Helge Skulstad

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 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.

Acute coronary occlusion in non-ST-elevation acute coronary syndrome: outcome and early identification by strain echocardiography

Objectives To compare infarct size and left ventricular ejection fraction in patients with non-ST-elevation myocardial infarction (NSTEMI) with and without acute coronary occlusions, and determine if myocardial strain by speckle-tracking echocardiography can identify acute occlusions in patients presenting with non-ST-elevation acute coronary syndrome (NSTE-ACS). Methods 111 patients with suspected NSTE-ACS were enrolled shortly after admittance. Echocardiographic measurements were performed a median of 1 h (interquartile range 0.5–4) after admittance, and coronary angiography 36±21 h after onset of symptoms. Territorial longitudinal and circumferential strain was calculated based on the perfusion territories of the three major coronary arteries in a 16-segment model of the left ventricle, and compared with traditional echocardiographic parameters. Long-term follow-up was by echocardiography and contrast-enhanced magnetic resonance imaging (ceMRI). Results Patients with NSTEMI due to acute coronary occlusion had higher peak troponin T than patients with NSTEMI without acute occlusions (4.9±4.7 vs 0.9±1.1 μg/l, p<0.001), larger infarct size by ceMRI (13±8% vs 3±3%, p<0.001) and poorer left ventricular ejection fraction (48±6% vs 57±6%, p<0.001) at follow-up. Territorial circumferential strain was the best parameter for predicting acute coronary occlusion. A territorial circumferential strain value >−10.0% had 90% sensitivity, 88% specificity and area under the curve=0.93 for identification of acute occlusions. Conclusions Patients with NSTEMI due to acute coronary occlusions develop larger infarcts and more impaired left ventricular function than patients with NSTEMI without occlusions, regardless of infarct-related territory. Territorial circumferential strain by echocardiography enables very early identification of acute coronary occlusions in patients with NSTE-ACS and may be used for detection of patients requiring urgent revascularisation.

Strain Echocardiography and Wall Motion Score Index Predicts Final Infarct Size in Patients With Non–ST-Segment–Elevation Myocardial Infarction

Background—Infarct size is a strong predictor of mortality and major adverse cardiovascular events after myocardial infarction. Acute reperfusion therapy limits infarct size and improves survival, but its use has been confined to patients with ST-segment–elevation myocardial infarction. The purpose of this study was to assess the relationship between echocardiographic parameters of left ventricular (LV) systolic function obtained before revascularization and final infarct size in patients with non–ST-segment–elevation myocardial infarction, as well as the ability of these parameters to identify patients with substantial infarction. Methods and Results—Sixty-one patients with non–ST-segment–elevation myocardial infarction were examined by echocardiography immediately before revascularization, 2.1±0.6 days after hospitalization. LV systolic function was assessed by ejection fraction, wall motion score index, and circumferential, longitudinal, and radial strain in a 16-segment LV model. Global strain represents average segmental strain values. Infarct size was assessed after 9±3 months by late-enhancement MRI, as a percentage of total LV myocardial volume. A good correlation was found between infarct size and wall motion score index (r=0.74, P<0.001) and global longitudinal strain (r=0.68, P<0.001). Global longitudinal strain >−13.8% and wall motion score index >1.30 accurately identified patients with substantial infarction (≥12% of myocardium, n=13; area under the receiver operator curve, 0.95 and 0.92, respectively). Conclusions—Echocardiographic parameters of LV systolic function correlate to infarct size in patients with non–ST-segment–elevation myocardial infarction. Global longitudinal strain and wall motion score index are both excellent parameters to identify patients with substantial myocardial infarction, who may benefit from urgent reperfusion therapy.

Mechanisms of Abnormal Systolic Motion of the Interventricular Septum During Left Bundle-Branch Block

Background— In a majority of patients with left bundle-branch block (LBBB), there is abnormal leftward motion of the interventricular septum during the preejection phase. This motion was considered to be passive, caused by early rise in right ventricular (RV) pressure, and has therefore been excluded from most indices of left ventricular (LV) dyssynchrony. If considered active, however, the leftward motion reflects onset of septal activation and should be included. We therefore investigated if the motion was a passive response to pressure changes or caused by active contraction. Methods and Results— LBBB was induced in 8 anesthetized dogs with micromanometers. Cardiac dimensions were measured by sonomicrometry and echocardiography. Induction of LBBB resulted in preejection leftward motion of the septum, simultaneously with shortening of septal segments (P<0.01). In each experiment, preejection septal shortening occurred against rising LV pressure, consistent with active contraction. Furthermore, the LV pressure–segment length relationships were shifted upward (P<0.01) relative to the passive elastic curve, indicating stiffening of septal myocardium, confirming an active mechanism. Initially, RV pressure increased faster than LV pressure, suggesting that the leftward septal motion may have a passive pressure component. However, the passive component appeared to play a minor role. The magnitude of preejection septal shortening was modified by load alterations. Conclusions— Leftward preejection motion of the septum during LBBB is mainly a result of active septal contraction, whereas alterations in diastolic ventricular pressures modulate the amplitude of this motion. The findings imply that the preejection phase should be included when assessing LV dyssynchrony.

Achievements in Congenital Heart Defect Surgery: A Prospective, 40 Year Study of 7038 Patients

Background— This article presents an update of the results achieved by modern surgery in congenital heart defects (CHDs) over the past 40 years regarding survival and the need for reoperations, especially focusing on the results from the past 2 decades. Methods and Results— From 1971 to 2011, all 7038 patients <16 years of age undergoing surgical treatment for CHD at Rikshospitalet (Oslo, Norway) were enrolled prospectively. CHD diagnosis, date, and type of all operations were recorded, as was all-cause mortality until December 31, 2012. CHDs were classified as simple (3751/7038=53.2%), complex (2918/7038=41.5%), or miscellaneous (369/7037=5.2%). Parallel to a marked, sequential increase in operations for complex defects, median age at first operation decreased from 1.6 years in 1971 to 1979 to 0.19 years in 2000 to 2011. In total, 1033 died before January 1, 2013. Cumulative survival until 16 years of age in complex CHD operated on in 1971 to 1989 versus 1990 to 2011 was 62.4% versus 86.9% (P<0.0001). In the comparison of patients operated on in 2000 to 2004 versus 2005 to 2011, 1-year survival was 90.7% versus 96.5% (P=0.003), and 5-year cumulative survival was 88.8% versus 95.0% (P=0.0003). In simple versus complex defects, 434 (11.6%) versus 985 (33.8%) patients needed at least 1 reoperation before 16 years of age. In complex defects, 5-year cumulative freedom of reoperation among patients operated on in 1990 to 1999 versus 2000 to 2011 was 66% versus 73% (P=0.0001). Conclusions— Highly significant, sequential improvements in survival and reductions in reoperations after CHD surgery were seen. A future challenge is to find methods to reduce the need for reoperations and further reduce long-term mortality.Background— This article presents an update of the results achieved by modern surgery in congenital heart defects (CHDs) over the past 40 years regarding survival and the need for reoperations, especially focusing on the results from the past 2 decades. Methods and Results— From 1971 to 2011, all 7038 patients <16 years of age undergoing surgical treatment for CHD at Rikshospitalet (Oslo, Norway) were enrolled prospectively. CHD diagnosis, date, and type of all operations were recorded, as was all-cause mortality until December 31, 2012. CHDs were classified as simple (3751/7038=53.2%), complex (2918/7038=41.5%), or miscellaneous (369/7037=5.2%). Parallel to a marked, sequential increase in operations for complex defects, median age at first operation decreased from 1.6 years in 1971 to 1979 to 0.19 years in 2000 to 2011. In total, 1033 died before January 1, 2013. Cumulative survival until 16 years of age in complex CHD operated on in 1971 to 1989 versus 1990 to 2011 was 62.4% versus 86.9% ( P <0.0001). In the comparison of patients operated on in 2000 to 2004 versus 2005 to 2011, 1-year survival was 90.7% versus 96.5% ( P =0.003), and 5-year cumulative survival was 88.8% versus 95.0% ( P =0.0003). In simple versus complex defects, 434 (11.6%) versus 985 (33.8%) patients needed at least 1 reoperation before 16 years of age. In complex defects, 5-year cumulative freedom of reoperation among patients operated on in 1990 to 1999 versus 2000 to 2011 was 66% versus 73% ( P =0.0001). Conclusions— Highly significant, sequential improvements in survival and reductions in reoperations after CHD surgery were seen. A future challenge is to find methods to reduce the need for reoperations and further reduce long-term mortality. # CLINICAL PERSPECTIVE {#article-title-36}

A novel clinical method for quantification of regional left ventricular pressure-strain loop area: a non-invasive index of myocardial work.

Aims Left ventricular (LV) pressure–strain loop area reflects regional myocardial work and metabolic demand, but the clinical use of this index is limited by the need for invasive pressure. In this study, we introduce a non-invasive method to measure LV pressure–strain loop area. Methods and results Left ventricular pressure was estimated by utilizing the profile of an empiric, normalized reference curve which was adjusted according to the duration of LV isovolumic and ejection phases, as defined by timing of aortic and mitral valve events by echocardiography. Absolute LV systolic pressure was set equal to arterial pressure measured invasively in dogs (n = 12) and non-invasively in patients (n = 18). In six patients, myocardial glucose metabolism was measured by positron emission tomography (PET). First, we studied anaesthetized dogs and observed an excellent correlation (r = 0.96) and a good agreement between estimated LV pressure–strain loop area and loop area by LV micromanometer and sonomicrometry. Secondly, we validated the method in patients with various cardiac disorders, including LV dyssynchrony, and confirmed an excellent correlation (r = 0.99) and a good agreement between pressure–strain loop areas using non-invasive and invasive LV pressure. Non-invasive pressure–strain loop area reflected work when incorporating changes in local LV geometry (r = 0.97) and showed a strong correlation with regional myocardial glucose metabolism by PET (r = 0.81). Conclusions The novel non-invasive method for regional LV pressure–strain loop area corresponded well with invasive measurements and with directly measured myocardial work and it reflected myocardial metabolism. This method for assessment of regional work may be of clinical interest for several patients groups, including LV dyssynchrony and ischaemia.