Stig Urheim

Regional myocardial systolic function during acute myocardial ischemia assessed by strain Doppler echocardiography

OBJECTIVES We sought to evaluate if echocardiographic strain measurements could detect acute myocardial ischemia, and to compare this new method with myocardial velocity measurements and wall motion score index. BACKGROUND Tissue Doppler echocardiography (TDE) is a promising method for assessing regional myocardial function. However, myocardial velocities measured by tissue Doppler echocardiography (TDE) vary throughout the left ventricle (LV) because of tethering effects from adjacent tissue. Strain Doppler echocardiography (SDE) is a new tool for measuring regional myocardial deformation excluding the effect of adjacent myocardial tissue. METHODS Seventeen patients undergoing angioplasty of the left anterior descending coronary artery (LAD) were studied. Left ventricular longitudinal wall motion was assessed by TDE and SDE from the apical four-chamber view before, during and after angioplasty from multiple myocardial segments simultaneously. RESULTS Systolic strain values were uniformly distributed in the different nonischemic LV segments, whereas systolic velocities decreased from basis to apex. During LAD occlusion, strain measurement showed expansion in the apical septal segment in 16 of 17 patients (7.5 +/- 6.5% vs. -17.7 +/- 7.2%, p < 0.001) and reduced compression in the mid-septal segment (p < 0.05) compared with baseline. Segments not supplied by LAD remained unchanged. Tissue Doppler echocardiography showed reduced velocities in all septal segments (p < 0.05) during angioplasty even though LAD does not supply the basal septal segment. Negative systolic velocities were present in 11 of 17 patients. Wall motion score index increased during ischemia (1.3 +/- 0.4, p < 0.05). CONCLUSIONS The new SDE approach might be a more accurate marker than TDE for detecting systolic regional myocardial dysfunction induced by LAD occlusion.

Quantification of left ventricular systolic function by tissue Doppler echocardiography: added value of measuring pre- and postejection velocities in ischemic myocardium.

Background—Tissue Doppler imaging (TDI) is a potentially powerful method for diagnosing myocardial ischemia. This study was designed to investigate how velocity patterns in ischemic myocardium relates to regional function, and to determine whether timing of velocity measurements relative to ejection and isovolumic phases may increase the diagnostic power of TDI. Methods and Results—In 17 open-chest anesthetized dogs we measured pressures by micromanometers, myocardial longitudinal segment lengths by sonomicrometry, and velocities by TDI. Myocardial longitudinal strain rate was calculated as velocity divided by distance to the left ventricle apex. Moderate ischemia (left anterior descending coronary artery stenosis) caused parallel reductions in regional systolic shortening by sonomicrometry (P <0.05) and in peak systolic velocities by TDI (P <0.05). Severe ischemia (left anterior descending coronary artery occlusion), however, induced systolic lengthening by sonomicrometry (P <0.001), whereas peak TDI velocity during ejection remained positive (P <0.05). When velocities during isovolumic contraction (IVC) and isovolumic relaxation (IVR) were included, TDI correlated well with sonomicrometry; ie, systolic lengthening occurred predominantly during IVC and was evident as negative velocities (r =0.70, P <0.001), and postsystolic shortening during IVR (r =0.72, P <0.001) as positive velocities. In nonischemic myocardium peak systolic strain rates were more uniform than velocities. Conclusion—The present results indicate that peak ejection velocity is an inappropriate measure of function in severely ischemic myocardium. Dyskinetic myocardium deforms predominantly during the isovolumic phases, and therefore IVC and IVR velocities are better markers of function. When isovolumic as well as ejection velocities are measured, TDI has excellent ability to quantify regional myocardial dysfunction. Longitudinal strain rates are more uniform than velocities and may further improve the diagnostic power of TDI.

Postsystolic Shortening in Ischemic Myocardium Active Contraction or Passive Recoil

Background—Postsystolic shortening in ischemic myocardium has been proposed as a marker of tissue viability. Our objectives were to determine if postsystolic shortening represents active fiber shortening or passive recoil and if postsystolic shortening may be quantified by strain Doppler echocardiography (SDE). Methods and Results—In 15 anesthetized dogs, we measured left ventricular (LV) pressure, myocardial long-axis strains by SDE, and segment lengths by sonomicrometry before and during LAD stenosis and occlusion. Active contraction was defined as elevated LVP and stress during postsystolic shortening when compared with the fully relaxed ventricle at similar segment lengths. LAD stenosis decreased systolic shortening from 10.4±1.2% to 5.9±0.9% (P <0.05), whereas postsystolic shortening increased from 1.1±0.3% to 4.2±0.7% (P <0.05). In hypokinetic and akinetic segments, LV pressure–segment length and LV stress–segment length loop analysis indicated that postsystolic shortening was active. LAD occlusion resulted in dyskinesis, and postsystolic shortening increased additionally to 8.2±1.0% (P <0.05). After 3 to 5 minutes with LAD occlusion, the dyskinetic segment generated no active stress, and the postsystolic shortening was attributable to passive recoil. Elevation of afterload caused hypokinetic segments to become dyskinetic, and postsystolic shortening remained partly active. Postsystolic shortening by SDE correlated well with sonomicrometry (r =0.83, P <0.01). Conclusions—Postsystolic shortening is a relatively nonspecific feature of ischemic myocardium and may occur in dyskinetic segments by an entirely passive mechanism. However, in segments with systolic hypokinesis or akinesis, postsystolic shortening is a marker of actively contracting myocardium. SDE was able to quantify postsystolic shortening and might represent a clinical method for identifying actively contracting and hence viable myocardium.

Myocardial strain imaging: how useful is it in clinical decision making?

Abstract Myocardial strain is a principle for quantification of left ventricular (LV) function which is now feasible with speckle-tracking echocardiography. The best evaluated strain parameter is global longitudinal strain (GLS) which is more sensitive than left ventricular ejection fraction (LVEF) as a measure of systolic function, and may be used to identify sub-clinical LV dysfunction in cardiomyopathies. Furthermore, GLS is recommended as routine measurement in patients undergoing chemotherapy to detect reduction in LV function prior to fall in LVEF. Intersegmental variability in timing of peak myocardial strain has been proposed as predictor of risk of ventricular arrhythmias. Strain imaging may be applied to guide placement of the LV pacing lead in patients receiving cardiac resynchronization therapy. Strain may also be used to diagnose myocardial ischaemia, but the technology is not sufficiently standardized to be recommended as a general tool for this purpose. Peak systolic left atrial strain is a promising supplementary index of LV filling pressure. The strain imaging methodology is still undergoing development, and further clinical trials are needed to determine if clinical decisions based on strain imaging result in better outcome. With this important limitation in mind, strain may be applied clinically as a supplementary diagnostic method.

Myocardial acceleration during isovolumic contraction: Relationship to contractility

Background—Acceleration of the mitral ring during isovolumic contraction has been proposed as a load-independent index of global left ventricular (LV) contractility. This study investigates whether myocardial isovolumic acceleration (IVA) reflects regional contractility. Methods and Results—In acutely instrumented, anesthetized dogs, we measured LV pressure, myocardial long-axis velocities, and IVA by tissue Doppler imaging (TDI) and sonomicrometry at different levels of global LV contractility and preload and during regional myocardial ischemia (reduced flow in the left anterior descending coronary artery). Dobutamine caused dose-dependent increments in IVA from 3.6±0.6 (mean±SEM) to a maximum of 7.1±1.4 m/s2 (P<0.01) by TDI, and there were parallel increments in LV dP/dtmax (P<0.01). However, volume loading decreased IVA from 3.6±0.6 to 2.5±0.4 m/s2 (P<0.05), whereas LV dP/dtmax was unchanged, and LV pressure–segment length loop analysis confirmed unchanged regional contractility. During myocardial ischemia, sonomicrometry indicated severely depressed regional function, whereas IVA remained unchanged. These findings were confirmed when IVA was measured by sonomicrometry. In contrast to peak ejection velocity that increased from apex toward the LV base, peak IVC velocity was maximum midway between apex and base. The onset of IVA coincided with onset of the first heart sound by phonocardiography. Peak IVA occurred at a LV pressure of 14±1 mm Hg, ie, close to end-diastole. Conclusions—There was no consistent relationship between peak IVA and regional myocardial contractility. Peak IVA was markedly load dependent and did not reflect impaired myocardial function during ischemia. Peak IVA may reflect late-diastolic events and possibly wall oscillations that are related to global LV function. Peak IVA seems to have limited potential in the assessment of regional myocardial function.

Myocardial strain analysis in acute coronary occlusion : A tool to assess myocardial viability and reperfusion

Background— This study proposes 2 new echocardiographic indices with potential application in acute coronary artery occlusion to differentiate between viable and necrotic myocardium and to identify reperfusion. We investigated whether the ratio between systolic lengthening and combined late and postsystolic shortening (L-S ratio) could identify viable myocardium and whether systolic myocardial compliance, calculated as systolic lengthening divided by systolic pressure rise, could identify necrotic myocardium. Methods and Results— In anesthetized dogs, we measured left ventricular (LV) pressure and long-axis strain by Doppler echocardiography (SDE) and sonomicrometry. The left anterior descending coronary artery was occluded for 15 minutes with 3-hour reperfusion (n=6), for 4 hours with 3-hour reperfusion (n=6), or for 4 hours with no reperfusion (n=6). Myocardial work was quantified by pressure–segment length analysis, necrosis by triphenyltetrazolium chloride staining, and edema by water content. L-S ratio and systolic compliance were calculated by SDE. The L-S ratio ranged between 0.00 and 1.00 and was well correlated with regional myocardial work (r=0.77, P<0.0001). In entirely passive myocardium, the L-S ratio approached 1 and was similar in viable (0.88±0.02) and necrotic (0.81±0.03) myocardium. Compliance, however, was reduced in necrotic myocardium owing to edema (0.07±0.01%/mm Hg) but was preserved in viable myocardium (0.15±0.01%/mm Hg, P<0.05). Reperfusion of viable myocardium caused a reduction of the L-S ratio after 15 minutes (0.57±0.06, P<0.05), reflecting recovery of function. Reperfusion of necrotic myocardium caused no change in the L-S ratio, but compliance was further reduced within 15 minutes (0.03±0.01%/mm Hg, P<0.05). Conclusion— Myocardial L-S ratio and compliance by SDE identified active contraction and necrosis, respectively. These indices should be tested clinically for assessment of myocardial viability and reperfusion.

Semi-automated quantification of left ventricular volumes and ejection fraction by real-time three-dimensional echocardiography

BackgroundRecent studies have shown that real-time three-dimensional (3D) echocardiography (RT3DE) gives more accurate and reproducible left ventricular (LV) volume and ejection fraction (EF) measurements than traditional two-dimensional methods. A new semi-automated tool (4DLVQ) for volume measurements in RT3DE has been developed. We sought to evaluate the accuracy and repeatability of this method compared to a 3D echo standard.MethodsLV end-diastolic volumes (EDV), end-systolic volumes (ESV), and EF measured using 4DLVQ were compared with a commercially available semi-automated analysis tool (TomTec 4D LV-Analysis ver. 2.2) in 35 patients. Repeated measurements were performed to investigate inter- and intra-observer variability.ResultsAverage analysis time of the new tool was 141s, significantly shorter than 261s using TomTec (p < 0.001). Bland Altman analysis revealed high agreement of measured EDV, ESV, and EF compared to TomTec (p = NS), with bias and 95% limits of agreement of 2.1 ± 21 ml, -0.88 ± 17 ml, and 1.6 ± 11% for EDV, ESV, and EF respectively. Intra-observer variability of 4DLVQ vs. TomTec was 7.5 ± 6.2 ml vs. 7.7 ± 7.3 ml for EDV, 5.5 ± 5.6 ml vs. 5.0 ± 5.9 ml for ESV, and 3.0 ± 2.7% vs. 2.1 ± 2.0% for EF (p = NS). The inter-observer variability of 4DLVQ vs. TomTec was 9.0 ± 5.9 ml vs. 17 ± 6.3 ml for EDV (p < 0.05), 5.0 ± 3.6 ml vs. 12 ± 7.7 ml for ESV (p < 0.05), and 2.7 ± 2.8% vs. 3.0 ± 2.1% for EF (p = NS).ConclusionIn conclusion, the new analysis tool gives rapid and reproducible measurements of LV volumes and EF, with good agreement compared to another RT3DE volume quantification tool.

Constrained Active Appearance Models for Segmentation of Triplane Echocardiograms

This paper presents multiview and multiframe active appearance models (AAMs) for left ventricular segmentation in triplane echocardiograms. We describe a general way of integrating local edge detector based segmentation algorithms into the AAM framework. The feasibility of this approach is evaluated by comparing an AAM constrained by a dynamic programming (DP) based snake with an unconstrained AAM, and an AAM constrained by manually defined landmarks. A leave-one-out validation scheme was used for training and testing of the methods. Evaluation was done in 36 patients suffering from various heart diseases, using manually determined volumes and ejection fractions (EF) as reference. The segmentation was initialized by manual selection of the mitral annulus and apex in three imaging planes. The differences, in volume, between manual segmentation and the best automatic method (DP-constrained AAM) were -3.1 plusmn 20 ml (meanplusmnSD) at end-diastole and 0.61 plusmn 13 ml at end-systole. The difference in EF was -1.3 plusmn 6.3%, comparable to the interobserver variability. We show that 1) constraining the model to manually defined landmarks improves volume and EF estimates compared to unconstrained AAMs, 2) further improvement is achieved using a DP-constrained AAM, and 3) segmentation in triplane echocardiograms gives higher accuracy than single plane data.

Identification of a definite diabetic cardiomyopathy in type 2 diabetes by comprehensive echocardiographic evaluation: A cross-sectional comparison with non-diabetic weight-matched controls.

Subclinical left ventricular (LV) dysfunction is prevalent in type 2 diabetes (T2DM). As obesity has been proposed as one causal factor in the disease process, this could bias the reported prevalences. We wanted to characterize echocardiographic LV dysfunction in obese T2DM subjects as compared to non‐diabetic obese controls.

Controlled release metoprolol for aortic regurgitation: a randomised clinical trial

Objective Chronic aortic regurgitation (AR) creates a volume load on the left ventricle, which induces adaptive responses. With time, excessive left ventricular (LV) dilatation may precipitate heart failure. β-adrenergic receptor antagonists (β-blockers) are beneficial in patients with heart failure, but their effect in AR is unclear. This trial was designed to evaluate the effect of controlled release metoprolol on LV remodelling in patients with AR. Methods In this double blind trial, 75 asymptomatic patients aged 44±14 years, 89% males, fulfilling at least two echocardiographic criteria for moderate or severe chronic AR, were randomised to receive metoprolol CR/XL up-titrated to 200 mg/day, or matching placebo. The primary endpoint was LV end diastolic volume, measured by MRI after 6 months of treatment. Results After 6 months, the difference in the baseline-adjusted LV end diastolic volume between patients allocated to metoprolol and those allocated to placebo was 8 (95% CI −8 to 25) mL (p=0.32). The adjusted LV ejection fraction was 2.7 (95% CI 0.1 to 5.3) percentage points higher in the metoprolol group than in the placebo group (p=0.04). The exercise capacity and peak oxygen consumption did not differ between treatment arms. Serum concentrations of N-terminal pro-B-type natriuretic peptide were 138 (95% CI 71 to 205) pg/mL higher in the metoprolol group (p<0.001). There were no serious adverse events in either treatment arm. Conclusions Treatment with metoprolol of adults with chronic, moderate to severe AR had no effect on LV volumes. Trial registration number ClinicalTrials.gov Identifier: NCT01157572-results.