Nontransmural Infarction Research Articles

Non-transmural myocardial infarction associated with regional contractile function is an independent predictor of positive outcome: an integrated approach to myocardial viability

BackgroundCardiovascular magnetic resonance permits assessment of irreversible myocardial fibrosis and contractile function in patients with previous myocardial infarction. We aimed to assess the prognostic value of myocardial fibrotic tissue with preserved/restored contractile activity.MethodsIn 730 consecutive myocardial infarction patients (64 ± 11 years), we quantified left ventricular (LV) end-diastolic (EDV) and end-systolic (ESV) volumes, ejection fraction (EF), regional wall motion (WM) (1 normal, 2 hypokinetic, 3 akinetic, 4 dyskinetic), and WM score index (WMSI), and measured the transmural (1–50 and 51–100) and global extent of the infarct scar by late gadolinium enhancement (LGE). Contractile fibrotic (CT-F) segments were identified as those showing WM-1 and WM-2 with LGE ≤ or ≥ 50%.ResultsDuring follow-up (median 2.5, range 1–4.7 years), cardiac events (cardiac death or appropriate implantable defibrillator shocks) occurred in 123 patients (17%). At univariate analysis, age, LVEDV, LVESV, LVEF, WMSI, extent of LGE, segments with transmural extent > 50%, and CT-F segments were associated with cardiac events. At multivariate analysis, age > 65 years, LVEF < 30%, WMSI > 1.7, and dilated LVEDV independently predicted cardiac events, while CT-F tissue was the only independent predictor of better outcome. After adjustment for LVEF < 30% and LVEDV dilatation, the presence of CT-F tissue was associated with good prognosis.ConclusionsIn addition to CMR imaging parameters associated with adverse outcome (severe LV dysfunction, poor WM, and dilated EDV), the presence of fibrotic myocardium showing contractile activity in patients with previous myocardial infarction yields a beneficial effect on patient survival.

Elastin-like recombinamers-based hydrogel modulates post-ischemic remodeling in a non-transmural myocardial infarction in sheep.

Ischemic heart disease is a leading cause of mortality due to irreversible damage to cardiac muscle. Inspired by the post-ischemic microenvironment, we devised an extracellular matrix (ECM)-mimicking hydrogel using catalyst-free click chemistry covalent bonding between two elastin-like recombinamers (ELRs). The resulting customized hydrogel included functional domains for cell adhesion and protease cleavage sites, sensitive to cleavage by matrix metalloproteases overexpressed after myocardial infarction (MI). The scaffold permitted stromal cell invasion and endothelial cell sprouting in vitro. The incidence of non-transmural infarcts has increased clinically over the past decade, and there is currently no treatment preventing further functional deterioration in the infarcted areas. Here, we have developed a clinically relevant ovine model of non-transmural infarcts induced by multiple suture ligations. Intramyocardial injections of the degradable ELRs-hydrogel led to complete functional recovery of ejection fraction 21 days after the intervention. We observed less fibrosis and more angiogenesis in the ELRs-hydrogel-treated ischemic core region compared to the untreated animals, as validated by the expression, proteomic, glycomic, and histological analyses. These findings were accompanied by enhanced preservation of GATA4+ cardiomyocytes in the border zone of the infarct. We propose that our customized ECM favors cardiomyocyte preservation in the border zone by modulating the ischemic core and a marked functional recovery. The functional benefits obtained by the timely injection of the ELRs-hydrogel in a clinically relevant MI model support the potential utility of this treatment for further clinical translation.

Assessment of Myocardial Viability After Acute ST- Elevated Myocardial Infarction Using Stress Speckle Tracking Echocardiography and Cardiac MRI

Background: Speckle-tracking echocardiography has emerged as a unique technique for accurately evaluating myocardial function by analyzing the motion of speckles identified. Speckle-tracking measured under stress may offer an opportunity to improve the detection of dynamic regional abnormalities and myocardial viability. Objective: The aim of the current study was to evaluate stress speckle tracking to detect myocardial viability in comparison to cardiac MRI in post-STEMI patients. Patients and methods: 74 patients were prospectively enrolled in 18-month’s study. Dobutamine stress echocardiography was performed 4 days post-infarction accompanied with automated functional imaging analysis of left ventricle during rest and then during low dose stress. All patients underwent a follow up stress echocardiography at 3 months with speckle tracking analysis. Cardiac MRI took place concomitantly at 4 days post-infarction and 3 months. Results: Investigating strain rate obtained with stress speckle tracking after revascularization predicted the extent of myocardial scar, determined by contrast-enhanced magnetic resonance imaging. A good correlation was found between the global strain and total infarct size (R 0.75, p< 0.001). Furthermore, a clear inverse relationship was found between the segmental strain and the transmural extent of infarction in each segment. Meanwhile it provided 81.82% sensitivity and 82.6% specificity to detect transmural from non-transmural infarction at a cut-off value of -10.15. Conclusion: Strain rate obtained from speckle tracking during stress is a novel method of detecting myocardial viability after STEMI. Moreover, it carries a promising role in post-myocardial infarction risk stratification with a reasonable prediction of reversible cardiac-related hospital re-admission.

Magnetocardiographic recognition of abnormal depolarization and repolarization in patients with coronary artery lesions caused by Kawasaki disease.

Myocardial ischemia changes the electrophysiological properties of the myocardium, but it is difficult to detect the abnormalities of depolarization and repolarization noninvasively in patients with coronary artery disease. Depolarization and repolarization abnormalities were retrospectively investigated in 61 patients (48 males and 13 females) with coronary artery lesions (CALs) caused by Kawasaki disease (KD) from 2007 to 2014 using magnetocardiography (MCG). CAL had been diagnosed by selective coronary angiography. Current arrow maps (CAMs) were constructed during depolarization and repolarization [corrected]. The MCG findings were compared between the stenotic lesions group (SL group) and the non-stenotic lesions group (non-SL group). The incidence of MCG abnormalities was significantly higher in the SL group than in the non-SL group (p < 0.0001). The incidence of abnormal repolarization was significantly higher than that of abnormal depolarization (p < 0.0001). The number of coronary artery occlusions significantly affected the severity of abnormal repolarization (p = 0.02). Six (75%) of the patients with abnormal depolarization had a previous anteroseptal myocardial infarction. The transmural myocardial infarction affects on abnormalities of depolarization, and the non-transmural myocardial infarction might relate on abnormalities of repolarization. The myocardial electrical properties were preserved in patients except very severe coronary stenosis. MCG is possible to detect electrical myocardial abnormalities noninvasively in patients with CALs caused by KD.

Gaussian Process Regressions for Inverse Problems and Parameter Searches in Models of Ventricular Mechanics

Patient specific models of ventricular mechanics require the optimization of their many parameters under the uncertainties associated with imaging of cardiac function. We present a strategy to reduce the complexity of parametric searches for 3-D FE models of left ventricular contraction. The study employs automatic image segmentation and analysis of an image database to gain geometric features for several classes of patients. Statistical distributions of geometric parameters are then used to design parametric studies investigating the effects of: (1) passive material properties during ventricular filling, and (2) infarct geometry on ventricular contraction in patients after a heart attack. Gaussian Process regression is used in both cases to build statistical models trained on the results of biophysical FEM simulations. The first statistical model estimates unloaded configurations based on either the intraventricular pressure or the end-diastolic fiber strain. The technique provides an alternative to the standard fixed-point iteration algorithm, which is more computationally expensive when used to unload more than 10 ventricles. The second statistical model captures the effects of varying infarct geometries on cardiac output. For training, we designed high resolution models of non-transmural infarcts including refinements of the border zone around the lesion. This study is a first effort in developing a platform combining HPC models and machine learning to investigate cardiac function in heart failure patients with the goal of assisting clinical diagnostics.

Pathological changes of left ventricular myocardium in patients with calcified aortic stenosis and coronary artery disease

Objective To characterize autopsy pathological changes of the coronary artery and left ventricular myocardium in elderly patients with moderate to severe calcified aortic stenosis, and to analyze the causes of death. Methods Seventeen cases of moderate to severe calcified aortic stenosis were identified from an autopsy database of Beijing Hospital containing 909 elderly patients(aged from 60-100 years)collected from April 1, 1969 to October 31, 2013.All cases were confirmed by autopsy and were analyzed retrospectively.The characteristics of coronary artery lesions, myocardial pathological changes and causes of death were summarized. Results Aortic stenosis was detected in 1.1%(2/190), 1.9%(5/266), 3.7%(11/297)and 6.4%(10/156)of patients in the 60-69, 70-79, 80-89 and 90-100 age groups, increasingly prevalent with age(χ2=10.08, P=0.018). In addition, seventeen cases were confirmed to have moderate to severe calcified aortic stenosis.Of these cases, 13(76.5%)had coronary artery disease and 5(29.4%)had severe coronary stenosis.The left anterior descending(LAD)artery was most commonly involved(47.0%). No thrombus was found in the coronary arteries, and only one had chronic total occlusion(5.9%). Myocardial infarction was confirmed in all 13 patients with coronary artery disease, including six cases(35.3%)of AMI, 11 cases(64.7%)of OMI and four cases(23.5%)of AMI and OMI.Among AMI cases, transmural infarction was shown only in one case, with two cases of non-transmural infarction, two cases of subendocardial infarction and one case of focal myocardial infarction.Among OMI cases, transmural infarction was shown in one case, with two cases of non-transmural infarction, four cases of subendocardial infarction and four cases of focal myocardial infarction.The clinical misdiagnosis rate of OMI was as high as 81.8%.Patients died mainly from cardiovascular disease(70.6%), with six cases(35.3%)from myocardial infarction, three from heart failure(17.6%)and three from malignant arrhythmia(17.6%). Six of the cases suffered from sudden cardiac death(35.3%)with biopsy-confirmed myocardial infarction changes. Conclusions The incidence of CAD in elderly patients with calcific aortic stenosis is high.Pathological changes of myocardial infarction, especially of subendocardial and focal infarction, occur in patients with moderate to severe aortic stenosis and coronary heart disease with a high clinical misdiagnosis rate.Aortic stenosis implicates both the valve and myocardium.Assessment of myocardial lesions in patients with calcific aortic stenosis should be carefully conducted in clinical practice. Key words: Aortic valve stenosis; Coronary disease

Peak CK-MB has a strong association with chronic scar size and wall motion abnormalities after revascularized non-transmural myocardial infarction \u2013 a prospective CMR study

BackgroundLarge myocardial infarction (MI) is associated with adverse left ventricular (LV) remodeling (LVR). We studied the nature of LVR, with specific attention to non-transmural MIs, and the association of peak CK-MB with recovery and chronic phase scar size and LVR.MethodsAltogether 41 patients underwent prospectively repeated cardiovascular magnetic resonance at a median of 22 (interquartile range 9–29) days and 10 (8–16) months after the first revascularized MI. Transmural MI was defined as ≥75% enhancement in at least one myocardial segment.ResultsPeak CK-MB was 86 (40–216) μg/L in median, while recovery and chronic phase scar size were 13 (3–23) % and 8 (2–19) %. Altogether 33 patients (81%) had a non-transmural MI. Peak CK-MB had a strong correlation with recovery and chronic scar size (r ≥ 0.80 for all, r ≥ 0.74 for non-transmural MIs; p < 0.001). Peak CK-MB, recovery scar size, and chronic scar size, were all strongly correlated with chronic wall motion abnormality index (WMAi) (r ≥ 0.75 for all, r ≥ 0.73 for non-transmural MIs; p < 0.001). There was proportional scar size and LV mass resorption of 26% (0–50%) and 6% (− 2–14%) in median. Young age (< 60 years, median) was associated with greater LV mass resorption (median 9%vs.1%, p = 0.007).ConclusionsPeak CK-MB has a strong association with chronic scar size and wall motion abnormalities after revascularized non-transmural MI. Considerable infarct resorption happens after the first-month recovery phase. LV mass resorption is related to age, being more common in younger patients.

CT-based SPECT attenuation correction and assessment of infarct size: results from a cardiac phantom study.

Myocardial perfusion SPECT is a commonly performed, well established, clinically useful procedure for the management of patients with coronary artery disease. However, the attenuation of photons from myocardium impacts the quantification of infarct sizes. CT-Attenuation Correction (AC) potentially resolves this problem. This contention was investigated by analyzing various parameters for infarct size delineation in a cardiac phantom model. A thorax phantom with a left ventricle (LV), fillable defects, lungs, spine and liver was used. The defects were combined to simulate 6 infarct sizes (5-20% LV). The LV walls were filled with 100120kBq/ml 99mTc and the liver with 10-12kBq/ml 99mTc. The defects were filled with water of 50% LV activity to simulate transmural and non-transmural infarction, respectively. Imaging of the phantom was repeated for each configuration in a SPECT/CT system. The defects were positioned in the anterior as well as in the inferior wall. Data were acquired in two modes: 32 views, 30s/view, 180° and 64 views, 15s/view, 360° orbit. Images were reconstructed iteratively with scatter correction and resolution recovery. Polar maps were generated and defect sizes were calculated with variable thresholds (40-60%, in 5% steps). The threshold yielding the best correlation and the lowest mean deviation from the true extents was considered optimal. AC data showed accurate estimation of transmural defect extents with an optimal threshold of 50% [non attenuation correction (NAC): 40%]. For the simulation of non-transmural defects, a threshold of 55% for AC was found to yield the best results (NAC: 45%). The variability in defect size due to the location (anterior versus inferior) of the defect was reduced by 50% when using AC data indicating the benefit from using AC. No difference in the optimal threshold was observed between the different orbits. Cardiac SPECT/CT shows an improved capability for quantitative defect size assessment in phantom studies due to the positive effects of attenuation correction.

Echocardiographic Correlate of Subendocardial Myocardial Infarction

Nontransmural (subendocardial) myocardial infarcts produce classical discomfort. Electrocardiograms usually show localized T wave inversions. Routine echocardiography usually does not show supportive regional wall motion abnormalities. Detailed echocardiography, however, reveals endocardial sear in the affected region. This echocardiographic finding supports the clinical diagnosis of myocardial infarction. We are reporting such eleven cases.

Impact of Intramyocardial Hemorrhage and Microvascular Obstruction on Cardiac Mechanics in Reperfusion Injury: A Speckle-Tracking Echocardiographic Study

Intramyocardial hemorrhage (IMH) and microvascular obstruction (MVO) are two major mechanisms of reperfusion injury of the left ventricle after acute ST-segment elevation myocardial infarction (STEMI). The aim of this study was to assess the impact of IMH and MVO on left ventricular (LV) cardiac mechanics using two-dimensional speckle-tracking echocardiography during the acute phase of STEMI and on LV functional recovery. Eighty-one patients with STEMI who received primary reperfusion therapy were prospectively studied. Infarct segments were classified by cardiac magnetic resonance according to infarct transmurality and the presence or absence of IMH and/or MVO. Segmental systolic longitudinal strain, circumferential strain (CS), and radial strain were measured by two-dimensional speckle-tracking echocardiography. Adverse LV remodeling and major adverse cardiovascular events were assessed at 1year. MVO without IMH was much less frequent in nontransmural infarct segments than in transmural infarct segments (6.0% vs 19.1%, P=.000), while IMH was present only in transmural infarct segments. In nontransmural infarct segments, MVO was not associated with any significant changes in strain (P>.5). In transmural infarct segments, there were no differences in all types of strain between segments without reperfusion injury and those with MVO alone (P>.20). IMH was evident in the midmyocardial layer within the infarct zone in 196 segments (46.1%). The presence of IMH in addition to MVO decreased CS significantly (P=.004), but not longitudinal and radial strain(P>.5). A receiver operating characteristic curve analysis with cross-validation by k-folding showed that the sensitivity and specificity of CS using a cutoff of >-11.66% to diagnose IMH were 78.00% and 79.45%, respectively (area under the curve=0.86; P=.0001). At 1year, patients with major adverse cardiovascular events and LV remodeling had significantly lower baseline measurements of all types of global strain (P<.05). In the acute phase of STEMI, reperfusion MVO and IMH injury have differential effects on cardiac mechanics. IMH preferentially affects CS, presumably related to its location in the midmyocardial layer.

Detection of small subendocardial infarction using speckle tracking echocardiography in a rat model.

It is challenging to detect small nontransmural infarcts visually or automatically. As it is important to detect myocardial infarction (MI) at early stages, we tested the hypothesis that small nontransmural MI can be detected using speckle tracking echocardiography (STE) at the acute stage. Minimal nontransmural infarcts were induced in 18 rats by causing recurrent ischemia-reperfusion of the left anterior descending (LAD) coronary artery, followed by a 30-min ligation and by reperfusion. A week later, the scar size was measured by histological analysis. Each rat underwent three echocardiography measurements: at baseline, 1day post-MI, and 1week post-MI. To measure the peak circumferential strain (CS), peak systolic CS, radial strain (RS), and time-to-peak (TTP) of the CS, short-axis view of the apex was analyzed by a STE program. The TTP was normalized by the duration of the heart cycle to create percent change of heart cycle. Histological analysis after 1week showed scar size of 4±6% at the anterior wall. At 24h post-MI, the peak CS, peak systolic CS, and RS were reduced compared to baseline at the anterior wall due to the MI, and at the adjacent segments-the anterior septum and lateral wall, due to stunning (P<.05). However, only the anterior wall, the genuine damaged segment, showed prolonged TTP vs baseline (baseline 36%, 24h 48%, P<.05). The TTP of the CS can distinguish between regions adjacent to MI (stunned or tethered) and MI, even in small nontransmural infarcts.

DIAGNOSTICS ISSUES OF CHLAMYDOPHILA PNEUMONIAE INFECTION IN PATIENTS WITH ACUTE CORONARY SYNDROME

Chlamydophila pneumoniae is nadotrophic to endothelial, smooth muscle cells of blood vessels. Proven ability of the pathogen to initiate atherosclerosis and exacerbate it. The incidence of acute C. pneumoniae infection is higher in patients with acute coronary syndrome than in patients with chronic ischemic heart disease according to the published papers. The aim of the research was the diagnostics of C. pneumoniae infection in patients with acute coronary syndrome by two methods based on different principles. A total of 20 patients admitted to hospital with a preliminary acute coronary syndrome diagnosis. During the first hospital hours of stay based on complaints, medical history, physical examination, results of laboratory and instrumental examination those patients were diagnosed as unstable angina (n = 10) or nontransmural myocardial infarction (n = 10). According to treatment standart all patients underwent coronary angiography and angioplasty. Furthermore, these patients fulfilled fence of the clinical material as mucosal scrapings nasal passages and posterior wall of the oropharynx applied on glass slides. Also, there were samples of arterial blood smears, obtained from the conductors installed in the locations pointed to implement the coronary arteries and angioplasty. These samples were examined by indirect immunofluorescence with the form of specific monoclonal antibodies against the cell wall major outer membrane protein of C. pneumoniae. Serum was used for immunoassay to quantify classes A and G immunoglobulins against C. pneumoniae. When comparing the results of two diagnostics methods of C. pneumoniae chronic infection, it was diagnosed in 5 of the 20 patients studied. One patient was with unstable angina and 4 were with nontransmural myocardial infarction. The presence of acute infection C. pneumoniae has been proven in 9 of 20 patients, including 4 patients with unstable angina and 5 with nontransmural myocardial infarction. Also found that patients with acute coronary syndrome, the infection can occur both by seropositive and seronegative types. Thus, acute coronary syndrome may be associated with chronic or acute infection of C. pneumoniae. The relevance of further study of the infection in patients with atherosclerosis was confirmed once again.

Mechanisms for overestimating acute myocardial infarct size with gadolinium-enhanced cardiovascular magnetic resonance imaging in humans: a quantitative and kinetic study.

AimsIt remains controversial whether cardiovascular magnetic resonance imaging with gadolinium only enhances acutely infarcted or also salvaged myocardium. We hypothesized that enhancement of salvaged myocardium may be due to altered extracellular volume (ECV) and contrast kinetics compared with normal and infarcted myocardium. If so, these mechanisms could contribute to overestimation of acute myocardial infarction (AMI) size.Methods and resultsImaging was performed at 1.5T ≤ 7 days after AMI with serial T1 mapping and volumetric early (5 min post-contrast) and late (20 min post-contrast) gadolinium enhancement imaging. Infarcts were classified as transmural (>75% transmural extent) or non-transmural. Patients with non-transmural infarctions (n = 15) had shorter duration of symptoms before reperfusion (P = 0.02), lower peak troponin (P = 0.008), and less microvascular obstruction (P < 0.001) than patients with transmural infarcts (n = 22). The size of enhancement at 5 min was greater than at 20 min (18.7 ± 12.7 vs. 12.1 ± 7.0%, P = 0.003) in non-transmural infarctions, but similar in transmural infarctions (23.0 ± 10.0 vs. 21.9 ± 9.9%, P = 0.21). ECV of salvaged myocardium was greater than normal (39.5 ± 5.8 vs. 24.1 ± 3.1%) but less than infarcted myocardium (50.5 ± 6.0%, both P < 0.001). In kinetic studies of non-transmural infarctions, salvaged and infarcted myocardium had similar T1 at 4 min but different T1 at 8–20 min post-contrast.ConclusionThe extent of gadolinium enhancement in AMI is modulated by ECV and contrast kinetics. Image acquisition too early after contrast administration resulted in overestimation of infarct size in non-transmural infarctions due to enhancement of salvaged myocardium.

Relation of Functional Echocardiographic Parameters to Infarct Scar Transmurality by Magnetic Resonance Imaging

Identification of viable but dysfunctional myocardium after myocardial infarction is important for management, including the decision for revascularization. Assessment of infarct transmurality (TRM) by late contrast enhancement on magnetic resonance imaging (MRI) is frequently used for this task but has several limitations, particularly its availability. The goal of this study was to compare the value of several simple echocardiographic parameters measured at rest at the bedside for the identification of three degrees of infarct TRM, with contrast-enhanced MRI as the gold standard. In a prospective, single-center study, 41 patients (33 men; mean age, 62 ± 10 years; 32 with ST-segment elevation infarctions) underwent resting echocardiography and contrast-enhanced MRI <5 days after infarction. Wall motion score, preejection velocity by tissue Doppler, and longitudinal, circumferential, and radial peak systolic strain by speckle-tracking-based strain imaging were assessed, and the findings were compared with infarct TRM stratified by contrast-enhanced MRI (no scar, 0% TRM; nontransmural scar, 1%-50% TRM; and transmural scar, 51%-100% TRM). Four hundred segments showed no scar, 125 showed nontransmural scar, and 213 showed transmural scar on contrast-enhanced MRI. The sensitivity and specificity of visual wall motion scoring to detect any scar versus no scar were 71% and 81%, respectively, similar to values for circumferential strain (sensitivity and specificity both 81% with a cutoff of -14.5%). Longitudinal and radial strain performed less well, and the presence of preejection velocity performed distinctly worse (45% and 90%, respectively). The sensitivity and specificity for identifying nontransmural versus transmural infarction was better for circumferential strain (78% and 75%, respectively, with a cutoff of -10.5%) than for the other strain types, preejection velocity (52% and 67%, respectively), or visual wall motion scoring (50% and 81%, respectively, for a score > 2). Visual wall motion analysis alone is able to detect infarcted myocardium but cannot differentiate sufficiently between transmural and nontransmural infarction. This is best achieved at the bedside using speckle-tracking-based circumferential strain.

Cardioprotective Effects of Osteopontin-1 during Development of Murine Ischemic Cardiomyopathy

Repetitive brief ischemia and reperfusion (I/R) is associated with ventricular dysfunction in pathogenesis of murine ischemic cardiomyopathy and human hibernating myocardium. We investigated the role of matricellular protein osteopontin-1 (OPN) in murine model of repetitive I/R. One 15-min LAD-occlusion followed by reperfusion was performed daily over 3, 5, and 7 consecutive days in C57/Bl6 wildtype- (WT-) and OPN−/−-mice (n = 8/group). After echocardiography hearts were processed for histological and mRNA-studies. Cardiac fibroblasts were isolated, cultured, and stimulated with TGF-β1. WT-mice showed an early, strong, and cardiomyocyte-specific osteopontin-expression leading to interstitial macrophage infiltration and consecutive fibrosis after 7 days I/R in absence of myocardial infarction. In contrast, OPN−/−-mice showed small, nontransmural infarctions after 3 days I/R associated with significantly worse ventricular dysfunction. OPN−/−-mice had different expression of myocardial contractile elements and antioxidative mediators and a lower expression of chemokines during I/R. OPN−/−-mice showed predominant collagen deposition in macrophage-rich small infarctions. We found lower induction of tenascin-C, MMP-9, MMP-12, and TIMP-1, whereas MMP-13-expression was higher in OPN−/−-mice. Cultured OPN−/−-myofibroblasts confirmed these findings. In conclusion, osteopontin seems to modulate expression of contractile elements, antioxidative mediators, and inflammatory response and subsequently remodel in order to protect cardiomyocytes in murine ischemic cardiomyopathy.

Quantitative magnetic resonance imaging can distinguish remodeling mechanisms after acute myocardial infarction based on the severity of ischemic insult

The type and extent of myocardial infarction encountered clinically is primarily determined by the severity of the initial ischemic insult. The purpose of the study was to differentiate longitudinal fluctuations in remodeling mechanisms in porcine myocardium following different ischemic insult durations. Animals (N = 8) were subjected to coronary balloon occlusion for either 90 or 45 min, followed by reperfusion. Imaging was performed on a 3 T MRI scanner between day‐2 and week‐6 postinfarction with edema quantified by T2, hemorrhage by T2*, vasodilatory function by blood‐oxygenation‐level‐dependent T2 alterations and infarction/microvascular obstruction by contrast‐enhanced imaging. The 90‐min model produced large transmural infarcts with hemorrhage and microvascular obstruction, while the 45 min produced small nontransmural and nonhemorrhagic infarction. In the 90‐min group, elevation of end‐diastolic‐volume, reduced cardiac function, persistence of edema, and prolonged vasodilatory dysfunction were all indicative of adverse remodeling; in contrast, the 45‐min group showed no signs of adverse remodeling. The 45‐ and 90‐min porcine models seem to be ideal for representing the low‐ and high‐risk patient groups, respectively, commonly encountered in the clinic. Such in vivo characterization will be a key in predicting functional recovery and may potentially allow evaluation of novel therapies targeted to alleviate ischemic injury and prevent microvascular obstruction/hemorrhage. Magn Reson Med, 70:1095–1105, 2013. © 2012 Wiley Periodicals, Inc.

Quantitative magnetic resonance imaging can distinguish remodeling mechanisms after acute myocardial infarction based on the severity of ischemic insult

The type and extent of myocardial infarction encountered clinically is primarily determined by the severity of the initial ischemic insult. The purpose of the study was to differentiate longitudinal fluctuations in remodeling mechanisms in porcine myocardium following different ischemic insult durations. Animals (N = 8) were subjected to coronary balloon occlusion for either 90 or 45 min, followed by reperfusion. Imaging was performed on a 3 T MRI scanner between day-2 and week-6 postinfarction with edema quantified by T2, hemorrhage by T2*, vasodilatory function by blood-oxygenation-level-dependent T2 alterations and infarction/microvascular obstruction by contrast-enhanced imaging. The 90-min model produced large transmural infarcts with hemorrhage and microvascular obstruction, while the 45 min produced small nontransmural and nonhemorrhagic infarction. In the 90-min group, elevation of end-diastolic-volume, reduced cardiac function, persistence of edema, and prolonged vasodilatory dysfunction were all indicative of adverse remodeling; in contrast, the 45-min group showed no signs of adverse remodeling. The 45- and 90-min porcine models seem to be ideal for representing the low- and high-risk patient groups, respectively, commonly encountered in the clinic. Such in vivo characterization will be a key in predicting functional recovery and may potentially allow evaluation of novel therapies targeted to alleviate ischemic injury and prevent microvascular obstruction/hemorrhage.

Layer-specific analysis of myocardial deformation for assessment of infarct transmurality: comparison of strain-encoded cardiovascular magnetic resonance with 2D speckle tracking echocardiography

Separate analysis of endocardial and epicardial myocardial layer deformation has become possible using strain-encoded cardiovascular magnetic resonance (SENC) and 2D-dimensional speckle tracking echocardiography (Echo). This study evaluated and compared both modalities for the assessment of infarct transmurality as defined by late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR). In 29 patients (age 62.4 ± 11.7 years, 23 male) with ischaemic cardiomyopathy, SENC using 1.5 T CMR and Echo were performed. Peak circumferential systolic strain of the endocardial and the epicardial layer of 304 myocardial segments was assessed by SENC and by Echo. The segmental transmurality of myocardial infarction was determined as relative amount of LGE (0%: no infarction; 1-50%: non-transmural infarction; 51-100%: transmural infarction). Endocardial and epicardial strain defined by SENC and by Echo differed significantly between segments of different infarct transmurality determined by CMR. Endocardial layer circumferential strain analysis by Echo and by SENC allowed distinction of segments with non-transmural infarction from non-infarcted segments with similar accuracy [area under the curve (AUC) 0.699 vs. 0.649, respectively, P = 0.239]. Epicardial layer circumferential strain analysis by Echo and by SENC allowed distinction of transmural from non-transmural myocardial infarction defined by LGE CMR with similar accuracy (AUC 0.721 vs. 0.664, respectively, P = 0.401). Endocardial strain by SENC correlated moderately with endocardial strain by Echo (r = 0.50; standard error of estimate = 5.2%). Layer-specific analysis of myocardial deformation by Echo and by SENC allows discrimination between different transmurality categories of myocardial infarction with similar accuracy. However, accuracy of both methods is non-optimal, indicating that further tools for improvement should be evaluated in the future.

Differentiation of transmural and nontransmural infarction using speckle tracking imaging to assess endocardial and epicardial torsion after revascularization

Assessment of transmural extent (TME) of necrosis after acute myocardial infarction (MI) remains a major problem in clinical practice. The study sought to determine whether speckle tracking imaging (STI) could differentiate transmural from nontransmural acute MI by assessment of endocardial and epicardial torsion. TME of infarct was measured by contrast-enhanced magnetic resonance imaging. Patients were divided into two groups according to TME (transmural MI group [TME ≥ 50%, n = 36] and nontransmural MI group [TME < 50%, n = 35]). As a control group, 30 subjects without evidence of structural heart disease were included. Conventional echocardiography and STI were done in controls and patients before and 1 month after percutaneous coronary intervention. Compared with control subjects, endocardial and epicardial torsion in patients with transmural and nontransmural MI were all extremely decreased (all P < 0.01). One month after percutaneous coronary intervention, there was no significant increase in endocardial and epicardial torsion in transmural MI patients. However, apical rotation and left ventricular torsion resumed slightly but significantly in the epicardium (but not endocardium) in patient with nontransmural MI (3.11 ± 0.81 vs. 4.37 ± 1.15°, P < 0.01; 3.69 ± 1.07 vs. 5.52 ± 1.89°, P < 0.01, respectively). The combined evaluation of endocardial and epicardial torsion by STI may be used to differentiate transmural from nontransmural MI after revascularization.

Abstract 8229: Layer Specific Strain-Encoded Magnetic Resonance Imaging for Evaluation of Left Ventricular Function and Infarct Transmurality in Patients With Chronic Coronary Artery Disease

Background: Strain-encoded imaging (SENC) is a new technique for myocardial deformation analysis in cardiac magnetic resonance imaging (MRI). The study aimed to evaluate whether myocardial deformation imaging performed by SENC allows quantification of regional left ventricular (LV) function and is related to scar transmurality defined by contrast-enhanced MRI (ceMRI). Methods: 50 patients (age 62 ± 10 years) with chronic ischemic LV dysfunction underwent ceMRI using a clinical 1.5T scanner (Achieva, Philips, Best, The Netherlands). Strain-encoded images were acquired using a commercially available software to calculate myocardial endocardial and epicardial strain (Diagnosoft SENC version 2.05, Diagnosoft Inc., Palo Alto, USA). Layer-specific peak circumferential strain was measured from long-axis views and peak longitudinal strain was evaluated from short-axis views in a 16-segment model. The extent of myocardial infarction was determined semiautomatically (CAAS MRV 3.3, Pie Medical, Netherlands) for each segment as relative amount of hyperenhancement by ceMRI (0%: no infarction; 1-50%: non-transmural infarction; 51-100%: transmural infarction). Results: A total of 589 of 600 segments (98%) were analyzed. Endocardial and epicardial circumferential as well as longitudinal strain showed significant differences between visually defined segmental function states and differed also significantly between the degree of infarct transmurality (all p&lt;0.001). A cutoff peak circumferential endocardial strain value of -15% differentiated nontransmural from transmural infarcted myocardium with a sensitivity of 100% and a specificity of 86% (area under the curve (AUC) 0.94). Distinction of nontransmural infarcted myocardium from transmural infarcted myocardium was done more accurately using circumferential endocardial strain compared to longitudinal endocardial strain (AUC 0.94 vs. AUC 0.76, p=0.003). Conclusions: Layer-specific SENC provides objective quantification of regional myocardial function and allows accurate discrimination between different transmurality states of myocardial infarction. Circumferential endocardial strain showed the best distinction between the different degrees of infarct transmurality.