Severity Of Myocardial Injury Research Articles

Accumulation of endogenous Muse cells in the myocardium and its pathophysiological role in patients with fulminant myocarditis.

Multi-lineage differentiating stress-enduring (Muse) cells, identified as pluripotent surface marker SSEA-3(+) cells, are stress tolerant endogenous pluripotent-like stem cells, and are involved in tissue repair. However, the significance of Muse cells in acute myocarditis has not been evaluated. In the present study, we counted Muse cells/area in biopsied myocardial tissue samples from 17 patients with fulminant myocarditis, and 6 with non-inflammatory myocardial disease as controls. Compared with controls, patients with fulminant myocarditis had significantly more Muse cells (p = 0.00042). Patients with mechanical circulatory support (p = 0.006) and myocardial degeneration (p = 0.023) had significantly more Muse cells than those without them. The Muse cell number was correlated with acute phase CK-MB level (ρ = 0.547, p = 0.029), indicating the severity of myocardial injury, and was also correlatedwith acute/recovery phase ratio of CK-MB (ρ = 0.585, p = 0.023) and cardiac troponin I (ρ = 0.498, p = 0.047) levels, indicating resilience of myocardial injury. In fulminant myocarditis, the Muse cell number was associated with the severity of clinical features in the acute phase, and also with the recovery from myocardial damage in the chronic phase. Endogenous Muse cells might be mobilized and accumulate to the myocardial tissues in fulminant myocarditis, and might participate in the repair of injured myocardium.

Characterization of dynamic changes in cardiac microstructure after reperfused ST-elevation myocardial infarction by biphasic diffusion tensor cardiovascular magnetic resonance.

Microstructural disturbances underlie dysfunctional contraction and adverse left ventricular (LV) remodelling after ST-elevation myocardial infarction (STEMI). Biphasic diffusion tensor cardiovascular magnetic resonance (DT-CMR) quantifies dynamic reorientation of sheetlets (E2A) from diastole to systole during myocardial thickening, and markers of tissue integrity [mean diffusivity (MD) and fractional anisotropy (FA)]. This study investigated whether microstructural alterations identified by biphasic DT-CMR: (i) enable contrast-free detection of acute myocardial infarction (MI); (ii) associate with severity of myocardial injury and contractile dysfunction; and (iii) predict adverse LV remodelling. Biphasic DT-CMR was acquired 4 days (n = 70) and 4 months (n = 66) after reperfused STEMI and in healthy volunteers (HVOLs) (n = 22). Adverse LV remodelling was defined as an increase in LV end-diastolic volume ≥ 20% at 4 months. MD and FA maps were compared with late gadolinium enhancement images. Widespread microstructural disturbances were detected post-STEMI. In the acute MI zone, diastolic E2A was raised and systolic E2A reduced, resulting in reduced E2A mobility (all P < .001 vs. adjacent and remote zones and HVOLs). Acute global E2A mobility was the only independent predictor of adverse LV remodelling (odds ratio .77; 95% confidence interval .63-.94; P = .010). MD and FA maps had excellent sensitivity and specificity (all > 90%) and interobserver agreement for detecting MI presence and location. Biphasic DT-CMR identifies microstructural alterations in both diastole and systole after STEMI, enabling detection of MI presence and location as well as predicting adverse LV remodelling. DT-CMR has potential to provide a single contrast-free modality for MI detection and prognostication of patients after acute STEMI.

New Insights into Cardiovascular Diseases Treatment Based on Molecular Targets

Cardiovascular diseases (CVDs) which consist of ischemic heart disease, stroke, heart failure, peripheral arterial disease, and several other cardiac and vascular conditions are one of the most common causes of death worldwide and often co-occur with diabetes mellitus and lipid disorders which worsens the prognosis and becomes a therapeutic challenge. Due to the increasing number of patients with CVDs, we need to search for new risk factors and pathophysiological changes to create new strategies for preventing, diagnosing, and treating not only CVDs but also comorbidities like diabetes mellitus and lipid disorders. As increasing amount of patients suffering from CVDs, there are many therapies which focus on new molecular targets like proprotein convertase subtilisin/kexin type 9 (PCSK9), angiopoietin-like protein 3, ATP-citrate lyase, or new technologies such as siRNA in treatment of dyslipidemia or sodium-glucose co-transporter-2 and glucagon-like peptide-1 in treatment of diabetes mellitus. Both SGLT-2 inhibitors and GLP-1 receptor agonists are used in the treatment of diabetes, however, they proved to have a beneficial effect in CVDs as well. Moreover, a significant amount of evidence has shown that exosomes seem to be associated with myocardial ischaemia and that exosome levels correlate with the severity of myocardial injury. In our work, we would like to focus on the above mechanisms. The knowledge of them allows for the appearance of new strategies of treatment among patients with CVDs.

Cardiac magnetic resonance feature tracking myocardial strain analysis in suspected acute myocarditis: diagnostic value and association with severity of myocardial injury

BackgroundAlbeit that cardiac magnetic resonance feature tracking (CMR-FT) has enabled quantitative assessment of global myocardial strain in the diagnosis of suspected acute myocarditis, the cardiac segmental dysfunction remains understudied. The aim of the present study was using CMR-FT to assess the global and segmental dysfunction of the myocardium for diagnosis of suspected acute myocarditis.MethodsForty-seven patients with suspected acute myocarditis (divided into impaired and preserved left ventricular ejection fraction [LVEF] groups) and 39 healthy controls (HCs) were studied. A total of 752 segments were divided into three subgroups, including segments with non-involvement (SNi), segments with edema (SE), and segments with both edema and late gadolinium enhancement (SE+LGE). 272 healthy segments served as the control group (SHCs).ResultsCompared with HCs, patients with preserved LVEF showed impaired global circumferential strain (GCS) and global longitudinal strain (GLS). Segmental strain analysis showed that the peak radial strain (PRS), peak circumferential strain (PCS), and peak longitudinal strain (PLS) values significantly reduced in SE+LGE compared with SHCs, SNi, SE. PCS significantly reduced in SNi (-15.3 ± 5.8% vs. -20.3 ± 6.4%, p < 0.001) and SE (-15.2 ± 5.6% vs. -20.3 ± 6.4%, p < 0.001), compared with SHCs. The area under the curve (AUC) values of GLS (0.723) and GCS (0.710) were higher than that of global peak radial strain (0.657) in the diagnosis of acute myocarditis, but the difference was not statistically significant. Adding the Lake Louise Criteria to the model resulted in a further increase in diagnostic performance.ConclusionsGlobal and segmental myocardial strain were impaired in patients with suspected acute myocarditis, even in the edema or relatively non-involved regions. CMR-FT may serve as an incremental tool for assessment of cardiac dysfunction and provide important additional imaging-evidence for distinguishing the different severity of myocardial injury in myocarditis.

Admission and follow-up cardiac magnetic resonance imaging findings in BNT162b2 Vaccine-Related myocarditis in adolescents

Background There is limited data on the pattern and severity of myocardial injury in patients with COVID-19 vaccination associated myocarditis. Objective We aimed to define the myocardial damage occurring after BNT162b2 vaccination, raise awareness about adverse reactions developing after vaccination, and determine the patterns and scope of Cardiac magnetic resonance imaging (MRI) findings. Patients/Methods A total of 9 patients diagnosed with vaccine-associated myopericarditis were followed up. Results The mean age of the patient at diagnosis was 15.3 ± 1.0 (range: 14–17) years, and all patients were male. Seven patients presented with myocarditis symptoms after their second vaccine dose, one patient presented with pericarditis symptoms after his first dose, and the other patient presented with myocarditis symptoms after his booster dose. The median time at presenting to the hospital was 3 (range: 2–22) days. Seven (77.7%) patients had abnormal electrocardiography (ECG) findings, and the most prevalent finding was diffuse ST-segment elevation. Initial cardiac MRI results were abnormal in all patients, where 8 (88.8%) patients had late gadolinium enhancement, and 5 (55.5%) had myocardial edoema. Three patients showed local left ventricular wall-motion abnormalities. In their follow-up MRIs 3–6 months later, myocardial edoema was present in 2 (28.5%) patients, while late gadolinium enhancement was present in all patients (7/7, 100%, 2 patients did not have control MRI time). Hypokinetic segments were still present in one of the 3 patients. No negative cardiac events were observed in the short-term follow-up of any patient. Conclusion Further follow-up evaluation and larger multicenter studies are needed to determine the clinical significance of persistent cardiac MRI abnormalities.

Cardiac MRI findings in COVID-19 vaccine-related myocarditis: pooled analysis of 435 patients

Abstract Background Myocarditis following COVID-19 vaccination is a rare adverse event that was recently reported. Understanding the pattern and severity of myocardial injury in myocarditis caused by COVID-19 vaccination is imperative for improving care of the patients. Purpose To detect the pattern and severity of myocardial injury in patients with myocarditis following COVID-19 vaccination based on cardiac MRI findings. Study type Systematic review. Method Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement, we systematically reviewed the literature by screening 2404 databases using boolean operators and the relevant key terms covering COVID-19 vaccine, myocarditis, and Cardiac MRI. We included all observational MRI studies on patients with suspected myocarditis following COVID-19 vaccination. Cardiac MRI findings, including T1, T2, ECV, LGE, and left ventricular ejection fraction, were extracted from included studies. Statistical tests As a single case series, individual-level patient data (IPD) studies were pooled with aggregated–level data (AD) studies through two-stage analyses. For this purpose, first, data from all case series and case reports with IPD were aggregated using one-stage IPD analyses. Results Based on our two-stage pooled analyses of IPD and AD studies, diagnosis of myocarditis using lake luoise criteria was confirmed in 74% (95% confidence interval (CI): 49% to 94%) of patients. Cardiac MRI abnormalities included elevated T2 in 67% (95% CI: 45% to 87%), myocardial LGE in 91% (95% CI: 81% to 99%) [having a subepicardial/midwall pattern: 99.5%], impaired LVEF (&amp;lt;50%) in 4% (95% CI: 0.0% to 9.0%). Also, elevated T1 and ECV (&amp;gt;30), reported only by some IPD studies, was detected in 72.5% (66/91) and 32% (16/50) of patients, respectively. Data conclusion Myocardial injury in COVID-19 vaccine-associated myocarditis may have a similar pattern compared to other forms of acute myocarditis. Despite other myocarditis, Preserved LVEF is a common finding in these patients. Funding Acknowledgement Type of funding sources: None.

Impact of various periods of perfusion-pause and reperfusion on the severity of myocardial injury in the langenodorff model.

To explore impact of various periods of ischemia and reperfusion on the severity of myocardial injury. Langendorff model of isolated cardiac perfusion system was established in 56 rat hearts. They were randomly assigned into four groups with four different ischemia (perfusion-pause) time and reperfusion time. The levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and creatine kinase-MB (CK-MB) were measured and the size of myocardial infarction was assessed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. The levels of AST, ALT, LDH, and CK-MB in the heart tissues and perfusate were lowest in the group I (shortest time of perfusion-pause and reperfusion) followed by the groups II, III, and IV (longest time of perfusion-pause and reperfusion) (p < 0.05). The myocardial infarction size was smallest in the group I (6.63 ± 0.47) followed by group II (15.12 ± 1.03), group III (20.32 ± 2.18), and group IV (32.29 ± 5.42) (p < 0.05). Two-way ANOVA analysis revealed that period of perfusion-pause and reperfusion independently and significantly affected the levels of AST and ALT in both heart tissues and perfusate (p < 0.001). The interaction of pausing period and reperfusion significantly affected the level of AST (p = 0.046) and CK-MB (p = 0.001) in the perfusate. In addition, perfusion-pause period significantly affected levels of LDH and CK-MB only in the perfusate (p < 0.001). Neither perfusate nor heart tissue LDH level was significantly affected by the interaction of perfusion-pause and reperfusion period (p > 0.05). The severity of myocardial injury in the Langendorff model was affected by the period of perfusion-pause and reperfusion. The longer period of perfusion-pause followed by the longer the period of reperfusion, the severe myocardial injury was found.

Myocardial Injury Pattern at MRI in COVID-19 Vaccine-Associated Myocarditis.

BackgroundThere is limited data on the pattern and severity of myocardial injury in patients with COVID-19 vaccination associated myocarditis.PurposeTo describe myocardial injury following COVID-19 vaccination and to compare these findings to other causes of myocarditis.MethodsIn this retrospective cohort study, consecutive adult patients with myocarditis with at least one T1-based and at least one T2-based abnormality on cardiac MRI performed at a tertiary referral hospital between 2019-2021 were included. Patients were classified into one of three groups: myocarditis following COVID-19 vaccination, myocarditis following COVID-19 illness, and other myocarditis not associated COVID-19 vaccination or illness.ResultsOf the 92 included patients, 21 (22%) had myocarditis following COVID-19 vaccination (mean age 31 years ±14 [standard deviation]; 17 men; mRNA-1273 in 12 [57%] and BNT162b2 in 9 [43%]). Ten patients (11%) had myocarditis following COVID-19 illness (mean age 51 years ±14; 3 men), and 61 (66%) had other myocarditis (mean age 44 years ±18; 36 men). MRI findings in vaccine associated myocarditis included late gadolinium enhancement (LGE) in 17 (81%) and left ventricular dysfunction in 6 (29%). Compared with other causes of myocarditis, patients with vaccine associated myocarditis had higher left ventricular ejection fraction and less extensive LGE, even after controlling for age, sex, and duration between symptom onset and MRI. The most frequent location of LGE in all groups was subepicardial at the basal inferolateral wall, although septal involvement was less common in vaccine associated myocarditis. At short-term follow-up (median 22 [IQR 7-48] days), all patients with vaccine associated myocarditis were asymptomatic with no adverse events.ConclusionsCardiac MRI demonstrated a similar pattern of myocardial injury in vaccine associated myocarditis compared to other causes, although abnormalities were less severe, with less frequent septal involvement, and no adverse events over short-term follow-up.See also the editorial by Raman and Neubauer.

Sevoflurane ameliorates adriamycin-induced myocardial injury in rats through the PI3K/Akt/GSK-3β pathway.

The aim of this study was to explore the effects of sevoflurane (SEV) pretreatment on Adriamycin (ADR)-induced myocardial injury through the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β) pathway. A total of 24 rats weighing 200-250 g were divided into four groups, including: control group (C group), ADR injection group (ADR group), SEV pretreatment group (ADR + SEV group) and inhibitor group (ADR + SEV + LY group). H9c2 cells were cultured in vitro and were divided into control group (C group), ADR treatment group (ADR group), and SEV pretreatment group (ADR + SEV group) and inhibitor group (ADR + SEV + LY group) as well. Next, the content of aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and creatine kinase (CK) in the serum was detected via Enzyme-Linked Immunosorbent Assay (ELISA). Hematoxylin-eosin (HE) staining assay was performed to determine the severity of myocardial injury. Meanwhile, the apoptosis rate of cells was detected through terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assay. Additionally, Western blotting (WB) was employed to measure the protein expression levels of phosphorylated (p)-GSK-3β, p-PI3K, Akt and p-Akt. Compared with C group, ADR significantly increased the content of AST, LDH and CK in the serum (p<0.01), reduced protein expression levels of p-GSK-3β, p-PI3K and p-Akt (p<0.01), increased apoptosis rate (p<0.01), and induced myocardial injury. SEV pretreatment significantly alleviated the effect of ADR, manifested as significantly lowered content of AST, LDH and CK in the serum (p<0.01), distinctly elevated protein expression levels of p-GSK-3β, p-PI3K and p-Akt (p<0.01), notably reduced apoptosis rate (p<0.01), and relieved myocardial injury. LY294002 remarkably inhibited the protective effect of SEV against myocardial injury (p<0.01) CONCLUSIONS: SEV is able to prominently ameliorate ADR-induced myocardial injury by regulating the phosphorylation level of the PI3K/Akt/GSK-3β signaling pathway.

Abstract 17183: Severity of Myocardial Injury in COVID-19 Hospitalized Patients

Introduction: Myocardial injury in COVID19 is reported as high as 30% and associated with worsened prognosis (Cooper et al., Circulation). Along with elevated cardiac biomarkers, elevated inflammatory markers of cytokine storm and hemophagocytic lymphohistiocytosis (HLH) are associated with increased illness severity and mortality. Our study aimed to identify patients at highest risk for myocardial injury and subsequent cardiac decompensation. Methods: 279 consecutive patients with COVID19 from a major metropolitan academic center, discharged from 3-21-2020 to 5-17-2020, were analyzed. Primary data includes age, sex, race, and peak troponin I during hospitalization. Patients were further stratified to evaluate severe cases with acute respiratory distress syndrome (ARDS) requiring intubation (n=40), and peak levels of CRP, ferritin, and D-dimer were collected. Bivariate and multivariate measures of association between peak inflammatory marker and troponin I levels were estimated. Results: Average age of ARDS population patients was 61 +/- 15 years; 50% male and 50% female. Self-identified African Americans(AA) were 35%, Hispanic/Latinos(H/L) were 55%, and Others including two White Americans were 10%. Average peak troponin I in H/L was remarkably higher 0.51 +/-1.16 compared to AA 0.18 +/- 0.23 and Others 0.13 +/- 0.16. Per multivariate regression analysis, D-dimer had the most significant effect on the elevated troponin (p=0.027). Although weakly significant, H/L showed elevated troponin (p =0.09) compared to non-H/L. Conclusion: Elevated D-dimer is associated with increased morbidity in COVID19, and also correlates with elevated troponin concerning for increased myocardial injury. Furthermore, the H/L population may be at greater risk for developing myocardial injury and have more injury as shown by higher troponin I levels. Larger studies may better assess the relation between inflammatory markers such as CRP and ferritin and myocardial injury. Our study provides evidence of systemic inflammation contributing to significant myocardial injury in COVID19, especially in the H/L population. Identifying patients at highest risk for myocardial injury early may allow for more effective medical interventions and improved outcomes.

Dynamic fluctuations of advanced glycation end products and its C-terminal truncated receptor level in patients with acute ST-segment elevation myocardial infarction and undergoing diabetes or not: A retrospective study.

The role of advanced glycation end products (AGEs) and its C-terminal truncated receptor (soluble receptor for advanced glycation end products, sRAGE) in ST-segment elevation myocardial infarction (STEMI) patients with or without diabetes is unknown. We compared their levels in patients with and without STEMI, as well as with and without diabetes. A prospective observational study was performed between December 2014 and December 2015. Study group included STEMI patients with coronary artery disease; control group included patients without coronary artery disease. Levels of AGEs and sRAGE were tested on Days 0, 2, and 5 after STEMI. Levels of creatine kinase-MB (CK-MB), cardiac troponin I, and N-terminal pro-brain natriuretic peptide (NT-proBNP) were tested on Days 0, 1, 2, and 3. Patient's diabetic status was determined by medical history or oral glucose tolerance test. Compared to patients in the control group, STEMI patients showed elevated levels of AGEs and sRAGE. In the STEMI group, diabetic patients had higher levels of AGEs and sRAGE compared to nondiabetic patients. The level of AGEs correlated with peak level of CK-MB in the overall population of patients with STEMI and with peak level of NT-proBNP in diabetic patients with STEMI. Levels of AGEs and sRAGE were elevated after STEMI, especially among patients with diabetes. These markers could serve to indicate the severity of myocardial injury and cardiac insufficiency, and play a potential role in predicting the prognosis of patients with STEMI.

Low T3 syndrome improves risk prediction of in-hospital cardiovascular death in patients with acute myocardial infarction

BackgroundLow triiodothyronine (T3) syndrome (LT3S) is frequently seen in patients with acute myocardial infarction (AMI). We examined the association between LT3S and severity of myocardial injury and determined whether LT3S adds predictive value over thrombolysis in myocardial infarction (TIMI) risk score for in-hospital cardiovascular (CV) death. MethodsOf 2459 AMI patients, 529 pairs of euthyroid and LT3S individuals with similar baseline characteristics were identified using 1:1 propensity score matching. LT3S was defined as free T3 (fT3) <2.36pg/mL, normal values of thyroid-stimulating hormone and free thyroxin. Primary outcome was in-hospital CV death. Receiver operating characteristic curves were generated to assess the predictive effects of fT3, TIMI risk score, and TIMI-LT3S risk score on in-hospital CV death. ResultsLT3S was found in 23.3% of patients with AMI. The peak values of cardiac troponin I in ng/mL and N-terminal pro-brain natriuretic peptide in ng/mL were significantly higher in LT3S: 6.6 (1.3–19.6) vs. 3.5 (0.8–12.1), p<0.001 and 3625 (1046–12,776) vs. 2158 (774–6759), p<0.001. Patients with LT3S had significantly higher rate of in-hospital CV death than those without (4.7% vs. 1.7%, p=0.005). Lower levels of fT3 yielded an area under the curve (AUC) of 0.741 for predicting CV death. LT3S, when added to the TIMI risk score, significantly increased AUC for in-hospital CV death than TIMI risk score alone (0.775 vs. 0.738, p=0.005). ConclusionsLT3S was associated with more severe myocardial injury and increased in-hospital CV mortality in patients with AMI. Furthermore, it improved risk prediction of in-hospital CV death post-AMI when it was added to the TIMI risk score.

Comparison of myocardial injury in pediatric patients undergoing living-donor liver transplantation performed under propofol- versus sevoflurane-based anesthesia

Objective To compare the severity of myocardial injury in pediatric patients undergoing living-donor liver transplantation (LDLT) performed under propofol- versus sevoflurane-based anesthesia. Methods Forty American Society of Anesthesiologists physical status Ⅲ or Ⅳ pediatric patients of both sexes, aged 5-13 months, weighing 5-12 kg, scheduled for elective LDLT under general anesthesia, were divided into 2 groups (n=20 each) using a random number table: propofol-based anesthesia group (group P) and sevoflurane-based anesthesia group (group S). Anesthesia was induced with intravenously injected midazolam 0.15 mg/kg, fentanyl 2-5 μg/kg and cisatracurium 0.15 mg/kg.Anesthesia was maintained by IV infusion of propofol 9-15 mg·kg-1·h-1 (in group P), continuous inhalation of 2.6%-4.0% sevoflurane (in group S), intermittent IV boluses of fentanyl 1-3 μg/kg and IV infusion of cisatracurium 1-2 μg·kg-1·min-1.At 5 min of anesthesia induction, 30 min of anhepatic phase, 3 h of neohepatic stage and the end of surgery, blood samples were taken from the central vein for determination of concentrations of cardiac troponin I and creatine kinase-MB in serum and concentrations of tumor necrosis factor-alpha, interleukin-6 and high-mobility group box 1 protein in serum (by enzyme-linked immunosorbent assay). The occurrence of adverse cardiovascular events (hypertension or hypotention, myocardial ischemia and ventricular premature beat) was recorded during surgery. Results There was no significant difference in concentrations of tumor necrosis factor-alpha, interleukin-6, high-mobility group box 1 protein, cardiac troponin I and creatine kinase-MB in serum at each time point or incidence of adverse cardiovascular events between the two groups (P>0.05). Conclusion The severity of myocardial injury is comparable in pediatric patients undergoing LDLT performed under propofol- versus sevoflurane-based anesthesia. Key words: Anesthetics, inhalation; Propofol; Liver transplantation; Myocardial reperfusion injury; Child

Increased complements and high-sensitivity C-reactive protein predict heart failure in acute myocardial infarction.

The aim of the present study was to investigate whether the serum levels of complements and high-sensitivity C-reactive protein (hs-CRP) in patients with acute myocardial infarction (AMI) are associated with the severity of myocardial injury. Consecutive patients (n=110) with AMI and 33 healthy individuals, who served as control subjects, were enrolled from May 2013 to February 2015. These patients were divided into two groups, those with ST segment elevation MI (STEMI) and those with non-ST segment elevation MI (NSTEMI). The patients with STEMI exhibited progression to diastolic dysfunction and heart failure. Furthermore, the results revealed that the level of serum complement and hs-CRP in patients with AMI increased rapidly when compared with the subjects from the control group, particularly in the STEMI patients, at different time-points. A statistically significant elevation of the complement and hs-CRP levels was observed at day 3 after AMI in the STEMI group. The activation of complement and hs-CRP following AMI may serve as a specific marker to successfully predict left ventricular dysfunction. Thus, biomarker-based approaches may be adopted to identify the severity of AMI with distinct pathophysiologic responses in order to rationally implement clinical therapeutic strategies.

Myocardial extracellular volume fraction measurement in chronic total coronary occlusion: Association with myocardial injury, angiographic collateral flow, and functional recovery

To investigate whether myocardial extracellular volume fraction (ECV) measurement by cardiac MR is indicative of myocardial injury, angiographic collateral flow, and functional recovery in patients with chronic total coronary occlusion (CTO). A total of 50 CTO patients undergoing 1.5 Tesla MR were prospectively enrolled, and 28 underwent a second MR 6 months after revascularization. T1-mapping based indices, including pre- and postcontrast T1 values and ECV, were obtained from infarcted and non-infarcted myocardium, myocardial segments, and coronary territory. The severity of myocardial injury was rated by transmurality extent of infarction (TEI) and regional wall motion abnormalities (RWMA) score. Angiographic collateral flow was evaluated using Rentrop classification. Improvement in segmental wall motion at 6 months was also assessed. ECV and postcontrast T1 value significantly outperformed precontrast T1 value for identifying myocardial infarction (area under the receiver operating characteristic curve [AUC]: 0.998 and 0.953 versus 0.824, all P < 0.02). Myocardial ECV was strongly correlated with TEI (P = 0.000), RWMA score (P = 0.000), and collateral classification (P = 0.007 for left anterior descending artery [LAD] territory, P = 0.001 for non-LAD territory). Furthermore, the likelihood of functional recovery was better predicted by ECV than by late gadolinium enhancement (LGE) (AUC: 0.76 versus 0.68, P < 0.02). Myocardial ECV may be a useful surrogate to assess myocardial injury and angiographic collateral flow in CTO, and ECV provides incremental value to LGE in assessing functional recovery after revascularization. J. MAGN. RESON. IMAGING 2016;44:972-982.

Predictive value of the E­selectin for the severity of myocardial injury in the PICU patients

目的 探讨E-选择素与小儿心肌损伤严重程度的相关性及预测价值。 方法 检测64例心肌损伤患儿(心肌损伤组)和64例健康儿童(对照组)的E-选择素的表达水平，使用肌钙蛋白Ⅰ及肌酸激酶同工酶作为对比，观察E-选择素与心肌损伤严重程度的相关性，评估E-选择素对心肌损伤严重程度的判断价值。 结果 心肌损伤组和对照组的E-选择素水平分别为(45.16±5.34)μg/L、(12.78±3.18)μg/L，两组间差异有统计学意义(P<0.01)。E-选择素水平与心肌损伤严重程度呈正相关(r＝0.582，P<0.01)，显示与心肌损伤程度密切相关。 结论 E-选择素可作为评估心肌损伤严重程度的重要指标之一，具有较高的预测价值。

Donor pretreatment with carbon monoxide prevents ischemia/reperfusion injury following heart transplantation in rats.

Because inhaled carbon monoxide (CO) provides potent anti-inflammatory and antioxidant effects against ischemia reperfusion injury, we hypothesized that treatment of organ donors with inhaled CO would decrease graft injury after heart transplantation. Hearts were heterotopically transplanted into syngeneic Lewis rats after 8 hours of cold preservation in University of Wisconsin solution. Donor rats were exposed to CO at a concentration of 250 parts per million for 24 hours via a gas-exposure chamber. Severity of myocardial injury was determined by total serum creatine phosphokinase and troponin I levels at three hours after reperfusion. In addition, Affymetrix gene array analysis of mRNA transcripts was performed on the heart graft tissue prior to implantation. Recipients of grafts from CO-exposed donors had lower levels of serum troponin I and creatine phosphokinase; less upregulation of mRNA for interleukin-6, intercellular adhesion molecule-1, and tumor necrosis factor-α; and fewer infiltrating cells. Although donor pretreatment with CO altered the expression of 49 genes expressly represented on the array, we could not obtain meaningful data to explain the mechanisms by which CO potentiated the protective effects. Pretreatment with CO gas before organ procurement effectively protected cardiac grafts from ischemia reperfusion-induced injury in a rat heterotopic cardiac transplant model. A clinical report review indicated that CO-poisoned organ donors may be comparable to non-poisoned donors.

Correlation of serum cardiac troponin I and acute phase protein concentrations with clinical staging in dogs with degenerative mitral valve disease.

Cardiac troponin I (cTnI) correlates with severity of myocardial injury. Nonspecific inflammation in congestive heart failure (CHF) could be assessed by C-reactive protein (CRP), haptoglobin (Hp), and ceruloplasmin (Cp) measurements. The aim of the study was to determine whether serum cTnI, CRP, Hp, and Cp concentrations differ among various stages of mitral valve disease (MVD) in dogs. Dogs with MVD were allocated to 3 groups (I - asymptomatic; II - mild to moderate CHF; III advanced CHF) according to the scheme of the International Small Animal Cardiac Healthy Council (ISACHC). Concentrations of cTnI, CRP, Cp, and Hp were measured in all dogs upon admission, and cTnI and CRP were measured bimonthly during a 4-month follow-up period. In total 46 dogs with MVD were enrolled for the cross-sectional part (21 Group I, 11 Group II, 14 Group III), and 35 dogs were included in the longitudinal study. Initial mean Cp concentrations were similar among all groups. There was a statistically significant difference in Hp and CRP concentrations between group I (n = 21, P = .019) and III (n = 14, P < .001). There was a statistically significant decrease in CRP (P = .033) and cTnI (P = .009) concentrations over the longitudinal study (all groups). CRP concentrations were significantly higher in group I than III (P = .004). During the 6-month monitoring period of 35 dogs, there was a statistically significant positive correlation between cTnI and CRP (P < .001). Differences in CRP concentrations between clinical stages of MVD suggest a clinically and therapeutically relevant inflammatory component.

Cardiac biomarkers in blood, and pericardial and cerebrospinal fluids of forensic autopsy cases: A reassessment with special regard to postmortem interval

Previous studies suggested possible application of postmortem biochemistry of myocardial biomarkers to the investigation of sudden cardiac death; however, differences from clinical findings should be considered in autopsy materials. The present study involved a comprehensive investigation of cardiac troponin T and I (cTnT and cTnI), and creatine kinase MB (CK-MB) in cardiac and peripheral external iliac venous blood, pericardial fluid (PCF) and cerebrospinal fluid (CSF) for reassessment, with special regard to the estimated postmortem interval in relation to the cause of death, reviewing a large number of forensic autopsy cases (n=1923). These cardiac biomarkers showed cause-of-death- and postmortem-time-dependent differences: blood and PCF levels of each marker were higher in hyperthermia (heatstroke), bathwater drowning and chronic congestive heart disease in cases of postmortem interval (PMI) <12h. After 12h postmortem, these markers were also higher in fatal drug abuse, spontaneous cerebral/subarachnoid bleeding, electrocution and pulmonary embolism. In addition, most other causes of death, including ischemic heart disease, showed substantial elevations, while these markers remained low in acute hemorrhagic death from sharp instrument injury, hypothermia (cold exposure) and sea-/freshwater drowning during PMI of <48h. CSF cTnI and CK-MB showed similar findings. There was no difference between myocardial infarction and other causes of death to be discriminated, including asphyxiation, drowning and fire fatality. These findings are similar to clinical observations in critical ill patients, suggesting that elevated cardiac biomarkers cannot be a specific finding for death from acute ischemic heart disease, but indicate the severity of myocardial injury in postmortem investigation.

Abstract 13121: Different Presentation Mode of Acute Myocardial Infarction is Associated With Antecedent Therapy With Nitrates and β-blockers

Introduction: Brief episodes of ischemia increases cardiac tolerance to a subsequent major ischemic insult. Prehospital medication may affect the mode of presentation in acute myocardial infarction (AMI) and pharmacologically precondition the heart toward ischemic episodes. Hypothesis: We assessed the hypothesis that antecedent therapy confers cardioprotection in patients suffering an AMI. Methods: The Japanese Acute Coronary Syndrome Study (JACSS) is a retrospective and multicenter observational study that is being conducted at 35 medical institutions in Japan. The JACSS database includes information on consecutive 1,204 patients who were hospitalized within 48 hours after the onset of AMI. Results: A total of 1,010 ST-elevation myocardial infarction (STEMI) and 194 non STEMI (NSTEMI) patients were included and the differences of the mode of presentation, prehospital medication and coronary risk factors were investigated in the present study. Coronary risk factors such as sex, hypertension, diabetes mellitus, hypercholesterolemia, smoking, obesity and previous coronary artery disease were comparable between STEMI and NSTEMI groups. Prehospital medication with aspirin, nitrates, β-blockers and calcium-channel blockers but not with angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers and statins were associated with the onset as NSTEMI. A stepwise regression analysis including coronary risk factors and prehospital medication revealed that chronic therapy with nitrates and β-blockers reduced the onset as STEMI compared with that as NSTEMI (table) Conclusions: Antecedent therapy with nitrates and β-blockers was associated with reduced severity of myocardial injury in response to an acute coronary event. Our findings may help to explain the missing link between a shift away from STEMI in favor of NSTEMI and a combined capability of nitrates and β-blockers to act as pharmacological inducers of ischemic preconditioning.