Estimation Of Infarct Size Research Articles

Significance of QRS scoring system in left ventricular function recovery after acute myocardial infarction.

The Selvester scoring system has been derived from ECG parameters for estimating infarct size. However, there is still a lack of evidence for Selvester score as an alternative to cardiac magnetic resonance (CMR) myocardial injury makers for risk stratification and prediction of left ventricular function (LVF) recovery among patients with ST-segment elevation myocardial infarction (STEMI). This multicentre observational study enrolled 328 STEMI patients (88.4% men, 57.3±10.6years of age) undergoing CMR examination 1week post-reperfusion therapy. Patients with baseline left ventricular ejection fraction (LVEF)<50% underwent a follow-up CMR 6months later, categorized into baseline normal LVF (ejection fraction [EF]≥50% at baseline, n=155); recovered LVF (EF<50% at baseline and ≥50% after 6months, n=69); and reduced LVF (EF<50% at baseline and after 6months, n=104). The median follow-up was 4 (3-4) years for all patients, with 61 patients experiencing major adverse cardiovascular event (MACEs). Patients with reduced LVF had a higher risk of MACEs than those with baseline normal LVF (P=0.01), while the recovered LVF group had no significant difference (P>0.05). A Selvester score >10 doubled the risk of MACEs in patients with systolic dysfunction (1.91 [1.02 to 3.58], P=0.04). Additionally, Selvester score, baseline LVEF, transmural infarction, and peak CK-MB were independent predictors of recovered LVF, with Selvester score providing incremental predictive value to peak CK-MB in predicting recovered LVF (∆AUC=0.07, P<0.05). The Selvester score improves risk stratification among STEMI patients beyond LVEF and provide independent and incremental information to clinical parameters in predicting recovered LVF.

Inflammatory Type Focal Cerebral Arteriopathy of the Posterior Circulation in Children: A Comparative Cohort Study.

Inflammatory type focal cerebral arteriopathy (FCA-i) in the anterior circulation (AC) is well characterized, and the focal cerebral arteriopathy severity score (FCASS) reflects the severity of the disease. We identified cases of FCA-i in the posterior circulation (PC) and adapted the FCASS to describe these cases. In this comparative cohort study, patients from the Swiss NeuroPaediatric Stroke Registry with ischemic stroke due to FCA-i between January 2000 and December 2018 were analyzed. A comparison between PC and AC cases regarding pediatric National Institutes of Health Stroke Scale score and pediatric stroke outcome measure and FCASS was performed. We estimated infarct size by the modified pediatric Alberta Stroke Program Early Computed Tomography Score in children with AC stroke and the adapted Bernese posterior diffusion-weighted imaging score in the PC. Thirty-five children with a median age of 6.3 (interquartile range, 2.7-8.2 [95% CI, 0.9-15.6]; 20 male; 57.1%) years with FCA-i were identified. The total incidence rate was 0.15/100 000/year (95% CI, 0.11-0.21). Six had PC-FCA-i. Time to final FCASS was longer in the PC compared with AC; the evolution of FCASS did not differ. Initial pediatric National Institutes of Health Stroke Scale score was higher in children with FCA-i in the PC with a median of 10.0 (interquartile range, 5.75-21.0) compared with 4.5 (interquartile range, 2.0-8.0) in those with AC-FCA-i. Different from the anterior cases, PC infarct volume did not correlate with higher discharge, maximum, or final FCASS scores (Pearson correlation coefficient [r], 0.25, 0.35, and 0.54). FCA-i also affects the PC. These cases should be included in future investigations into FCA-i. Although it did not correlate with clinical outcomes in our cohort, the modified FCASS may well serve as a marker for the evolution of the arteriopathy in posterior FCA-i.

Simplified Selvester QRS Score as an Infarct Size Parameter in STEMI Patients Undergoing Pharmacoinvasive or Primary Percutaneous Coronary Intervention

Background:Cardiovascular disease especially acute myocardial infarct (AMI) is one of the highest cause of mortality worldwide. Majority of AMI comes in the form of ST elevation myocardial infarct (STEMI) that requires timely diagnosis and revascularization management to restore myocardial circulation. The simple method to estimate infarct size is by using simplified Selvester QRS Score to electrocardiogram records, which is a tested method that have good correlation with gold standard, namely cardiac magnetic resonance imaging. &#x0D; Objectives : To investigate difference of infarct size with simplified Selvester QRS score parameter between STEMI patients undergoing pharmacoinvasive compared to primary PCI.&#x0D; Methods: Eighty-two STEMI patients, 41 of pharmacoinvasive and 41 of primary PCI was scored with simplified Selvester QRS score from electrocardiogram recording. Patient data are retroactively taken form Sardjito Cardiovascular Intensive Care (SCIENCE) registry. Scoring of simplified Selvester QRS Score was done by two experienced cardiologist blinded to patient procedure, and results then measured for interobserver agreement with Bland-Altman test. Comparison of QRS Score in pharmacoinvasive and primary PCI group was done with independent sample T test followed with multivariable linear regression test.&#x0D; Results: The means of simplified Selvester QRS score in pharmacoinvasive and primary PCI group is 7.240±3.015 and 8.900±4.188, p=0.043, respectively. Independent sample T test shows significant difference in the simplified Selvester QRS score in pharmacoinvasive and primary PCI group. The multivariable analysis shows that variables other than revascularization method independently influences QRS score are onset, anterior segment ST elevation and ST segment elevation in more &gt; 3 leads in electrocardiogram.&#x0D; Conclusion: There is significant difference in infarct size measured by simplified Selvester QRS score betweem STEMI patient undergoing pharmacoinvasive method compared to primary PCI procedure, which is lower in the pharmacoinvasive group

Inosine attenuates post-stroke neuroinflammation by modulating inflammasome mediated microglial activation and polarization

To date, various agents and molecules have been developed to treat post-stroke neuroinflammation; however, none of them are clinically successful. Post-stroke neuroinflammation is primarily attributed to microglial polarization as the generation of inflammasome complexes shifts microglia to their M1 phenotype and regulates the downstream cascade. Inosine, an adenosine derivative reported to maintain cellular energy homeostasis in stressed conditions. Although the exact mechanism is still unexplored, various studies have reported that it can stimulate axonal sprouting in different neurodegenerative diseases. Hence, our present study aims to decipher the molecular mechanism of inosine mediated neuroprotection by modulating inflammasome signaling towards altered microglial polarization in ischemic stroke. Inosine was administered intraperitoneally to male Sprague Dawley rats at 1 h post-ischemic stroke and was further evaluated for neurodeficit score, motor coordination and long-term neuroprotection. Brains were harvested for infarct size estimation, biochemical assays and molecular studies. Inosine administration at 1 h post ischemic stroke decreased infarct size, neurodeficit score, and improved motor co-ordination. Normalization of biochemical parameters were achieved in the treatment groups. Microglial polarization towards its anti-inflammatory phenotype and modulation of inflammation were evident by relevant gene and protein expression studies. The outcome provides preliminary evidence of inosine mediated alleviation of post-stroke neuroinflammation via modulation of microglial polarization towards its anti-inflammatory form through regulating the inflammasome activation.

Correlation of serial high-sensitivity cardiac troponin t values to infarct mass determined by cardiac magnetic resonance imaging

Abstract Funding Acknowledgements Type of funding sources: None. Background/Introduction The extent of myocardial injury is strongly associated with adverse outcome after acute myocardial infarction (AMI). Contrast-enhanced magnetic resonance imaging (CE-MRI) is the preferred technique for myocardial imaging. Its use in daily clinical practise, however, is restricted due to limited availability and high costs. High-sensitivity cardiac troponin T (hs-cTnT) correlates well with the extent of myocardial injury and may therefore be a cost effective and widely available surrogate for the estimation of infarct size. Purpose To validate correlations between CE-MRI infarct mass and hs-cTnT values at different time points in patients with confirmed AMI. Methods Patients presenting with AMI and with available CE-MRI between January 1, 2018 and December 31, 2020 were included. Correlation coefficients between hs-cTnT on admission, after 24h, 48h, 72h, 96h and peak hs-cTnT values and CE-MRI infarct mass were calculated. Correlations between hs-cTnT and CE-MRI infarct mass were compared to those of a 3rd generation cTnT assay from a previously published study of our group. Results 137 patients were included for the present analysis. Median CE-MRI infarct mass was 12,5 g (95%CI: 9.8-16.2 g). Hs-cTnT values and infarct mass correlated well at all time points including admission (r=0.474, [95%CI: 0.331-0.560], p&amp;lt;0.0001), 24h (r=0.508, [95%CI: 0.370-0.625], p&amp;lt;0.0001), 48h (r=0.547, [95%CI: 0.404-0.664], p&amp;lt;0.0001), 72h (r=0.489, [95%CI: 0.320-0.628], p&amp;lt;0.0001), 96h (r=0.509, [95%CI: 0.330-0.653], p&amp;lt;0.001) including peak hs-cTnT values (r=0.547, [95%CI: 0.416-0.656], p&amp;lt;0.0001) and maximum absolute delta changes within 96h (r=0.507, [95%CI: 0.369-0.622], p&amp;lt;0.001). Correlations of the 3rd generation assay could be confirmed for hs-cTnT at all time points. A superior correlation with CE-MRI infarct mass was observed for hs-cTnT values on admission. Conclusions Hs-cTnT values at different time points correlate well with CE-MRI infarct mass. Correlations of admission hs-cTnT values are superior to those of a 3rd generation assay.

Post-stroke Depression is Alleviated by Apelin-13 via Regulating BDNF Mediated Phosphorylation of Forkhead box O 3A Protein in Rat Model of Ischemic Stroke (P3-5.004)

<h3>Objective:</h3> To explore the role of Apelin-13 in alleviating post-stroke depression via regulation of BDNF mediated phosphorylation of forkhead box O 3A protein (FOXO3A) in rodent model of ischemic stroke. <h3>Background:</h3> Post-stroke depression (PSD) is a common complication in patients. Studies suggest that patients developing depression is associated with low-level serum brain derived neurotrophic factor (BDNF) that may increase the susceptibility to develop PSD. Treatment of PSD utilizes conventional drugs that are used to treat non stroke related mood disorders. However, limited success of these drugs have led researchers to investigate novel therapeutic strategies that can treat PSD. Apelin-13 is an adipocytokine that has been reported to exhibit beneficial effects in stroke as well as depression. Therefore, the present study aims to explore the role of Apelin-13 in alleviating PSD via regulation of BDNF mediated phosphorylation of forkhead box O 3A protein (FOXO3A) in rodent model of ischemic stroke. <h3>Design/Methods:</h3> Apelin-13 was administered to male SD rats post stroke and acute depression was induced. Rats were evaluated for functional and motor outcome at 24 h of reperfusion. Brains were harvested for infarct size estimation, biochemical assays, comparative histology and molecular studies. <h3>Results:</h3> Apelin-13 rendered neuroprotection in PSD rats and alleviated depressive like behavior. It reduced infarct size and improved functional, and behavioral outcome. Normalization of biochemical parameters were achieved in Apelin-13 treated group. Reduction of FOXO3A phosphorylation with relation to BDNF expression was evident by relevant protein expression studies. <h3>Conclusions:</h3> This study provides a preliminary evidence of the role of Apelin-13 in ameliorating PSD which can further provide a rationale to explore it as a treatment approach. <b>Disclosure:</b> Aishika Datta has nothing to disclose. Miss Sarmah has nothing to disclose. Mr. Sahu has received research support from National Institute Of Pharmaceutical Education and Research, Ahmedabad. Ms. Ghosh has received research support from National Institute of Pharmaceutical Education and Research, Ahmedabad. Ms. Rana has received research support from NIPER-Ahmedabad. Dr. Bhattacharya has nothing to disclose.

Clinically Acquired High Sensitivity Cardiac Troponin T is a Poor Predictor of Reduced Left Ventricular Ejection Fraction After ST Elevation Myocardial Infarction: A National Cohort Study-ANZACS-QI 65.

Cardiac troponins (cTn) have been used historically to estimate infarct size in ST elevation myocardial infarction (STEMI). Within a resource constrained health care environment, cTn could therefore be used for prioritisation of patients for cardiac imaging, in particular echocardiography. We aimed to determine how useful routinely collected cTn would be in predicting significant left ventricular (LV) impairment. All patients in the All New Zealand Acute Coronary Syndrome Quality Improvement (ANZACS-QI) registry with their first episode of STEMI between January 2013 and November 2018, who had high sensitivity troponin T measured, were included. We excluded patients with no left ventricular ejection fraction (LVEF) assessment, known LV dysfunction, or prior myocardial infarction. In total,3,698 patients were included in the analysis. A higher mean hsTnT (admission and peak) was seen in patients with more severely impaired LV function but there was significant overlap in the range of hsTnT between the different LVEF categories. Cardiac troponins demonstrated poor discriminative ability to either predict or exclude significant LV impairment (LVEF <40%). At an optimal cutpoint of 3,405 ng/L, peak hsTnT had a sensitivity of 56.5% (95% confidence interval [CI] 42-62%), a specificity of 65.3% (95% CI 62-79%) and an area under the receiver operating curve of 0.62 (95% CI 0.60-0.64). This is the largest study comparing clinically measured troponin levels and LV function in patients presenting with STEMI. A definite, but weak, association was seen between peak troponin and the degree of LV dysfunction, with significant overlap in troponin levels between levels of myocardial dysfunction. Routinely acquired troponin is not suitable for clinical use as a method of prioritising patients for cardiac imaging.

Non-Invasive Myocardial Infarction Ischemic Area Estimation Through Four-Dimensional Ultrasound

Background/Objective: Following myocardial infarction, infarct size and cardiac function are significant predictors of long-term prognosis. Most echocardiography studies rely on two-dimensional analysis for estimation of left ventricular function and electrical activity analysis for estimation of infarct area. Other imaging modalities, such as cardiac magnetic resonance imaging, are limited by time, cost, availability, patient tolerance, and incompatible implantable devices. Using an experimental mouse model of myocardial infarction, we hypothesize that four-dimensional ultrasound offers a possible alternative for easy, quick, and reliable estimation of infarct size. &#x0D; Methods: A cohort of 10 mice underwent four-dimensional cardiac imaging at baseline using a small animal high frequency ultrasound. A thoracotomy was subsequently performed, and a suture placed to ligate the left coronary artery approximately midway down the left ventricle. Sequential four-dimensional ultrasound was performed at six time points over 28 days, following which the mice were euthanized. The hearts were then removed and sent for embedding and sectioning into seven uniform segments stained using both H&amp;E and Masson’ s Trichrome.&#x0D; Results: Thus far, we have segmented the imaging and collected end diastolic volume, peak systolic volume, stroke volume, ejection fraction, transmural thickness, and circumferential strain. Additionally, four-dimensional models of the left ventricles have been rendered. Histological embedding, sectioning, and staining is still in progress, and therefore validation against the gold standard is still in process.&#x0D; Conclusion and Impact: Treatment and monitoring of myocardial infarction patients is reliant upon accurate assessment of patient status and prognosis. This study provides initial evidence for the validity of four-dimensional ultrasound as a tool for estimation of myocardial infarction size, providing an alternative to current two-dimensional methods that are less accurate and a more accessible alternative to highly specialized and costly equipment. Improved and accessible imaging methods have the potential to enhance patient care, ultimately improving overall health outcomes.

Tissue processing and optimal visualization of cerebral infarcts following sub-acute focal ischemia in rats

Transient cerebral ischemia followed by reperfusion in an infarcted brain comes with predictable acute and chronic morphological alterations in neuronal and non-neuronal cells. An accurate delineation of the cerebral infarct is not a simple task due to the complex shapes and indistinct borders of the infarction. Thus, an exact macroscopic histological approach for infarct volume estimation can lead to faster and more reliable preclinical research results. This study investigated the effect(s) of confounding factors such as fixation and tissue embedding on the quality of macroscopic visualization of focal cerebral ischemia by anti-microtubule-associated-protein-2 antibody (MAP2) with conventional Hematoxylin and Eosin (HE) staining serving as the control. The aim was to specify the most reliable macroscopic infarct size estimation method after sub-acute focal cerebral ischemia based on the qualitative investigation. Our results showed that the ischemic area on the MAP2-stained sections could be identified macroscopically on both cryo-preserved and paraffin-embedded sections from both immersion- and perfusion-fixed brains. The HE staining did not clearly depict an infarct area for macroscopic visualization. Therefore both immersion-fixed and perfused-fixed-MAP2 stained sections can be used reliably to quantify cerebral infarcts.

Association of Troponin levels with angiographic findings among patients with non-ST segment elevation myocardial infarction

The assessment of Troponin levels at admission is essential for risk stratification of non-ST-segment elevation myocardial infarction (NSTEMI) and estimation of infarct size. The aim of this study is to confirm whether the troponin level at admission can predict the angiographic severity of coronary artery disease (CAD) regarding NSTEMI patients. A retrospective study of 81 patients with NSTEMI hospitalized in the Intensive Cardiac Unit of the Cardiology Department of AVERROES Hospital, Casablanca. All the patients had cardiac biomarker assessment and were scheduled for coronary angiography. ACC/AHA classification was used to determine the anatomical complexity of CAD. Mean age was 59.3 years, and most patients were male (70.4%). Thirty-four patients were chronic smoker while 7 patients were weaned tobacco user. Forty-two percent were hypertensive while 25.9% of the patients were diabetic. Seventy-five patients had coronary angiography. The others did not because of complications (stroke, hemodynamically unstable AF). Among the patients, 59.3% had coronary artery angioplasty, 11.1% were scheduled for coronary artery bypass grafting, while medical treatment was decided for the rest of patients. Mean heartbeat was 78.5 bpm and mean arterial pressure was 120/70 mmHg. Mean left ventricular ejection fraction was 52%. Mean troponin level was 9718 ng/mL. Troponin level in patients presenting with simple CAD was 1317 ng/mL versus 15,342 ng/mL in patients with complex CAD. Positive linear correlation was found between the hsTn levels and the complexity of CAD ( P = 0.041). Troponin level at admission may predict the complexity of CAD. In our series, high hsTn were associated either with multivessel disease, LM or proximal LAD significant stenosis.

Validation of a simple ECG score for infarct size estimation in patients with first-time ST-elevation myocardial infarction

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Austrian Science Fund Background The magnitude of myocardial damage after acute ST-elevation myocardial infarction (STEMI) is a crucial prognostic determinant. Cardiac magnetic resonance (CMR) imaging offers a precise infarct severity assessment after STEMI; however, limited to restricted availability in daily clinical routine. Recently, a simple ECG score (DETERMINE score) was developed for infarct size (IS) estimation in STEMI patients with prior infarction. We sought to validate this score in patients with first-time STEMI for the assessment of myocardial injury visualized by CMR. Methods In this validation study, 423 revascularized first-time STEMI patients (median age 56, 17% women) were included. ECG was conducted at discharge for evaluation of the DETERMINE and Selvester score. CMR imaging was performed at a median of 3 days for the assessment of infarct characteristics (IS and microvascular obstruction [MVO]). Results Median DETERMINE score of the overall cohort was 8 points (interquartile range: 5-11). Patients presenting with a score &amp;gt; 8 points had more often anterior infarct localization (64% vs. 29%, p &amp;lt; 0.001) and higher peak hs-TnT levels (6957 ng/l vs. 3117 ng/l, p &amp;lt; 0.001). In linear and binary multivariable logistic regression analysis, the DETERMINE score remained as independent associate of IS (odds ratio [OR]: 1.09, 95% confidence interval [CI] 1.00 to 1.18, p = 0.047) and MVO (OR: 1.09, 95% CI 1.02 to 1.16, p = 0.016), after adjustment for Selvester score and peak hs-cTnT. Conclusions In survivors of first-time STEMI, the DETERMINE score provides an easy and inexpensive tool for suitable IS estimation. Moreover, the DETERMINE score showed significant and independent association with MVO. Thus, this simple ECG score might help identify patients at high risk of large infarct burden who might benefit from more aggressive treatment strategies.

Estimating the extent of myocardial damage in patients with STEMI using the DETERMINE score

BackgroundRecently, a simple ECG score (DETERMINE score) has been proposed for estimating myocardial scar in patients with ischaemic cardiomyopathy. We sought to evaluate the usefulness of the DETERMINE score for...

Texture-based machine learning in LGE-CMRI for automatic scar assessment

Abstract Background Conventional methods for the estimation of infarct size by late-enhanced cardiac magnetic resonance imaging use analyzes from each slice which in turn is added to generate a volume. We present a novel method based on machine learning, called texture based probability mapping (TPM). TPM is based upon expressing the probability of scarring in a pixel based upon analysing textural information in patches around each pixel. Purpose To explore our method and assess its utility as a tool to scar size and compare it with four established methods. Methods In 54 patients with ischemic scars, our method was compared with four 2D methods. 2 patients were excluded due to low image quality and artefacts. The most basal and apical short axis image slices were exclude due to partial volume artefacts. Myocardial infarction (MI) size was estimated manually, and TPM performed. Cardiac segments were defined as myocardial regions with pixel probabilities within a specified range. By varying the lower probability threshold while keeping the upper threshold fixed at 1, different cardiac segments were defined. Using the Sørensen-Dice coefficient the optimal probability range with the highest correlation to manual estimation of infarct size was identified. Results TPM-range 0.341–1.0 is best correlated to manual demarcation (median Dice 0.70). The method demonstrated stronger correlations between scar size and left ventricular remodeling parameters (LV ejection fraction: r=−0.731, p&amp;lt;0.0005; LV end-diastolic volume: r=0.641, p&amp;lt;0.0005; LV end-systolic volume: r=0.672, p&amp;lt;0.0005) compared with manual method. Conclusion Using TPM, infarct size can be measured automatically without using signal intensity as a reference value. It is without the need for manual demarcation of the scar and is less time consuming and less vulnerable to interobserver variability. It has a strong correlation with left ventricular remodeling parameters crucial in guiding further medical therapy. The use of this method is however not primarily dedicated for scar size estimation, but a tool to evaluate different properties of the tissue that cannot be visualized by the naked eye. It's an important step towards better understanding of myocardial damage pattern causing ventricular arrhythmia and SCD. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Helse Vest

Effects of salvianolate on myocardial perfusion after primary percutaneous catheter intervention in patients with ST-segment elevation myocardial infarction: a multicenter, randomized, double-blind, placebo-controlled study.

BackgroundDespite prompt revascularization following acute myocardial infarction, poor myocardial perfusion commonly occurs due to impaired microvascular circulation and is an independent predictor of adverse outcomes. The current trial sought to examine the effects of salvianolate on myocardial perfusion in patients with ST-segment-elevation myocardial infarction (STEMI) who were undergoing primary percutaneous coronary intervention (PCI).MethodsThis randomized, double-blind, placebo-controlled, multicenter study evaluated the effects of intravenous salvianolate on the achievement of complete epicardial and myocardial reperfusion after PCI, defined as thrombolysis in myocardial infarction flow grade 3 and thrombolysis in myocardial infarction myocardial perfusion grade 3. We also measured plasma total creatine kinase-mass band fraction (CK-MB)-estimated infarct size and echocardiography-derived left ventricular ejection fraction and recorded the 30-day clinical and safety outcomes. A total of 536 patients presenting with acute STEMI were randomized to receive either an i.v. infusion of salvianolate (n=265) or placebo (n=271).ResultsSalvianolate administration exerted beneficial effects on coronary microcirculation. There was a trend of reduced myocardial infarct size in the salvianolate group compared to the placebo group (P=0.070), although no significant difference in left ventricular ejection fraction was found between the two groups.ConclusionsSalvianolate administration is associated with improved myocardial perfusion in patients with STEMI undergoing PCI. A larger study is required to assess the impact of this therapy on clinical cardiac outcomes.

Growth Differentiation Factor-8 (GDF8)/Myostatin is a Predictor of Troponin I Peak and a Marker of Clinical Severity after Acute Myocardial Infarction.

Objective: Growth differentiation factor-8 (GDF8), also known as myostatin, is a member of the transforming growth factor-β superfamily that inhibits skeletal muscle growth. We aimed to investigate the association between GDF8 and peak troponin I levels after acute myocardial infarction (AMI). Methods: All consecutive patients admitted from June 2016 to February 2018 for type 1 AMI in the Coronary Care Unit of University Hospital of Dijon Bourgogne (France) were included in our prospective study. Blood samples were harvested on admission, and serum levels of GDF8 were measured using a commercially available enzyme-linked immunosorbent assay kit. Results: Among the 296 patients with type 1 AMI, median age was 68 years and 27% were women. GDF8 levels (median (IQR) = 2375 ng/L) were negatively correlated with age, sex and diabetes (p < 0.001 for all). GDF8 levels were higher in patients with in-hospital ventricular tachycardia or fibrillation (VT/VF) than those without in-hospital VT/VF. GDF8 was positively correlated with troponin I peak (r = 0.247; p < 0.001). In multivariate linear regression analysis, log GDF8 (OR: 21.59; 95% CI 34.08–119.05; p < 0.001) was an independent predictor of troponin I peak. Conclusions: These results suggest that GDF8 levels could reflect the extent of myocardial damage during AMI, similar to peak troponin I, which is currently used to estimate infarct size. Further studies are needed to elucidate the underlying mechanisms linking the GDF8 cytokine with troponin I levels.

Decreased atrioventricular plane displacement after acute myocardial infarction yields a concomitant decrease in stroke volume.

Acute myocardial infarction (AMI) can progress to heart failure, which has a poor prognosis. Normally, 60% of stroke volume (SV) is attributed to the longitudinal ventricular shortening and lengthening evident in the atrioventricular plane displacement (AVPD) during the cardiac cycle, but there is no information on how the relationship changes between SV and AVPD before and after AMI. Therefore, the aim of this study was to determine how SV depends on AVPD before and after AMI in two swine models. Serial cardiac magnetic resonance imaging was carried out before and 1–2 h after AMI in a microembolization model (n = 12) and an ischemia-reperfusion model (n = 14). A subset of pigs (n = 7) were additionally imaged at 24 h and at 7 days. Cine and late gadolinium enhancement images were analyzed for cardiac function, AVPD measurements and infarct size estimation, respectively. AVPD decreased (P < 0.05) in all myocardial regions after AMI, with a concomitant SV decrease (P < 0.001). The ischemia-reperfusion model affected SV to a higher degree and had a larger AVPD decrease than the microembolization model (−29 ± 14% vs. −15 ± 18%; P < 0.05). Wall thickening decreased in infarcted areas (P < 0.001), and A-wave AVPD remained unchanged (P = 0.93) whereas E-wave AVPD decreased (P < 0.001) after AMI. We conclude that AVPD is coupled to SV independent of infarct type but likely to a greater degree in ischemia-reperfusion infarcts compared with microembolization infarcts. AMI reduces diastolic early filling AVPD but not AVPD from atrial contraction. These findings shed light on the physiological significance of atrioventricular plane motion when assessing acute and subacute myocardial infarction.NEW & NOTEWORTHY The link between cardiac longitudinal motion, measured as atrioventricular plane displacement (AVPD), and stroke volume (SV) is investigated in swine after acute myocardial infarction (AMI). This cardiac magnetic resonance study demonstrates a close coupling between AVPD and SV before and after AMI in an experimental setting and demonstrates that this connection is present in ischemia-reperfusion and microembolization infarcts, acutely and during the first week. Furthermore, AVPD is equally and persistently depressed in infarcted and remote myocardium after AMI.

Enhanced functional recovery by levodopa is associated with decreased levels of synaptogyrin following stroke in aged mice

Levodopa is a precursor to dopamine that has been shown to improve functional recovery following stroke partly achieved through mechanisms of brain plasticity. This study investigates if dopamine might affect plasticity by having a direct effect on synaptic plasticity through alterations in neurotransmitter release and re-uptake. Synaptogyrin is a synaptic vesicle protein that has been suggested to be involved in dopamine re-uptake in the synaptic terminal. Therefore, we investigated if levodopa has an effect on the expression of synaptogyrin 1. Thy1-YFP mice were subjected to photothrombosis as an experimental model of stroke. Starting two days after surgery they were treated with either levodopa or a vehicle solution (saline) on a daily basis until day seven following surgery. On day seven they were sacrificed and their brains stained for Dopamine 1 receptor (D1R), Dopamine 2 receptor (D2R) and Parvalbumin (PV). Neu-N stainings were used to estimate infarct size. A second group of mice were subjected to photothrombosis and also treated with either levodopa or a vehicle solution in the same manner as previously mentioned. On day seven they were then sacrificed, and samples of brain tissue were taken for protein determination. Western blots were carried out to investigate possible differences in synaptogyrin expression between the two groups. Immunofluorescent stains showed the presence of dopamine receptors on the YFP-positive neurons and on PV-expressing neurones. Our Western Blot analysis showed a significant decrease in the expression of synaptogyrin in levodopa-treated mice. Our stains showed co-localisation with Thy-1 neurones and PV-expressing neurones for both D1 and D2 receptors. This indicates that dopamine has the ability to bind to, and directly influence cortical neurons, as well as inhibitory interneurons. We discovered a considerable decrease in synaptogyrin expression through levodopa treatment, suggesting that this might be a mechanism for regulating brain plasticity.

Complete versus simplified Selvester QRS score for infarct severity assessment in ST-elevation myocardial infarction

BackgroundComplete and simplified Selvester QRS score have been proposed as valuable clinical tool for estimating myocardial damage in patients with ST-elevation myocardial infarction (STEMI). We sought to comprehensively compare both scoring systems for the prediction of myocardial and microvascular injury assessed by cardiac magnetic resonance (CMR) imaging in patients with acute STEMI.MethodsIn this prospective observational study, 201 revascularized STEMI patients were included. Electrocardiography was conducted at a median of 2 (interquartile range 1–4) days after the index event to evaluate the complete and simplified QRS scores. CMR was performed within 1 week and 4 months thereafter to determine acute and chronic infarct size (IS) as well as microvascular obstruction (MVO).ResultsComplete and simplified QRS score showed comparable predictive value for acute (area under the curve (AUC) = 0.64 vs. 0.67) and chronic IS (AUC = 0.63 vs. 0.68) as well as for MVO (AUC = 0.64 vs. 0.66). Peak high sensitivity cardiac troponin T (hs-cTnT) showed an AUC of 0.88 for acute IS and 0.91 for chronic IS, respectively. For the prediction of MVO, peak hs-cTnT represented an AUC of 0.81.ConclusionsIn reperfused STEMI, complete and simplified QRS score displayed comparable value for the prediction of acute and chronic myocardial as well as microvascular damage. However, both QRS scoring systems provided inferior predictive validity, compared to peak hs-cTnT, the clinical reference method for IS estimation.

Validation of contemporary electrocardiographic indices of area at risk and infarct size in acute ST elevation myocardial infarction (STEMI)

BackgroundElectrocardiographic (ECG) methods to assess area at risk (AAR) and infarct size (IS) in patients with ST-elevation myocardial infarction (STEMI) have been previously established but not validated against contemporary benchmark Cardiac Magnetic Resonance (CMR) measures. We compared ECG-determined and CMR-determined measures for (a) AAR, (b) IS, and (c) myocardial salvage. MethodsSixty patients with ECG evidence of STEMI and CMR imaging performed within 13 days were included. The ECG-determined (a) AAR scores (Aldrich and Wilkins), (b) IS (Selvester score), and (c) myocardial salvage (i.e. [AAR-IS] / AAR × 100%), were compared with CMR-determined measures. ResultsCompared with CMR-determined AAR, both the Wilkins & Aldrich scores underestimated AAR, although the Wilkins (r = 0.72, p < 0.001) showed a better correlation than the Aldrich (r = 0.54, p < 0.001). Bland-Altman analysis revealed a bias of 2.6% (95% limits of agreement: 18.5%, −13.3%) for the Wilkins and 5.9% (95% limits of agreement: 25.6%, −13.8%) for the Aldrich. Estimation of IS was similar between the Selvester score and CMR, with good correlation (r = 0.77, p < 0.001) and agreement (fixed bias 0.4%, 95% limits of agreement 20.8%, −15.5%). However, ECG-determined myocardial salvage significantly underestimated CMR-determined myocardial salvage, with an inverse correlation (r = −0.33, p = 0.01). ConclusionsThe Wilkins score is superior to Aldrich score as an ECG-AAR index, Selvester score is a reasonable ECG estimate of infarct size, though ECG derived myocardial salvage does not have enough accuracy to be used in the clinical setting; it may be an inexpensive surrogate for myocardial salvage in large research studies. Further validation and prognostic studies are required.

Three-dimensional myocardial strain correlates with murine left ventricular remodelling severity post-infarction.

Heart failure continues to be a common and deadly sequela of myocardial infarction (MI). Despite strong evidence suggesting the importance of myocardial mechanics in cardiac remodelling, many MI studies still rely on two-dimensional analyses to estimate global left ventricular (LV) function. Here, we integrated four-dimensional ultrasound with three-dimensional strain mapping to longitudinally characterize LV mechanics within and around infarcts in order to study the post-MI remodelling process. To induce infarcts with varying severities, we separated 15 mice into three equal-sized groups: (i) sham, (ii) 30 min ischaemia-reperfusion, and (iii) permanent ligation of the left coronary artery. Four-dimensional ultrasound from a high-frequency small animal system was used to monitor changes in LV geometry, function and strain over 28 days. We reconstructed three-dimensional myocardial strain maps and showed that strain profiles at the infarct border followed a sigmoidal behaviour. We also identified that mice with mild remodelling had significantly higher strains in the infarcted myocardium than those with severe injury. Finally, we developed a new approach to non-invasively estimate infarct size from strain maps, which correlated well with histological results. Taken together, the presented work provides a thorough approach to quantify regional strain, an important component when assessing post-MI remodelling.