Subendocardial Infarction Research Articles

Cardiovascular Magnetic Resonance Before Invasive Coronary Angiography in Suspected Non–ST-Segment Elevation Myocardial Infarction

BackgroundIn suspected non–ST-segment elevation myocardial infarction (NSTEMI), this presumed diagnosis may not hold true in all cases, particularly in patients with nonobstructive coronary arteries (NOCA). Additionally, in multivessel coronary artery disease, the presumed infarct-related artery may be incorrect. ObjectivesThis study sought to assess the diagnostic utility of cardiac magnetic resonance (CMR) before invasive coronary angiogram (ICA) in suspected NSTEMI. MethodsA total of 100 consecutive stable patients with suspected acute NSTEMI (70% male, age 62 ± 11 years) prospectively underwent CMR pre-ICA to assess cardiac function (cine), edema (T2-weighted imaging, T1 mapping), and necrosis/scar (late gadolinium enhancement). CMR images were interpreted blinded to ICA findings. The clinical care and ICA teams were blinded to CMR findings until post-ICA. ResultsEarly CMR (median 33 hours postadmission and 4 hours pre-ICA) confirmed only 52% (52 of 100) of patients had subendocardial infarction, 15% transmural infarction, 18% nonischemic pathologies (myocarditis, takotsubo, and other forms of cardiomyopathies), and 11% normal CMR; 4% were nondiagnostic. Subanalyses according to ICA findings showed that, in patients with obstructive coronary artery disease (73 of 100), CMR confirmed only 84% (61 of 73) had MI, 10% (7 of 73) nonischemic pathologies, and 5% (4 of 73) normal. In patients with NOCA (27 of 100), CMR found MI in only 22% (6 of 27 true MI with NOCA), and reclassified the presumed diagnosis of NSTEMI in 67% (18 of 27: 11 nonischemic pathologies, 7 normal). In patients with CMR-MI and obstructive coronary artery disease (61 of 100), CMR identified a different infarct-related artery in 11% (7 of 61). ConclusionsIn patients presenting with suspected NSTEMI, a CMR-first strategy identified MI in 67%, nonischemic pathologies in 18%, and normal findings in 11%. Accordingly, CMR has the potential to affect at least 50% of all patients by reclassifying their diagnosis or altering their potential management.

Comparison of coronary artery lesion complexity and body component parameters measured by TANITA.

Obesity is one of the main reversible causes of coronary artery disease. To investigate the relationship between body component measurements calculated with TANITA and SYNTAX score (SXscore), which indicates coronary complexity. 200 acute subendocardial myocardial infarction patients were included in our study. Body component measurements were made with the TANITA BC-601 device. After coronary angiography, patients were divided into two groups: high SXscore (≥ 22) and low-medium SXscore (< 22). When the high SXscore group (50 patients) was compared with the low medium SXscore group (150 patients); for waist height ratio (p = 0.001), total fat weight (p = 0.001), total fat percentage (p = 0.006), total water percentage (p = 0.001), trunk fat percentage (p = 0.001), internal fat (p = 0.001) and metabolic age (p < 0.001), a statistical difference was found. In the correlation analysis, a correlation was detected between high SXscore and the waist height ratio (p = 0.042), trunk fat percentage (p = 0.047), internal fat (p < 0.001) and metabolic age (p = 0.009). ROC curve analysis for prediction of high SXscore detection; the cut-off value for internal fat and metabolic age was found to be 13.5-60.5 with 60-64% sensitivity and 61.3-62.7% specificity. We demonstrated the relationship between parameters such as internal fat, trunk fat percentage and metabolic age calculated by TANITA and SXscore, which is the coronary complexity score. We recommend that patients with high values detected during TANITA measurements be followed more carefully in terms of primary preventive medicine.

Novel Approach for Assessing Postinfarct Myocardial Injury and Inflammation Using Hybrid Somatostatin Receptor Positron Emission Tomography/Magnetic Resonance Imaging.

Novel Approach for Assessing Postinfarct Myocardial Injury and Inflammation Using Hybrid Somatostatin Receptor Positron Emission Tomography/Magnetic Resonance Imaging.

Novel Application of Post-contrast T1map for Detection of Subendocardial Infarction

In cardiac magnetic resonance (CMR) for myocardial infarction, there have been quite a few cases of obscure image contrast between subendocardial lesion and left ventricular (LV) blood pool on late gadolinium enhancement (LGE) images. This study was motivated by confirmation of usefulness of post-contrast T1map for detection of subendocardial infarction. From June 2017 to May 2018, forty-eight consecutive patients who underwent contrast-enhanced CMR to assess myocardial infarction were reviewed. We measured the contrast ratio (CR) between the infarcted myocardium and LV blood pool on LGE and on post-contrast T1map images, and compared them. The CR (mean±standard deviation) was -0.04±0.11 for LGE images and 0.02±0.04 for post-contrast T1map images (P<0.05). These results suggest that the post-contrast T1map, which uses the difference in T1 value as image contrast rather than magnitude image, can clearly depict the boundary between the infarcted myocardium and LV blood pool. The addition of post-contrast T1map to image interpretation might provide valuable information in the evaluation of subendocardial infarction.

Abstract 15675: Mid-Ventricular Hypertrophic Cardiomyopathy Presenting With Minoca

Background: Mid-ventricular hypertrophic obstructive cardiomyopathy (HOCM) is an uncommon form of cardiomyopathy that is linked to an apical aneurysm, increasing the risk of sudden death. Cases: We described four patients who presented with chest pain or SOB. Troponin elevation, acute myocardial infarction on cardiac MRI and absence of obstructive coronary disease confirmed the diagnosis of MINOCA. Echo revealed a pressure gradient between the apical and basal chambers of the left ventricle. Cardiac MRI showed mid-ventricular HOCM and mid-cavity obliteration with akinetic apical chamber LGE revealed areas of sub-endocardial or transmural myocardial infarction at the level of obstruction and at the apical segments distal to the obstruction. The presence of myocardial edema on tissue mapping in the same area suggested acute myocardial injury (Figure). Discussion: The pathogenesis of development of apical myocardial scarring and aneurysm formation in mid-ventricular HOCM remains unknown. Other variant of hypertrophic cardiomyopathy shows mid-myocardial foci of scar inside the hypertrophied segments, indicating fibrosis. Whereas in our patients, the LGE revealed a sub-endocardial or transmural infarct (myocardial infarction pattern) - an uncommon pattern in other hypertrophic cardiomyopathy variants. This pattern and elevation of troponin during the acute phase of illness supports the hypothesis that apical aneurysm is due to apical myocardial ischemia in mid-ventricular HOCM. Tissue characterization and pattern of scar by cardiac MRI in these patients could be useful in understanding the pathophysiology of this type of HOCM.

Improved myocardial scar visualization with fast free-breathing motion-compensated black-blood T1-rho-prepared late gadolinium enhancement MRI

PurposeClinical guidelines recommend the use of bright-blood late gadolinium enhancement (BR-LGE) for the detection and quantification of regional myocardial fibrosis and scar. This technique, however, may suffer from poor contrast at the blood-scar interface, particularly in patients with subendocardial myocardial infarction. The purpose of this study was to assess the clinical performance of a two-dimensional black-blood LGE (BL-LGE) sequence, which combines free-breathing T1-rho-prepared single-shot acquisitions with an advanced non-rigid motion-compensated patch-based reconstruction. Materials and methodsExtended phase graph simulations and phantom experiments were performed to investigate the performance of the motion-correction algorithm and to assess the black-blood properties of the proposed sequence. Fifty-one patients (37 men, 14 women; mean age, 55 ± 15 [SD] years; age range: 19–81 years) with known or suspected cardiac disease prospectively underwent free-breathing T1-rho-prepared BL-LGE imaging with inline non-rigid motion-compensated patch-based reconstruction at 1.5T. Conventional breath-held BR-LGE images were acquired for comparison purposes. Acquisition times were recorded. Two readers graded the image quality and relative contrasts were calculated. Presence, location, and extent of LGE were evaluated. ResultsBL-LGE images were acquired with full ventricular coverage in 115 ± 25 (SD) sec (range: 64–160 sec). Image quality was significantly higher on free-breathing BL-LGE imaging than on its breath-held BR-LGE counterpart (3.6 ± 0.7 [SD] [range: 2–4] vs. 3.9 ± 0.2 [SD] [range: 3–4]) (P <0.01) and was graded as diagnostic for 44/51 (86%) patients. The mean scar-to-myocardium and scar-to-blood relative contrasts were significantly higher on BL-LGE images (P < 0.01 for both). The extent of LGE was larger on BL-LGE (median, 5 segments [IQR: 2, 7 segments] vs. median, 4 segments [IQR: 1, 6 segments]) (P < 0.01), the method being particularly sensitive in segments with LGE involving the subendocardium or papillary muscles. In eight patients (16%), BL-LGE could ascertain or rule out a diagnosis otherwise inconclusive on BR-LGE. ConclusionFree-breathing T1-rho-prepared BL-LGE imaging with inline motion compensated reconstruction offers a promising diagnostic technology for the non-invasive assessment of myocardial injuries.

Distribution of evoked delayed potential and delayed potential in a patient with subendocardial inferior infarction and transmural postero-lateral infarction: A case report

A 47-year-old man with transmural posterolateral myocardial infarction (MI) and subendocardial inferior MI underwent catheter ablation for monomorphic ventricular tachycardia (VT). Right ventricular extra stimulation could unmask evoked delayed potentials in the subendocardial infarction area without delayed potentials in the sinus rhythm. Extra stimulation mapping for VT is useful for hidden VT substrates, particularly in the subendocardial infarction area.

Medium-Term Cardiac Outcomes in Young People with Multi-system Inflammatory Syndrome: The Era of COVID-19.

Multi-system inflammatory syndrome in children (MIS-C) causes widespread inflammation including a pancarditis in the weeks following a COVID infection. As we prepare for further coronavirus surges, understanding the medium-term cardiac impacts of this condition is important for allocating healthcare resources. A retrospective single-center study of 67 consecutive patients with MIS-C was performed evaluating echocardiographic and electrocardiographic (ECG) findings to determine the point of worst cardiac dysfunction during the admission, then at intervals of 6–8 weeks and 6–8 months. Worst cardiac function occurred 6.8 ± 2.4 days after the onset of fever with mean 3D left ventricle (LV) ejection fraction (EF) 50.5 ± 9.8%. A pancarditis was typically present: 46.3% had cardiac impairment; 31.3% had pericardial effusion; 26.8% demonstrated moderate (or worse) valvar regurgitation; and 26.8% had coronary dilatation. Cardiac function normalized in all patients by 6–8 weeks (mean 3D LV EF 61.3 ± 4.4%, p < 0.001 compared to presentation). Coronary dilatation resolved in all but one patient who initially developed large aneurysms at presentation, which persisted 6 months later. ECG changes predominantly featured T-wave changes resolving at follow-up. Adverse events included need for ECMO (n = 2), death as an ECMO-related complication (n = 1), LV thrombus formation (n = 1), and subendocardial infarction (n = 1). MIS-C causes a pancarditis. In the majority, discharge from long-term follow-up can be considered as full cardiac recovery is expected by 8 weeks. The exception includes patients with medium sized aneurysms or greater as these may persist and require on-going surveillance.

Cardiac arrest with successful cardiopulmonary resuscitation and survival induce histologic changes that correlate with survival time and lead to misdiagnosis in sudden arrhythmic death syndrome

BackgroundSudden arrhythmic death syndrome (SADS), defined as sudden cardiac death (SCD) with a morphologically normal heart, is an important cause of sudden death. Hypoperfusion due to cardiac arrest followed by successful cardiopulmonary resuscitation (CPR) may induce histologic changes that mimic pathologic conditions. Detailed characterisation of such features and whether they could confound SADS diagnosis are not described. MethodsRetrospective observational study analysing all consecutive cases of sudden death prospectively referred to a UK national cardiac pathology centre between 2017 and 2021. Cases showing hypoperfusion features were identified after review of clinical information and examination by expert cardiac pathologists. ResultsOut of 2,568 SCD cases, 126 (4.9%) were identified with hypoperfusion changes. Macroscopically, the commonest finding was left ventricular focal or diffuse subendocardial haemorrhage (13.5%). Microscopically, haemorrhage and contraction band necrosis (n = 50, 37.7%), subendocardial acute infarction (n = 44, 34.1%), interstitial mixed inflammatory cell infiltrates (n = 31, 24.9%), healing granulation tissue (n = 9, 7.1%) and subendocardial fibrosis (n = 1, 0.7%) were observed. These changes correlated to duration of survival following resuscitation. In a subcohort of 41 cases, autopsy pathologists misinterpreted such changes as ischaemic myocardial infarction (n = 7; 17%), myocarditis (n = 5; 12.1%), or other pathologies (n = 2; 4.8%) in 14 SADS cases. ConclusionWe provide a comprehensive characterisation of hypoperfusion-related changes in the heart following successful CPR with survival, which are time related. These features can lead to diagnostic confusion among pathologists but knowledge of history of resuscitation with survival should help with general and expert pathology assessment and improve SADS diagnostic yield, prompting genetic screening of decedents’ relatives.

Simplified image acquisition and detection of ischemic and non-ischemic myocardial fibrosis with fixed short inversion time magnetic resonance late gadolinium enhancement.

Late gadolinium enhancement with fixed short inversion time (LGEshort) provides excellent tissue contrast with dark scar and bright blood pool and does not need prior myocardial nulling. We hypothesize better visibility of ischemic scars and equal visibility of non-ischemic LGE in LGEshort compared to clinically established LGE (LGEstandard). LGEshort and LGEstandard were retrospectively evaluated in 179 patients (3043 segments) with suspected or known coronary artery disease by four blinded readers (reader A: most experienced - D: least experienced). The amount of ischemic and non-ischemic LGE as well as visibility (4: very good - 1: poor) of ischemic LGE was visually assessed. All readers detected more infarcted segments in LGEshort compared to LGEstandard (378 segments reported as infarcted; A:p = 0.5, B:p = 0.8, C,D:p = 0.03). Scar visibility was scored higher in LGEshort by all readers (A,B:p = 0.03; C,D:p = 0.02), especially for subendocardial infarcts (A,B:p = 0.04, C,D:p = 0.02). Less experienced readers detected significantly more infarcted papillary muscles (C:p = 0.02, D:p = 0.03) in a shorter reading time in LGEshort (C:p = 0.04, D:p = 0.02). Non-ischemic LGE was equally visible in both sequences (A:p = 0.9, B:p = 0.8, C,D:p = 0.6). LGEshort detects more ischemic LGE with improved scar visibility compared to LGEstandard, independent of experience level. The visibility of non-ischemic LGE is equivalent to LGEstandard. Less experienced readers can diagnose ischemic and non-ischemic LGE faster in LGEshort. LGEshort with its maximal operational simplicity can be used for visualization of all types of fibrosis - ischemic and non-ischemic - instead of LGEstandard, independent of experience level.

Pathobiology of Myocardial Ischemia and Reperfusion Injury: Models, Modes, Molecular Mechanisms, Modulation, and Clinical Applications.

This review presents an integrated approach to the analysis of myocardial ischemia and reperfusion injury and the modulating influence of myocardial conditioning during the evolution of acute myocardial infarction (AMI) and other clinical settings. Experimental studies have involved a spectrum of in vitro, ex vivo, and in vivo models, and guidelines have been developed for the conduct of rigorous preclinical studies and for the identification of various forms of cell injury and death in evolving AMI. AMI in vivo is dominated by oncosis (cell injury with swelling) leading to necroptosis and final necrosis of ischemic cardiomyocytes (CMCs), without or with contraction band formation. Early after coronary occlusion, reperfusion salvages a significant amount of ischemic myocardium in the subepicardium while reperfusion injury contributes up to 50% of the final subendocardial infarct. AMI progression is mediated by damage (or danger)-associated molecular patterns, also known as alarmins, which activate pattern recognition receptors and initiate the inflammatory response. In preclinical studies, lethal reperfusion injury can largely be prevented with preconditioning or postconditioning by pharmacologic or physical means due to effects on both the CMC and microvasculature. Conditioning involves triggers, cytosolic mediators, and intracellular effectors. Mitochondria have a central role in the maintenance and loss of viability of CMCs. Reperfusion of severely ischemic myocardium leads to sustained opening of the mitochondrial permeability transition pore (MPTP). Once the MPTP is opened, the mitochondrial membrane potential (ΔΨm) is rapidly lost and energy production ceases. Conditioning blocks the sustained opening of the MPTP. Translation of conditioning strategies to the clinical management of patients has been challenging. The status of translation of experimental findings to approaches to modulate and ameliorate ischemic and reperfusion injury is discussed for the clinical settings of acute coronary syndromes treated with percutaneous interventions and cardiac preservation during open heart surgery and cardiac transplantation.

From Q/Non-Q Myocardial Infarction to STEMI/NSTEMI: Why It's Time to Consider Another Simplified Dichotomy; a Narrative Literature Review.

Acute coronary syndromes (ACSs) are classified as ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) based on the presence of guideline-recommended ST-segment elevation (STE) criteria on the electrocardiogram (ECG). STEMI is associated with acute total coronary occlusion (ATO) and transmural myocardial necrosis and is managed with emergent reperfusion therapy, and NSTEMI is supposedly synonymous with subendocardial myocardial infarction without ATO. However, coronary angiograms reveal that a significant proportion of patients with NSTEMI have ATO. Here, we review articles that studied the frequency and cardiovascular outcomes of ATO in NSTEMI patients compared with those without ATO. We discuss ECG patterns of patients with suspected acute myocardial infarction that do not fulfill STEMI criteria but are associated with ATO. Under-recognition of these atypical patterns results in delays to reperfusion therapy. We also advocate revision of the current STEMI/NSTEMI paradigm because consideration of STE, by itself, out of context of other clinical and ECG features, leads to the ECG diagnosis of STEMI when the ECG actually represents a mimic ["Pseudo-STEMI"],and suggest renaming the ACSs classification as the Occlusion Myocardial Infarction (OMI)/Non-Occlusion Myocardial Infarction (NOMI) paradigm.

Stable Gastric Pentadecapeptide BPC 157 Therapy for Primary Abdominal Compartment Syndrome in Rats.

Recently, the stable gastric pentadecapeptide BPC 157 was shown to counteract major vessel occlusion syndromes, i.e., peripheral and/or central occlusion, while activating particular collateral pathways. We induced abdominal compartment syndrome (intra-abdominal pressure in thiopental-anesthetized rats at 25 mmHg (60 min), 30 mmHg (30 min), 40 mmHg (30 min), and 50 mmHg (15 min) and in esketamine-anesthetized rats (25 mmHg for 120 min)) as a model of multiple occlusion syndrome. By improving the function of the venous system with BPC 157, we reversed the chain of harmful events. Rats with intra-abdominal hypertension (grade III, grade IV) received BPC 157 (10 µg or 10 ng/kg sc) or saline (5 ml) after 10 min. BPC 157 administration recovered the azygos vein via the inferior–superior caval vein rescue pathway. Additionally, intracranial (superior sagittal sinus), portal, and caval hypertension and aortal hypotension were reduced, as were the grossly congested stomach and major hemorrhagic lesions, brain swelling, venous and arterial thrombosis, congested inferior caval and superior mesenteric veins, and collapsed azygos vein; thus, the failed collateral pathway was fully recovered. Severe ECG disturbances (i.e., severe bradycardia and ST-elevation until asystole) were also reversed. Microscopically, transmural hyperemia of the gastrointestinal tract, intestinal mucosa villi reduction, crypt reduction with focal denudation of superficial epithelia, and large bowel dilatation were all inhibited. In the liver, BPC 157 reduced congestion and severe sinusoid enlargement. In the lung, a normal presentation was observed, with no alveolar membrane focal thickening and no lung congestion or edema, and severe intra-alveolar hemorrhage was absent. Moreover, severe heart congestion, subendocardial infarction, renal hemorrhage, brain edema, hemorrhage, and neural damage were prevented. In conclusion, BPC 157 cured primary abdominal compartment syndrome.

Abstract 16747: Rapidly Lethal Dilated Cardiomyopathy Secondary To Generalized Arterial Calcification Of Infancy

Case Presentation: A previously healthy 3-month-old infant presented with cardiorespiratory arrest, from which she was successfully resuscitated. A dilated cardiomyopathy with severely depressed systolic function was diagnosed. ECG showed high voltage QRS complexes and generalized alteration of repolarization. In the following 12 hours, she suffered 2 other cardiac arrests, recuperated with defibrillation. Hemodinamic stability was achieved but brain death was diagnosed 36 hours after the onset of symptoms. Autopsy showed striking calcification of the right and left coronary arteries, with narrowing of the arterial lumen, causing extensive subendocardial infarction. Calcification also affected the aorta, pulmonary arteries, thyroid, kidney and other splanchnic arteries. Generalized arterial calcification of infancy (GACI) was diagnosed and a genetic study found two biallelic variants in ABCC6 gene: p.Arg1114Cys and p.Trp38Ser, both previously described in elastic pseudoxanthoma (PXE), but not in GACI. Genotyping of the healthy parents confirmed genetic segregation with biallelic variants. Discussion: GACI is an extremely rare genetic disease characterized by widespread arterial calcification and narrowing of large and medium-sized vessels. The usual clinical presentation is heart failure in fetal life or in the first months of infancy. In most cases it is lethal, with death occurring within a few hours or days after the onset of symptoms, although clinical involvement is highly variable and cases with long survival have been described. GACI is an autosomal recessive disease secondary to biallelic variants in the ENPP1 gene (67% of cases) and in the ABCC6 gene (9%). The variants found in our patient had not been previously described in GACI, just in PXE, a much milder disease with usually normal lifespan. This case confirms that both entities reflect two extremes of a clinical spectrum of ectopic calcification instead of two different disorders. The aim of presenting this case is to remind clinicians of this rare etiology in neonates or infants with dilated cardiomyopathy. In case of death, autopsy should always be requested. When this condition is diagnosed, genetic study will be positive in 75% of cases, allowing prenatal counseling.

Robert's Intragastric Alcohol-Induced Gastric Lesion Model as an Escalated General Peripheral and Central Syndrome, Counteracted by the Stable Gastric Pentadecapeptide BPC 157.

We redefined Robert’s prototypical cytoprotection model, namely the intragastric administration of 96% alcohol in order to generate a general peripheral and central syndrome similar to that which occurs when major central or peripheral veins are occluded in animal models. With this redefinition, we used Robert’s model to examine the cytoprotective effects of the stable gastric pentadecapeptide BPC 157. The intragastric administration of alcohol induced gastric lesions, intracranial (superior sagittal sinus) hypertension, severe brain swelling and lesions, portal and vena caval hypertension, aortal hypotension, severe thrombosis, inferior vena cava and superior mesenteric vein congestion, azygos vein failure (as a failed collateral pathway), electrocardiogram disturbances, and heart, lung, liver and kidney lesions. The use of BPC 157 therapy (10 µg/kg or 10 ng/kg given intraperitoneally 1 min after alcohol) counteracted these deficits rapidly. Specifically, BPC 157 reversed brain swelling and superior mesenteric vein and inferior vena caval congestion, and helped the azygos vein to recover, which improved the collateral blood flow pathway. Microscopically, BPC 157 counteracted brain (i.e., intracerebral hemorrhage with degenerative changes of cerebral and cerebellar neurons), heart (acute subendocardial infarct), lung (parenchymal hemorrhage), liver (congestion), kidney (congestion) and gastrointestinal (epithelium loss, hemorrhagic gastritis) lesions. In addition, this may have taken place along with the activation of specific molecular pathways. In conclusion, these findings clarify and extend the theory of cytoprotection, offer an approach to its practical application, and establish BPC 157 as a prospective cytoprotective treatment.

Microstructural characteristics of chronic infarct segments assessed using diffusion tensor imaging

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): British Heart Foundation Background The microstructural changes following myocardial infarction (MI) can be characterised in-vivo with cardiac diffusion tensor imaging (cDTI) imaging, using mean diffusivity (MD), fractional anisotropy (FA), secondary eigenvector angle (E2A) and helix angle (HA) maps. In this study, we use cDTI to explore the microstructural differences between subendocardial and transmural chronic infarct segments. Method Twenty STEMI patients (15 men, 5 women, mean age 59) underwent 3T CMR scan at 3 months following presentation (mean interval 107 ± 18 days). Scan protocol included: second order motion compensated (M012) free-breathing spin echo DTI (3 slices, 18 diffusion directions at b-values 100s/mm2[3], 200s/mm2[3] and 500s/mm2[12], acquired resolution was 2.20x2.27x8mm3; cine gradient echo and LGE imaging. Average MD, FA, E2A and HA parameters were calculated on a 16-AHA-segmental level. HA maps were described by dividing values into left-handed HA (LHM, -90° &amp;lt; HA &amp;lt; -30°), circumferential HA (CM, -30° &amp;lt; HA &amp;lt; 30°), and right-handed HA (RHM, 30° &amp;lt; HA &amp;lt; 90°) and reported as relative proportions. Infarct segments were identified using LGE; patients were categorised according to the maximal transmurality of their infarct segments, into subendocardial (&amp;lt;50% LGE) or transmural (&amp;gt;50% LGE) MI. Results DTI acquisition was successful in all patients (acquisition time 13 ± 5mins). Ten patients had transmural MI. The results are shown in table 1. Transmurally infarcted segments had significantly lower FA (FA subendocardial MI = 0.27 ± 0.04, FA transmural MI = 0.23 ± 0.02, p &amp;lt; 0.01), lower E2A (E2A subendocardial MI = 47 ± 7°, E2A transmural MI = 38 ± 6°, p &amp;lt; 0.01) and lower proportions of right-handed cardiomyocytes (RHM subendocardial MI = 21 ± 5%, RHM transmural MI = 14 ± 5%, p &amp;lt; 0.01) than subendocardial infarct segments. Conclusion Compared to subendocardial MI segments, the diffusion of water molecules is more isotropic in transmurally infarcted myocardium as evidenced by lower FA values, signifying increased structural disarray. The significantly lower E2A values suggest that laminar sheetlets of transmural infarct segments remain fixed at shallower angles during systole and are unable to reach their usual contractile configuration. The lower proportions of RHM on HA maps highlight the significantly greater loss of subendocardial cardiomyocytes in transmural infarct segments. Further studies are required to assess if these segmental changes can be predictive of long-term LV remodelling.

Post myocardial infarction ionic remodelling promotes repolarisation dispersion and electrocardiogram abnormalities in acute and chronic stages

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Wellcome Trust Background Sudden cardiac death (SCD) occurs in both acute and chronic stages post myocardial infarction (MI), and the left ventricular ejection fraction (LVEF) and electrocardiogram (ECG) characteristics are important biomarkers for clinical decision making. While various ionic remodelling has been reported in literature at various stages post-MI, the effect of them on clinical biomarkers have not been fully explored. Purpose Evaluate the effects of cellular ionic remodelling in acute and chronic post myocardial infarction on ECG and LVEF biomarkers through computational modelling and simulations of human biventricular electromechanics. Methods An electromechanical coupled biventricular model with ToR-ORd (Tomek 2019) human electrophysiology coupled with human excitation-contraction machinery (Land 2017) and orthotropic passive mechanics (Holzapfel 2009) was used as baseline model. The 12-lead ECG were simulated at standard body-surface electrode locations, and the biventricular pressure volume loop was simulated to quantify the simulated LVEF. A cardiac magnetic resonance (CMR) derived human biventricular geometry (Strocchi 2020) was used in combination with rigidly aligned torso geometry (Minchole 2019). An anterior sub-endocardial infarction was delineated with infarct, border zone (BZ) and remote zone (RZ) regions. For acute infarction, three types of BZ ionic remodelling from literature, and their effects on simulated LVEF and ECG characteristics were quantified. For chronic infarction, a single chronic BZ ionic remodelling was combine with two different models of RZ ionic remodelling from literature, and the effects of these remodelling on the simulated LVEF and ECG were quantified. The electromechanical properties of the sub-endocardial infarct region did not significantly affect simulated ECG or LVEF biomarkers. Results For the acute phase, simulations showed pre-cordial ECG abnormalities for all three BZ models, with T-wave inversion and QT prolongation (80 ms) in BZ1, ST-segment elevation with T-wave inversion in BZ2, and decreased T-wave amplitude in BZ3. Activation maps showed conduction block in BZ2 simulations, leading to ST-segment elevation. Repolarisation maps showed high dispersion in BZ1 simulations, leading to T-wave inversion. LVEF for BZ2 decreased by 4% (from 57% in control) due to conduction block in BZ and lack of contraction in that region, LVEF remained constant for BZ1 and BZ3 simulations. For the chronic phase, there was QT prolongation in both RZ1 (80 ms) and RZ2 (170 ms) as well as decreased T-wave amplitude, reflected by elevated repolarisation dispersion. LVEF was not significantly altered for either simulations. Conclusions Post-MI ionic remodelling at the acute and chronic stages cause varying degrees of dispersion of repolarisation and T-wave and ST-segment abnormalities, with minimal effect on mechanical function, except in the case of severe conduction abnormality. Abstract Figure.

Role of speckle tracking echocardiography in patients with myocardial infarction

All over the world cardiovascular diseases are one of the main reason of morbidity and mortality in the structure of non-communicable diseases, and myocardial infarction has a leading role. Markers of modern advanced ultrasound techniques, speckle tracking echocardiography, play significant role in the detection and assessment of cardiovascular disease. Deviation of them can detect myocardial ischemia, hypertrophy, dystrophy and infiltration, severe systemic diseases, cardiotoxicity of the drugs, etc. This technology significantly improves diagnostic capabilities of transthoracic echocardiography, it allows to assess myocardial function in all three planes (longitudinal, circumferential and radial), in which myocardium moves during cardiac cycle. Speckle tracking echocardiography can determine the volume of myocardial damage, differentiate subendocardial and transmural myocardial infarction, identify viable and fibrous areas of the myocardium, that is confirmed by the results of magnetic resonance imaging. Besides, this method helps to detect and assess mechanical dyssynchrony and also predict the risk of pathological left ventricular remodeling and life-threatening adverse cardiovascular events (arrhythmias, increasing of heart failure, recurrent myocardial infarction, stroke, death, etc.), that is important for patients with acute myocardial infarction to identify high-risk patients. The most studied markers of this technique are longitudinal, circumferential and radial strain, mechanical dispersion and postsystolic shortening. Markers of this ultrasound technique significantly complete other markers of transthoracic echocardiography, such as left ventricular ejection fraction, to assess risk stratification of cardiovascular complications. The value of speckle-tracking echocardiography markers has been demonstrated alone or in combination with other markers.

Inverse association of mortality and body mass index in patients with left ventricular systolic dysfunction of both ischemic and non-ischemic etiologies.

BackgroundObesity is a worldwide epidemic that has been associated with poor outcomes. Previous studies have demonstrated an inverse relationship between body mass index (BMI) and outcomes, the 'obesity paradox', in several diseases.HypothesisWe sought to evaluate whether the obesity paradox is present in patients with left ventricular systolic dysfunction (LVSD) of all etiologies, using all‐cause mortality as the primary endpoint and hospitalization as the secondary endpoint.MethodsWe conducted a retrospective cohort study of LVSD patients (n = 18 003) seen within the University of Pittsburgh Medical Center network between January 2011 and December 2017. Patients were divided into four BMI categories (underweight, normal weight, overweight, and obese) and stratified by left ventricular ejection fraction (LVEF): <20%, 20–35%, and 35–50%.ResultsOver a median follow‐up of 2.28 years, higher BMI (mean 28.9 ± 6.8) was associated with better survival for the overall cohort and within LVEF strata (p < .0001). The most common cause of hospitalization was subendocardial infarction among underweight and normal weight patients and heart failure among overweight and obese patients. Cox proportional hazards model showed that BMI, age, and comorbid conditions of diabetes mellitus, chronic obstructive pulmonary disease, chronic kidney disease, and prior myocardial infarction are independent predictors of death.ConclusionsOur results support the existence of an obesity paradox impacting all‐cause mortality in patients with LVSD of ischemic and non‐ischemic etiologies even after adjusting for LVEF and comorbidities. Additional research is needed to understand the effect of weight loss on survival once a diagnosis of LVSD is established.

Human biventricular electromechanical simulations on the progression of electrocardiographic and mechanical abnormalities in post-myocardial infarction.

AimsDevelop, calibrate and evaluate with clinical data a human electromechanical modelling and simulation framework for multiscale, mechanistic investigations in healthy and post-myocardial infarction (MI) conditions, from ionic to clinical biomarkers. Methods and resultsHuman healthy and post-MI electromechanical simulations were conducted with a novel biventricular model, calibrated and evaluated with experimental and clinical data, including torso/biventricular anatomy from clinical magnetic resonance, state-of-the-art human-based membrane kinetics, excitation–contraction and active tension models, and orthotropic electromechanical coupling. Electromechanical remodelling of the infarct/ischaemic region and the border zone were simulated for ischaemic, acute, and chronic states in a fully transmural anterior infarct and a subendocardial anterior infarct. The results were compared with clinical electrocardiogram and left ventricular ejection fraction (LVEF) data at similar states. Healthy model simulations show LVEF 63%, with 11% peak systolic wall thickening, QRS duration and QT interval of 100 ms and 330 ms. LVEF in ischaemic, acute, and chronic post-MI states were 56%, 51%, and 52%, respectively. In linking the three post-MI simulations, it was apparent that elevated resting potential due to hyperkalaemia in the infarcted region led to ST-segment elevation, while a large repolarization gradient corresponded to T-wave inversion. Mechanically, the chronic stiffening of the infarct region had the benefit of improving systolic function by reducing infarct bulging at the expense of reducing diastolic function by inhibiting inflation.ConclusionOur human-based multiscale modelling and simulation framework enables mechanistic investigations into patho-physiological electrophysiological and mechanical behaviour and can serve as testbed to guide the optimization of pharmacological and electrical therapies.