-diastolic cavity area or cardiac output. The time course for nicardipine bolus was consistent with a two-compartment pharmacokinetic model with rapid redistribution from a small central compartment. Nicardipine was effective for selectively decreasing arterial blood pressure acutely, but had no effects on ventricular preload or cardiac output. The absence of dose-dependent changes in cardiac output, left ventricular systolic performance, and left ventricular afterload despite significant decreases in arterial pressure suggested that nicardipine had a small negative inotropic action.

Nicardipine Intravenous Bolus Dosing for Acutely Decreasing Arterial Blood Pressure During General Anesthesia for Cardiac Operations: Pharmacokinetics, Pharmacodynamics, and Associated Effects on Left Ventricular Function

The objective of this study was to evaluate the efficacy of nicardipine, a dihydropyridine calcium channel antagonist, administered as an IV bolus dose to acutely decrease arterial pressure in anesthetized cardiac surgical patients. We performed a double-blind, randomized, self-controlled, dose-ranging study in 40 adult cardiac surgical patients to determine the pharmacokinetics and pharmacodynamics of nicardipine 0.25 mg, 0.50 mg, 1.00 mg, and 2.00 mg administered as an IV bolus. Transesophageal echocardiography was used to assess left ventricular preload, afterload, and global systolic function. Plasma nicardipine concentration was measured using high-performance liquid chromatography. Nicardipine selectively decreased arterial pressure in a dose-dependent manner with a maximum response within 100 s and recovery to half the maximum response within 3–7 min without associated changes in heart rate. The decreases in arterial pressure were associated with only small decreases in left ventricular end-systolic wall stress and small increases in global left ventricular systolic function without changes in left ventricular end-diastolic cavity area or cardiac output. The time course for nicardipine bolus was consistent with a two-compartment pharmacokinetic model with rapid redistribution from a small central compartment. Implications Nicardipine was effective for selectively decreasing arterial blood pressure acutely, but had no effects on ventricular preload or cardiac output. The absence of dose-dependent changes in cardiac output, left ventricular systolic performance, and left ventricular afterload despite significant decreases in arterial pressure suggested that nicardipine had a small negative inotropic action.

Temporal dissociation of left ventricular function and remodeling following experimental myocardial infarction in rats

Background: Left ventricular function early after myocardial infarction (MI) predicts subsequent clinical outcome. Nevertheless, the relationship between early changes in left ventricular function and subsequent left ventricular remodeling has not been well defined. Methods and Results: To explore the temporal relationship between left ventricular function and remodeling after MI, rats (n = 63) underwent coronary artery ligation with and without reperfusion at 45 or 180 minutes or a sham operation. All animals were followed up by serial echocardiography preligation; 4, 24, and 48 hours; and 1, 2, 3, 4, 6, and 9 weeks after MI. Measures of global left ventricular size and function and regional wall motion were obtained at physiological heart rates. Histological infarct sizes (range, 0% to 52%) were determined in all animals. Within 4 hours of MI, fractional area change (FAC) decreased dramatically in association with an increase in left ventricular systolic cavity area, whereas diastolic area increased more gradually. Early FAC was related to infarct size ( r = −0.82; P < .000), predicted the extent of left ventricular enlargement ( P = .0001), and remained depressed throughout the duration of follow-up. Regional wall motion excursion and systolic wall thickness decreased in the infarcted and noninfarcted regions in animals with large infarctions. Conclusions: The rate of left ventricular dilatation after MI in rats is proportional to initial left ventricular function, although left ventricular function remains relatively constant as the ventricle progressively enlarges. Regional myocardial function after a large MI is abnormal in noninfarcted as well as infarcted regions.

Load-Independent Indices of Left Ventricular Function Using Automated Border Detection.

Echocardiographic automated border detection is the ability to assess left ventricular (LV) cross-sectional cavity areas and volumes on line. This capability has enabled the use of LV pressure-volume relationships as a means to determine LV function in a manner relatively independent of loading conditions. This discussion reviews previous validation studies in animal models and humans using LV cross-sectional area as a surrogate for LV volume and the clinical applications of LV pressure-area relations. Applications of arterial pressure as a substitute for LV ejection pressure to assess pressure-area relations are also reviewed, along with the use of pressure-area relations to assess right ventricular performance. Last, preload-adjusted maximal power as an alternative load-insensitive means to determine LV performance is discussed.

Intracardiac echocardiography: computerized detection of left ventricular borders.

A semi-automated method for two- and three-dimensional analysis of intracardiac echocardiography (ICE) images and image sequences is reported based on detection of epicardial and endocardial borders using graph searching. The border detection method was applied to 50 ICE images acquired in vivo in five dogs and to 108 images in 16 volumetric ICE image sequences from eight cadaveric pig hearts. The ICE images from the in vivo study showed good correlation between computer-detected and observer-defined left ventricular (LV) cavity areas and epicardial areas (r = 0.99, y = 0.98x + 0.43 [cm2]; r = 0.99, y = 0.98x + 1.11 [cm2]; respectively). In the cadaveric hearts, the LV volumes were determined with the volume measurement error of 7.6 +/- 7.7% and 11.3 +/- 11.2% for the aortic valve and mitral valve image sequences, respectively. Our method facilitates an accurate and computationally efficient approach for the quantitative assessment of ICE image data in 2D and 3D.

Echocardiographic estimation of left ventricular cavity area with a newly developed automated contour tracking method

Development of an automated contour tracking method provides detection and tracking of the endocardial boundary using the energy minimization method without tracing a region of interest. The purpose of this study was to compare the automated contour tracking method and manually drawn methods for the measurement of left ventricular cavity areas and fractional area change. Apical four-chamber view was visualized and recorded for off-line analysis in 11 patients by means of two-dimensional echocardiography. The automated contour tracking method automatically traces the endocardial border from the recorded images and calculates left ventricular cavity areas (end-diastole and end-systole) and fractional area change. In the same images selected as end-diastole and end-systole in the automated contour tracking method, left ventricular endocardial border was manually traced to calculate left ventricular cavity areas and fractional area change. Both methods were compared by linear regression analysis for the measurement of cavity areas and fractional area change. Left ventricular areas measured by the automated contour tracking method showed an excellent correlation with those by the manual method (end-diastole: r = 0.99, y = 0.83x + 2.6, standard error of the estimate = 1.5 cm 2; end-systole: r = 0.99, y = 0.96x –0.8, standard error of the estimate = 1.2 cm 2). The mean differences between the automated contour tracking and manual methods were –3.1 ± 5.1 cm 2 and –1.6 ± 2.4 cm 2 at end-diastole and end-systole, respectively. Fractional area change determined by the automated contour tracking method correlated well with that by the manual method ( r = 0.95, y = 1.17x –6.5, standard error of the estimate = 3.4%). The mean difference between the automated contour tracking and manual methods was –0.8% ± 7.1%. In conclusion, a newly developed automated contour tracking method correlates highly with the manual method for the estimation of left ventricular cavity areas and fractional area change in high-quality images. This suggests that this new technique may be useful in the automated quantitation of left ventricular function in patients with high-quality images with no dropout and no intercavity artifact or structure. (J Am Soc Echocardiogr 1997;10:822-9.)

Intracardiac Versus Transthoracic Echocardiographic Imaging of Translation and Rotation of Left Ventricular Center of Cavity Area in Dogs

Motion of the left ventricular cavity center during the cardiac cycle was compared using transthoracic and intracardiac echocardiography. Rotation was comparable for the 2 methods, however, translation of the left ventricular cavity area center was greater with intracardiac echocardiography.

Comparison of echocardiographic acoustic quantification system and radionuclide ventriculography for estimating left ventricular ejection fraction: Validation in patients without regional wall motion abnormalities

Echocardiographic automated border detection of blood-endocardium interface is made on the basis of the principle of acoustic quantification. The automated border system is capable of providing on-line left ventricular (LV) cavity area and function. Recently, ABD algorithms have been devised to estimate LV volume on line from a long-axis image, calculated by established area-length method or Simpson's formula. To test the clinical validity of this newly developed echocardiographic method, LV volumes and ejection fraction measured by real-time acoustic quantification were compared with radionuclide ejection fraction in 24 subjects on the same day. Patients were included in the study if ≥75% of their endocardium was visualized with conventional two-dimensional echocardiography. Sixteen (66%) of 24 patients had a technically adequate conventional echocardiogram with a broad range of ventricular dimensions and systolic function. None of the study patients had regional wall motion abnormalities. Echocardiographic measurements were obtained from the LV apical four-chamber, long-axis view. Ejection fraction, determined by the acoustic quantification and by radionuclide ventriculography, showed a strong linear relation ( r = 0.92, standard error of the estimate = 4.4, p < 0.05). However, acoustic quantification overestimated the radionuclide ejection fraction with rather wide limits of agreement (3.8% ± 16.4%; bias ± 2 SD). Thus echocardiographic automated border detection technique is a reasonably accurate method for on-line assessment of LV function. (Am Heart J 1997;133:359-63.)

Left ventricular performance assessed by echocardiographic automated border detection and arterial pressure.

Automated echocardiographic measures of left ventricular (LV) cavity area are closely correlated with changes in volume and can be coupled with LV pressure (PLV) to construct pressure-area loops in real time. The objective was to rapidly estimate LV contractility from end-systolic relationships of cavity area (as a surrogate for LV volume) and central arterial pressure (Pa) (as a surrogate for PLV) in a canine model using automated algorithms. In eight anesthetized mongrel dogs, we simultaneously measured PLV, LV area, and Pa (fluid-filled catheter). End-systolic pressure-area relationships in terms of pressure-area elastance (E'es)] from pressure-area loops during inferior vena caval occlusions were determined during basal conditions (control), dobutamine infusion (5-10 micrograms.mg-1.min-1), and after bolus propranolol (2 mg/kg) with both PLV and Pa by semiautomated and automated iterative regression methods. E'es increased during dobutamine infusion and decreased after propranolol infusion in all animals and with all iterative methods. Estimates of Ees from Pa were closely correlated with E'es from PLV by both the semiautomated and automated methods (r = 0.93; P < 0.01). The relationship between E'es obtained from Pn for the two methods was also closely correlated. Although the automated methods displayed larger differences from the semiautomated iterative technique by Bland-Altman analysis, the change in E'es with all techniques during dobutamine infusion and after propranolol infusion was of similar magnitude and direction among the three techniques. Greater variability with the dobutamine runs was partially due to abnormally conducted ventricular beats that minimized the number of consecutive beats that could be used for these analyses. We conclude that on-line Pa recordings from fluid-filled catheters can be used with echocardiographic automated border detection to rapidly calculate E'es as a means to estimate LV contractility.

研究 新しい心エコー法,Acoustic quantification法による左室断面積の測定

研究 新しい心エコー法,Acoustic quantification法による左室断面積の測定

Early diastolic left ventricular inflow pressures in normal subjects and patients with dilated cardiomyopathy. Reconstruction from pulsed Doppler echocardiography.

To estimate early diastolic left ventricular inflow pressures in normal subjects and patients with dilated cardiomyopathy, and thus to assess the potential effect of restoring forces. Early diastolic left ventricular inflow pressures were reconstructed using the ventricular blood as an accelerometer, by measuring velocity at 1 cm intervals within the left ventricle from mitral ring to apex by pulsed Doppler echocardiography, and differentiating the records to obtain the acceleration. Aortic component of second heart sound (A2) was used to fix relative timings. The local pressure gradient was determined from the acceleration at each level, and the total pressure drop during the acceleration (+ peak PD) and deceleration (- peak PD) phases of the filling interval were determined by summing the local increments. The total stroke volume (SV) at the left ventricular outflow tract and the mitral stroke distances (MSD) were also determined, using the time-velocity integral at mitral ring level. Effective flow orifice area was thus SV/MSD. Inflow jet width across the mitral valve was estimated by cross sectional colour Doppler flow mapping. 32 patients with dilated cardiomyopathy with a dominant mitral E or summation wave, and 24 normal subjects of similar ages. Normal + peak PD was 3.9 (SD 0.7) v 7.4 (2.2) mm Hg in dilated cardiomyopathy (P < 0.01). Normal - peak PD was 2.5 (0.9) v 5.6 (2.8) mm Hg in cardiomyopathy (P < 0.01). Normal effective flow orifice area was 5.9 (1.3) v 1.9 (0.8) [range 0.9 approximately 3.7] cm2 in cardiomyopathy (P < 0.01). This corresponded to 71 (18)% of the end systolic cavity cross section in normals v 11 (6)% in dilated cardiomyopathy (P < 0.01). Normal cross sectional colour inflow jet width was 2.7 (0.3) v 1.5 (0.4) cm in cardiomyopathy (P < 0.01). The jet width correlated with flow width calculated from effective flow orifice area (r = 0.82, P < 0.01). (1) Total early diastolic positive and negative peak pressure drop are normally low, so that significant negative left ventricular pressures are not needed to explain normal resting early diastolic mitral flow velocities. (2) These low pressure drops are only possible with a large effective orifice area approaching end systolic left ventricular cavity area. (3) Atrioventricular pressure drops are much greater in dilated cardiomyopathy, where increased inflow accelerations are due to reduced effective flow orifice area. These disturbances will impair filling independently of any abnormality of relaxation or compliance.

Automated echocardiographic measures of right ventricular area as an index of volume and end-systolic pressure-area relations to assess right ventricular function.

On-line determination of right ventricular (RV) volume to assess its function is clinically difficult. Echocardiographic automated border detection measures of left ventricular (LV) cavity area have been shown to reflect changes in volume, and pressure-area relations have been used to estimate LV contractility. The potential for RV cavity area to estimate changes in volume and to assess RV function, however, has not been evaluated. Accordingly, the objective of this study was to determine the relation between echocardiographic automated border-detected RV cross-sectional area and true volume and to assess the potential for end-systolic pressure-area relations to estimate RV function in an isovolumically contracting isolated canine heart preparation. Eight excised dog hearts with both right and left intraventricular balloons were perfused in an ex vivo apparatus in which both ventricular volumes were controlled independently. RV area data from the level of the left midventricular short-axis plane and pressure data were recorded on a computer through a customized hardware and software interface with the ultrasound system. RV volumes were varied from 9.4 +/- 3.9 to 43.8 +/- 6.9 mL at each of three different LV volume ranges (low range, 12.5 +/- 3.8 mL; medium range, 23.9 +/- 5.6 mL; and high range, 37.5 +/- 5.4 mL). The variation of RV area during isovolumic contraction, which we called deformational area change, was considerable (1.49 +/- 0.68 cm2 mean +/- SD) but did not change significantly with changing RV and LV volumes. Linear regression analysis correlated the maximum, minimum, and mean automated border-detected RV area during isovolumic contraction with absolute volume. A predominantly linear relation was observed, with the group mean r = .98 (y = 0.16x + 0.97; SEE = 0.21 cm2). The effect of LV volume on RV area-volume relation was a significant parallel downward shift (P < .05) by increases in LV volume. End-systolic pressure-area and pressure-volume relations using simultaneously RV pressure were both highly linear and covaried with changing LV volume. Echocardiographic automated border-detected RV area reflects changes in RV volume under a constant LV volume, and the derived end-systolic pressure-area relation has potential for on-line assessment of RV function.