Regional Left Ventricular Wall Thickness Research Articles

Ct Assessment Of Left Ventricular Myocardial Thickness As A Marker Of Viability: A Head-to-head Comparison With Cardiac Magnetic Resonance Late Gadolinium Enhancement

Introduction: Cardiac computed tomography is increasingly being performed prior to CTO procedures to assess the anatomy of the occluded coronary segment, to help define interventional strategy and predict success rates. Assessment of myocardial viability is predominantly a domain of echocardiography, SPECT and magnetic resonance imaging. On the other hand, CT allows particularly accurate assessment of myocardial thickness. We therefore assessed the diagnostic value of regional left ventricular wall thickness in CT to identify myocardial viability compared to myocardial late gadolinium enhancement (LGE) in cardiac magnetic resonance (CMR) imaging.

Cardiac Resynchronization Therapy for Improving Non-Uniform Thickening of Left Ventricular Wall: Assessment by Quantitative Gated Myocardial Perfusion SPECT.

Cardiac resynchronization therapy (CRT) improves cardiac dyssynchrony in heart failure patients with a wide QRS electrocardiogram (ECG). Assessment of left ventricular (LV) dyssynchrony using echocardiography or other imaging modalities is important to predict CRT effectiveness. In this study, we retrospectively evaluated cardiac nuclear imaging of ECG-gated myocardial perfusion single-photon emission computed tomography (SPECT) with 99mTc-sestamibi for CRT candidate (n = 120) with severe heart failure and wide QRS (> 120 msec) in ECG. To analyze LV non-uniformity, we used the quantitative gated SPECT (QGS) software to calculate changes in regional LV wall thickness during a cardiac cycle (i.e., wall thickening scores). Cardiac events (heart failure, ventricular arrhythmias and cardiac death) after CRT during 38 ± 22 (SD) months were also evaluated. In 97 of 120 patients who underwent QGS before and 6 months after CRT, CRT homogenized non-uniform wall thickening between septal and lateral of the LV especially in CRT responders. This observation was indicated as increase in the lateral deflection (XWT) of wall thickening scores before CRT and its decrease after CRT. In 120 patients with QGS before CRT, the larger XWT before CRT (≥ 16.5) predicted better prognoses after CRT. This finding was similarly observed even in patients with narrower baseline QRS (≤ 140 msec; n = 41 of 120), who usually have less benefits from CRT. In conclusion, CRT improved non-uniformity of wall thickening between the LV septal and lateral regions evaluated using QGS, which is predictive of better prognosis in the chronic phase after CRT.

Prevalence of Unexplained Left Ventricular Hypertrophy by Cardiac Magnetic Resonance Imaging in MESA.

BackgroundHypertrophic cardiomyopathy is defined as unexplained left ventricular (LV) hypertrophy (wall thickness ≥15 mm) and is prevalent in 0.2% of adults (1:500) in population‐based studies using echocardiography. Cardiac magnetic resonance imaging (MRI) allows for more accurate wall thickness measurement across the entire ventricle than echocardiography. The prevalence of unexplained LV hypertrophy by cardiac MRI is unknown. MESA (Multi‐Ethnic Study of Atherosclerosis) recruited individuals without overt cardiovascular disease 45 to 84 years of age.Methods and ResultsWe studied 4972 individuals who underwent measurement of regional LV wall thickness by cardiac MRI as part of the MESA baseline exam. American Heart Association criteria were used to define LV segments. We excluded participants with hypertension, LV dilation (≥95% predicted end‐diastolic volume) or dysfunction (ejection fraction ≤50%), moderate‐to‐severe left‐sided valve lesions by cardiac MRI, severe aortic valve calcification by cardiac computed tomography (aortic valve Agatston calcium score >1200 in women or >2000 in men), obesity (body mass index >35 kg/m2), diabetes mellitus, and current smoking. Sixty‐seven participants (aged 64±10 years, 9% female) had unexplained LV hypertrophy (wall thickness ≥15 mm in at least 2 adjacent LV segments), representing 1.4% (1 in 74) participants, 2.6% of men and 0.2% of women. Prevalence was similar across categories of race/ethnicity. Hypertrophy was focal in 17 (25.4%), intermediate in 44 (65.7%), and diffuse in 5 (7.5%) participants.ConclusionsThe prevalence of unexplained LV hypertrophy in a population‐based cohort using cardiac MRI was 1.4%. This may have implications for the diagnosis of patients with hypertrophic cardiomyopathy and will require further study.

Cardioprotection by placenta-derived stromal cells in a murine myocardial infarction model

BackgroundAutologous cells for cell therapy of ischemic cardiomyopathy often display age- and disease-related functional impairment, whereas an allogenic immunotolerant cell product would allow off-the-shelf application of uncompromised donor cells. We investigated the cardiac regeneration potential of a novel, clinical-grade placenta-derived human stromal cell product (PLX-PAD). MethodsPLX-PAD cells derived from human donor placentas and expanded in a three-dimensional bioreactor system were tested for surface marker expression, proangiogenic, anti-inflammatory, and immunomodulatory properties in vitro. In BALB/C mice, the left anterior descending artery was ligated and PLX-PAD cells (n = 10) or vehicle (n = 10) were injected in the infarct border zone. Four weeks later, heart function was analyzed by two-dimensional and M-mode echocardiography. Scar size, microvessel density, extracellular matrix composition, myocyte apoptosis, and PLX-PAD cell retention were studied by histology. ResultsIn vitro, PLX-PAD cells displayed both proangiogenesis and anti-inflammatory properties, represented by the secretion of both vascular endothelial growth factor and angiopoietin-1 that was upregulated by hypoxia, as well as by the capacity to suppress T-cell proliferation and augment IL-10 secretion when co-cultured with peripheral blood mononuclear cells. Compared with control mice, PLX-PAD-treated hearts had better contractile function, smaller infarct size, greater regional left ventricular wall thickness, and less apoptosis after 4 wk. PLX-PAD stimulated both angiogenesis and arteriogenesis in the infarct border zone, and periostin expression was upregulated in PLX-PAD-treated hearts. ConclusionsClinical-grade PLX-PAD cells exert beneficial effects on ischemic myocardium that are associated with improved contractile function, and may be suitable for further evaluation aiming at clinical pilot trials of cardiac cell therapy.

Underestimation of the ejection fraction using the quantitative gated SPECT for patients with myocardial hypertrophy

The aim of the present study is to quantify the degree of the error as a function of the left ventricular (LV) wall thickness, in calculation of the ejection fraction (EF) using gated single-photon emission computed tomography (SPECT). The essential error of quantitative gated SPECT (QGS) software in patients with myocardial hypertrophy has not been quantitatively estimated. Forty-six patients with known or suspected hypertrophic cardiomyopathy underwent gated myocardial perfusion SPECT and cardiac magnetic resonance (MR) imaging. The EF value was automatically calculated from gated SPECT using the QGS software. Twelve points of regional LV wall thickness and the EF value were estimated from MR images. Only a fair correlation was found between the QGS-EF and the MR-EF values (r = 0.48, y = 0.49x + 26.80, p < 0.01), and the QGS-EF was underestimated (r = 0.25, y = 0.90x) in 30 patients with myocardial hypertrophy (mean wall thickness > 12 mm). The magnitude of the error of the EF quantification from gated SPECT showed a significant negative correlation with the mean 12-point LV wall thickness in all 46 patients (r = -0.67, y = -4.12x + 40.44, p < 0.0001). The degree of the error of the ESV and that of the EDV showed positive correlation with the mean LV wall thickness (r = 0.55, y = 5.46x - 56.13, p < 0.0001; r = 0.31, y = 4.20x - 55.28, p < 0.05, respectively). The underestimation of EF increases with the degree of myocardial hypertrophy, because of the overestimation of the LV cavity especially in the end-systolic phase.

Preoperative Regional Left Ventricular Wall Thickening Determined by Quantitative Gated SPECT as a Predictor of Mid-Term Surgical Results for Ischemic and Nonischemic Cardiomyopathy

This study aimed to elucidate whether regional left ventricular wall thickening (LVWT) determined by quantitative gated SPECT (QGS) is useful in predicting surgical outcomes for ischemic (ICM) and nonischemic cardiomyopathy (NICM). The study group comprised 53 patients with either ICM (n=30, left ventricular ejection fraction (LVEF)=24.7±7.1%) or NICM (n=23, LVEF=24.0±6.3%) scheduled for surgical repair underwent preoperative QGS to evaluate regional LV function. LVWT of 20 segments derived from QGS was normalized by being divided by the normal value of each LV level. Normalized values of the segments were summed to be representative of each area. For 16 of the 30 patients with ICM and 17 of the 23 patients with NICM, surgical ventricular restoration and papillary muscle approximation (PMA) were performed for surgical repair and, for the rest, PMA alone was done for both ICM and NICM patients. Adjunctive coronary artery bypass grafting for ICM patients was added when necessary. Mean follow-up periods were 2.5±1.8 years for ICM and 2.2±2.4 years for NICM. Posterior regional LVWT in NICM (normalized sum value <0.61 n=7, ROC: AUC=0.80) predicted cardiac events (chronic heart failure and cardiac-caused death). The one-year cardiac event-free rates were 22.2% and 85.1% and the 2 years rates were 11.1% and 48.6% for the lower posterior WT group and higher posterior WT group respectively (P=0.003). Posterior LVWT can be a predictor for postoperative cardiac events in patients with NICM.

Effects of hypertrophy and fibrosis on regional and global functional heterogeneity in hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is a disease that typically has heterogeneous hypertrophy and dysfunction of the myocardium. Cardiac magnetic resonance imaging (CMR) can be used to accurately assess ventricular wall thickness and regional fibrosis. We investigated the effects of hypertrophy and fibrosis on the heterogeneity of regional and global myocardial function in HCM. Forty patients who were diagnosed with HCM were consecutively enrolled. Echocardiography and CMR with delayed hyper-enhancement imaging (DHE) was performed for each patient. Left ventricular (LV) regional and global longitudinal strain (SL(R) and SL(G)) were obtained by two-dimensional speckle tracking method on echocardiography. With CMR, regional myocardial wall thickness was measured, and the amount of DHE was calculated semi-quantitatively in each segment. Overall, 720 segments were analyzed. SL(R) was significantly decreased in the hypertrophied segments (thickness>11mm) and segments with DHE (P<0.001). SL(R) was correlated with myocardial wall thickness (r=0.47, P=0.001) and amount of regional DHE (r=0.39, P<0.001). On multivariate analysis, regional LV wall thickness and amount of DHE were the only independent determinants of SL(R). SL(G) was associated with LV diastolic functional parameters in echocardiography, total DHE volume, and LV mass index. Total DHE volume and LV mass index were independent determinants of SL(G) on multivariate analysis. The extent of regional myocardial fibrosis is associated with regional myocardial function independently of morphological changes of the myocardium, and the correlation extended to global LV function. In this context, DHE may be a useful parameter to discover early myocardial dysfunction independently of LV hypertrophy.

Left Ventricular Endocardial and Epicardial Border Length Delineation with Perflutren Contrast during Transthoracic Echocardiography

Precise estimation of wall motion abnormalities during routine echocardiography rests on optimal endocardial border visualization. Endocardial "dropout" may result in the misinterpretation of regional wall motion. Left ventricular opacification (LVO) with intravenous contrast improves the visualization of the left ventricular endocardial border length (EnBL). The purpose of this study was to determine if contrast also improves the visualization of the epicardial border length (EpBL) in addition to the EnBL. This is a single center retrospective observational study. From 200 consecutive patients referred to the Echocardiography Laboratory for the assessment and evaluation of coronary artery disease, 73 patients who received contrast were enrolled. All the images were standardized using offline software. The visualized segments of the epicardium and endocardium were measured in diastole and systole, without and with contrast-enhancement and these segments were summed to provide the total visualized EnBL and EpBL. Contrast enhanced imaging improved EnBL by 65% and 45% in end-diastolic and end-systolic views, respectively. Similarly, EpBL was improved by 61% and 57% in end-diastolic and end-systolic views, respectively (all P values <0.05). Contrast LVO improves the EnBL as previously reported. Additionally, based upon the blinded review of 1,752 regional myocardial wall segments, this study is the first to suggest that contrast also enhances the visualization of the EpBL. This finding has direct clinical implications as the improvement in both EnBL and EpBL with contrast may assist in evaluation of regional left ventricular wall thickening which is a critical parameter used to assess for myocardial ischemia.

Significance of Maximal and Regional Left Ventricular Wall Thickness in Association With Arrhythmic Events in Patients With Hypertrophic Cardiomyopathy

Increased maximal left ventricular wall thickness (LVWT; >30 mm) is a marker of risk for sudden cardiac death in hypertrophic cardiomyopathy (HCM). Patients with mild left ventricular hypertrophy (LVH) are not free of events. Regional heterogeneity of LVH may contribute to arrhythmic vulnerability. 157 HCM patients underwent assessment of maximal and regional LVWT by 2-dimensional echocardiography, and arrhythmic burden in a follow-up of a median 3.7 years. 45 patients with ventricular arrhythmic events (VAEs+ group) had larger maximal LVWT and regional LVWTs (basal anterior-B12 and equatorial inferior-EQ6 segments, P=0.05). Maximal LVWT and B12 above a cut-off value of 15 mm were associated with a significant 4.5-fold (95% confidence interval (CI) 1.1-18.8, P=0.04), 3.2-fold (95%CI 1.5-6.7, P<0.002), and EQ6 above 19 mm with 5.9-fold (95%CI 2.0-16.9, P<0.001) increased the relative risk of VAEs. Multivariate analysis identified the 2 regional measures as the only predictors, independently associated with arrhythmic risk. Non-invasive imaging measures, such as LVWT, do have a role in identifying the patients at risk of VAEs. In addition to maximal LVWT, the key regional LVWTs provide complementary information of incremental value to the conventional risk stratification model.

Quantitative assessment of regional left ventricular wall thickness and thickening using 16 multidetector-row computed tomography: comparison with cine magnetic resonance imaging

The purpose of this study was to investigate the feasibility of retrospective electrocardiography-gated multidetector-row computed tomography (MDCT) in the assessment left ventricular (LV) wall thickness and thickening and to test its validity compared to cine magnetic resonance imaging (MRI) as a standard of reference. We enrolled 19 patients who underwent both cardiac MDCT and cine MRI. End-diastolic wall thickness (EDWT) and end-systolic wall thickness (ESWT) were measured in 16 myocardial segments. Percent systolic wall thickening (%SWT) was generated from the EDWT and ESWT. Nondiagnostic myocardial segments were excluded. Correlation and agreement between MDCT and cine MRI were analyzed. Segmental assessability values were 86.2% (262/304) and 92.1% (280/304) for MDCT and cine MRI, respectively. In assessable segments by both modalities (80.9%, 246/304), a significant correlation between MDCT and MRI was found (r = 0.89, 0.85, and 0.61, for EDWT, ESWT, and %SWT, respectively; all P < 0.05). Mean EDWT and ESWT values by MDCT were slightly lower than those by cine MRI (9.8 +/- 3.6 vs. 10.0 +/- 3.7 mm and 13.8 +/- 4.4 vs. 14.1 +/- 4.3 mm, respectively; both P < 0.01). Bland-Altman analysis revealed acceptable limits of agreement between MDCT and Cine MRI. MDCT is a feasible method to assess regional LV wall thickness and systolic thickening.

Infarct transmurality and adjacent segmental function as determinants of wall thickening in revascularized chronic ischemic heart disease

There are many factors which influence regional left ventricular wall thickening (WT) in ischemic heart disease (IHD). We used magnetic resonance imaging (MRI) to explore, in patients with chronic ischemic heart disease (CIHD), how regional WT is affected by both infarct transmurality (IT) and the function of adjacent segments. We also compared these findings with a group of healthy volunteers (controls). Twenty patients (20 men, mean age 63, range 45-80 years) were imaged with cine MRI for function and delayed enhancement MRI for infarction 6 months after revascularization. Twenty age and sex matched controls underwent cine MRI. Short-axis images were analysed using a 12-segment per slice model in four midventricular slices per subject. WT and IT were inversely related (r(2) = 0.11, P<0.001). WT of non-infarcted segments in patients was lower than corresponding segments in controls (5.1 versus 4.6 mm, P<0.001). WT in patients decreased with an increasing number of dysfunctional adjacent segments (P<0.001) and increasing IT (P<0.001). WT was more strongly influenced by the number of dysfunctional adjacent segments (t = -22.93, P<0.001) than by IT (t = -4.50, P<0.001). The number of dysfunctional adjacent segments is a greater determinant than infarct transmurality on regional wall thickening.

1279 Regional left-ventricular wall thickness and strain: new reperfusion and viability markers

1279 Regional left-ventricular wall thickness and strain: new reperfusion and viability markers

Automated Tracking of Left Ventricular Wall Thickening with Intracardiac Echocardiography

Objective . We developed and evaluated a new method to automatically measure regional left ventricular wall thickening by analyzing the radiofrequency backscatter signal from an intracardiac echocardiographic catheter. Methods . We inserted 10-MHz echocardiographic catheters in 11 dogs. Wall thickness was perturbed by altering loading conditions and inotropic state. The backscatter signal from a single selected radial scan line was digitized. An automated algorithm identified the digitized endocardial and epicardial signals, tracked them throughout the cardiac cycle, and plotted the spatial difference over time. Pressure-thickness loops were generated. Results . End-systolic and end-diastolic thickness and percent wall thickening from the unedited, unsmoothed signals compared favorably with independent manual analysis of transthoracic echocardiographic images of the same region: r = 0.89 for wall thickness and 0.81 for systolic thickening. Conclusion . The backscatter signal from an intracardiac echocardiographic device can be analyzed automatically to continuously assess regional left ventricular wall thickening and generate pressure-thickness loops. (J Am Soc Echocardiogr 1998;11:1020-6.)

Left Stellate Ganglion Block Impairs Left Ventricular Function

Stellate ganglion block (SGB) is an established procedure for the diagnosis and treatment of chronic pain. SGB results in an acute sympathetic denervation of a part of the left ventricular (LV) wall innervated by the blocked ganglion, which may impair regional contractility. The resulting imbalance of myocardial contractility in different LV regions may affect LV function adversely by increasing LV asynchrony. Seven anesthetized open chest dogs were instrumented for measurement of aortic and LV pressure (tip manometers), cardiac output (CO, thermodilution), and regional LV wall thickness (WT, sonomicrometry) in the anteroapical (predominantly innervated by the right stellate ganglion) and posterobasal wall (left stellate ganglion). The contractility of both regions was assessed using the relationship between preload recruitable stroke work and end-diastolic WT relationship (MW). The timing of regional myocardial wall motion was evaluated by means of the phase of the first harmonic of the Fourier transform of the WT signals, LV asynchrony by the phase difference (PD) between both regions, and LV diastolic function by the time constant of isovolumic relaxation (tau). Measurements were performed before and after left SGB (LSGB). Mean arterial pressure was 105 +/- 25 (mean +/- SD) before and 97 +/- 10 mm Hg after LSGB (not significant). CO remained unchanged (3.09 +/- 1.03 vs 2.93 +/- 1.07 L/min). LSGB significantly reduced contractility in the posterobasal myocardium (MW -162 +/- 26 vs -80 +/- 7 mm Hg; P < 0.01), accompanied by a delay of regional wall motion within the cardiac cycle (phase 202 +/- 18 vs 223 +/- 17 degrees; P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of cilazapril on regional left ventricular wall thickness and chamber dimension following acute myocardial infarction: In vivo assessment using MRI

The primary goal of the current study was to assess in situ, using magnetic resonance imaging, the effect of a new angiotensin-converting enzyme inhibitor, cilazapril in reducing left ventricular remodeling after acute myocardial infarction. Three groups of animals were investigated: (1) sham-operated rats ( n = 19); (2) infarcted rats receiving no treatment ( n = 23); and (3) infarcted rats receiving cilazapril (100 mg/L drinking water, n = 20). Treatment with cilazapril began on the third day postocclusion and continued for 3 to 4 months. Myocardial infarction was produced by ligation of the left coronary artery, and electrocardiographic (ECG)-gated short-axis images were acquired 3 to 4 months later. Sham-operated animals were subjected to the same procedure but the left coronary artery was not ligated. From the image acquired in the middle of the left ventricle (equatorial slice), left ventricular wall thicknesses, chamber diameters, and surface area measurements of the cavities were determined. At autopsy examination infarct size and tissue water content were determined. The results demonstrate that magnetic resonance imaging has the potential to assess in situ the alterations of left ventricular dimensions and mass after acute myocardial infarction and can be used to document the influence of therapeutic interventions. Cilazapril provided protection against the deleterious remodeling changes such as ventricular dilation and wall thinning consequent to acute myocardial infarction.

Analysis of beat-to-beat cardiovascular hemodynamic variables obtained from long-term biotelemetry

Manual methods of large volume data storage, retrieval, and analysis are difficult, time consuming, and present numerous opportunities for calculation errors. We have designed and implemented a comprehensive computer-based system for performing these functions. Development of this system was necessary since left ventricular (LV) blood pressure and two regional LV wall thickness measurements were obtained during long-term extracorporeal biotelemetry of miniswine for 24-h periods. During a single recording period over 100 000 individual cardiac cycles were recorded on analog tape and later analysed for determination of global myocardial oxygen demand and regional myocardial function. In addition, custom designed software was developed to determine the extent and duration of myocardial dysfunction. Batch file commands enabled the customized software to operate without prompting by the user thus optimizing the time usage of the computer, and the computer based data acquisition and analysis system. Although this system was designed specifically for analysing cardiovascular hemodynamic variables, it is flexible and can be applied to other experimental applications.

Biotelemetry of cardiovascular hemodynamic measurements in miniswine

A three-channel biotelemetry system has been designed and implemented for use in a chronically instrumented animal model of cardiovascular disease. A dual-channel ultrasonic transit-time micrometer allows monitoring of left-ventricular wall motion for the regions perfused by the left circumflex and left anterior descending coronary arteries. A third channel provides left ventricular blood pressure obtained from a high-fidelity blood pressure transducer implanted in the left ventricle. The biotelemetry system features a high voltage dc-dc converter for improved ultrasonic signal strength, a time-to-voltage converter that is highly immune to synchronization frequency variations, low power consumption (approx. 100 mW), small size (4 x 6 x 12 cm), and low weight (approx. 200 g). This three-channel system has enabled our laboratory to continuously monitor untethered animals for 24-h periods. Data obtained from this miniature biotelemetry system can be utilized to quantify myocardial oxygen demand and regional left-ventricular wall thickening.

Simulated left ventricular aneurysm and aneurysm repair in swine

Patch reconstruction of left ventricular aneurysm may be superior to linear closure, but this hypothesis has not been tested experimentally. Accordingly, six anesthetized domestic pigs were instrumented to measure regional left ventricular wall thickening, stroke volume, systolic left ventricular pressure, and myocardial oxygen consumption. With total bypass and cardioplegia, a 6 by 8 cm Dacron patch was inserted into the anteroapical left ventricle. Simulations were as follows: left ventricular aneurysm, patch open; patch reconstruction, 50% patch plication; standard repair, ventriculotomy edges approximated. Global function, from stroke work (stroke volume x integral of left ventricular pressure)-left ventricular end-diastolic pressure curves, was depressed in all three simulations compared with control. A tendency for stroke work to be greater for standard repair than for left ventricular aneurysm and patch reconstruction at higher preloads was not statistically significant. Mechanical efficiency, from stroke work/myocardial oxygen consumption (joules per milliliter oxygen per beat), was 2.43 +/- 0.52 (mean +/- standard error of the mean) (control), 2.22 +/- 0.94 (standard repair), 1.27 +/- 0.39 (patch reconstruction), and 1.09 +/- 0.37 (left ventricular aneurysm) (no significant differences). Regional work was calculated as regional left ventricular wall thickening x integral of left ventricular pressure. The slope of the regional work-end-diastolic wall thickness relation decreased in the posterior wall 14.0 +/- 2.9 (control) versus 8.4 +/- 2.0 (left ventricular aneurysm), 6.9 +/- 1.4 (patch reconstruction), and 7.4 +/- 1.4 (standard repair) (p less than 0.05). In the anterior wall, contractility did not change significantly (7.4 +/- 1.2, control; 7.8 +/- 2.7, left ventricular aneurysm; 5.0 +/- 0.4, patch reconstruction; and 5.3 +/- 0.4, standard repair). Decreased end-diastolic wall thinning anteriorly suggested tethering. These results in the normal left ventricle suggest that patch ventriculoplasty is of no greater benefit than linear repair. Either repair may impede function of adjacent myocardium through restriction of regional diastolic lengthening.

Relation of lactate production to postischaemic reduction in function and myocardial oxygen consumption after partial coronary occlusion in swine.

Postischaemic myocardial dysfunction (stunning) induced by partial occlusion of the left anterior descending coronary artery and its relation to lactate production during reperfusion were studied in nine swine. A 40% reduction in regional left ventricular wall thickening, as measured by ultrasonic crystals, was prospectively defined as stunning. A perfusion pressure of 20 mmHg was maintained with a hydraulic occluder for each ischaemic period and was monitored by a distal arterial catheter. To achieve a 40% reduction in function, four animals required three ischaemic periods (mean ischaemic flow reduction 73%), four two (86% flow reduction), and one one (93% flow reduction). At 25 min of reperfusion transmural flow was slightly reduced from 0.67 ml.g-1.min-1 at control to 0.58 ml.g-1.min-1 (p less than 0.05), whereas regional flow endocardial to epicardial flow ratio was unchanged. At 60 min reperfusion, percentage systolic wall thickening was reduced to 25% from a control of 39% (p less than 0.01) and parallel reductions in regional myocardial oxygen consumption from 4.3 ml.min-1 to 2.7 ml.min-1 occurred (p less than 0.01). Lactate extraction was depressed at 15 min reperfusion (-4.0% compared with control +18.0% (p less than 0.05)) but returned to control values by 30 min. It is concluded that postischaemic myocardial dysfunction (stunning) can be induced by partial coronary occlusions and that the extent of dysfunction depends on the degree of flow reduction. The reductions in myocardial oxygen consumption parallel those of wall thickening during reperfusion after stunning. Finally, lactate production occurs during early reperfusion but does not persist with the postischaemic reductions in function and myocardial oxygen consumption.

End-systolic dimension-wall thickness relations during myocardial ischemia in conscious dogs: A new approach for defining regional function

Overall and regional left ventricular (LV) function was studied during progressive coronary stenosis in conscious dogs by determining the relations at end-systole between LV pressure, chamber dimensions, and regional LV wall thickness. An index of regional wall stress was also analyzed. Using ultrasonic dimension gauges, measurements were made of LV wall thickness in control and ischemic regions, and the external long- and short-axis LV diameters were determined; an implanted micromanometer measured LV pressure. Internal LV diameters were obtained from the external diameters by subtraction of wall thickness, and the index of regional wall stress employed a thick-walled ellipsoidal model. During regional ischemia, the LV long axis at end-systole did not change, whereas the short-axis diameter progressively increased (from 24 ± 7 mm [standard deviation] to 30 ± 9 mm, p < 0.001, indicating a more spherical LV shape during ischemia). The end-systolic pressure did not change, and therefore the end-systolic pressure-diameter relation shifted progressively, suggesting a global decrease in LV contactility. The end-systolic points relating LV wall thickness in the ischemic region to the end-systolic LV pressure revealed the regional nature of the abnormality, showing a progressive displacement to the left, whereas there was no significant displacement of this relation in the control region. The application of this index over a range of loading conditions during partial vena caval occlusion was illustrated. Thus, the regional endsystolic wall thickness-pressure relation provides a new index for defining the regional contractile state of the LV myocardium which is potentially load-independent and offers the possibility for echocardiographic application.