Myocardial Damage In Patients Research Articles

Myocardial dysfunction in patients with rheumatoid arthritis in the speckle-tracking echocardiography and its relationship with the clinical characteristics of the disease

patients with RA have an approximately 50% increased risk of cardiovascular events and cardiovascular death. Cardiovascular diseases lead to a decrease in life expectancy, and the determination of the mechanisms of myocardial damage in patients with RA is of great importance for the development of methods for the early prevention of heart failure. The aim of our study was to study myocardial dysfunction using speckle tracking echocardiography (STE) in patients with RA and to find out possible correlations with the course of the disease and risk factors for cardiovascular diseases. Materials and methods. 29 RA patients were examined (5 in remission, 17.2%). Rheumatoid factor (RF), the level of antibodies to cyclic citrullinated peptides (a-CRP), quantitative C-reactive protein (CRP) was determined in the blood of all patients, and echocardiography and speckle-tracking echocardiography were performed to determine indicators of longitudinal deformation of the left ventricle. Disease activity was determined using the DAS28 index (CRP) and other functional and laboratory indicators. The results. The study of STE indicators is much better than "classical" echocardiography, revealing latent preclinical heart lesions. We established a significant decrease in Global Longitudinal Strain in the basal anterior and basal antero-septal segments (-17.24±3.01% and 15.94±9.37%, respectively) and preservation of local strain in the apical and middle segments (respectively -26.95+4.95% and -21.69+3.05%). In general, 41.2% of patients with RA had lesions of the basal segments. When analyzing the correlation between disease activity and deformation in STE, an inverse relationship between the DAS28 index and apical deformation (API Strain) was established (r=-0.50, р=0.06). The highest correlations were found between STE and functional status of disease: HAQ-DI score (r=-0.51, p=0.05) and VAS activity (r=-0.64, p=0.01). Conclusions. Functional activity according to the HAQ-DI score and VAS had a significantly greater relationship with preclinical manifestations of heart damage (detected by STE) than standard cardio-vascular risk factors. It is necessary to continue the search for other important factors that can lead to the formation of heart lesions and are related to both the activity of the disease and the functional status of patients. It is expedient to conduct comparative studies of STE in RA and coronary artery disease to clarify the differences in the processes of formation of myocardial damage.

Association of epicardial fat volume with subclinical myocardial damage in patients with type 2 diabetes mellitus.

In type 2 diabetes mellitus (T2DM) patients, left ventricular systolic dyssynchrony (LVSD) with normal left ventricular ejection fraction (LVEF) and normal myocardial perfusion could referred to as subclinical myocardial damage, which is difficult to diagnose at an early stage. Epicardial adipose tissue, a distinctive heart-specific visceral fat, is closely related to various cardiovascular diseases. The objective of this study was to investigate the correlation between epicardial fat volume (EFV) and subclinical myocardial damage in T2DM patients. This retrospective cross-sectional study included 117 T2DM patients with normal myocardial perfusion by single photon emission computed tomography-computed tomography (SPECT-CT) and normal LVEF by echocardiography. The study was conducted from January 2018 to December 2022. Patient data were collected through electronic medical records including basic patient information, medical history, laboratory tests, and medication data. The EFV was quantified through a non-contrast CT scan. Quantitative indicators of LVSD including phase standard deviation (PSD) and phase histogram bandwidth (PBW) were obtained through phase analysis of the gated rest myocardial perfusion imaging (MPI). Additionally, 83 healthy individuals at the same time were selected to gain the reference threshold of LVSD indicators (13.1° for PSD and 37.6° for PBW). Univariate and multivariable logistic regression models were performed to analyze factors influencing LVSD. A generalized additive model (GAM) was applied to explore the relationship between EFV and LVSD. The receiver operating characteristic (ROC) curve was used to analyze the diagnostic value of EFV for LVSD. Among all patients, 32 (27.4%) patients had LVSD. Compared with the non-LVSD group, the body mass index (BMI) and EFV were higher in the LVSD group (25.83±2.66 vs. 23.94±3.13 kg/m2; 142.41±44.17 vs. 108.01±38.24 cm3, respectively, both P<0.05). Multivariate regression analysis revealed that EFV was independently associated with LVSD [odds ratio (OR) =1.19; 95% confidence interval (CI): 1.06-1.34; P=0.003]. Age, BMI, incidence of hypertension, and LVSD were increased with tertiles of EFV (all P<0.05). The GAM indicated a linear association between EFV and LVSD. The ROC curve analysis concluded that the area under the curve (AUC) of EFV for predicting subclinical myocardial damage in T2DM patients was 0.732 (95% CI: 0.633-0.831, P<0.001), with the optimal threshold of 122.26 cm3, sensitivity of 71.9%, and specificity of 69.4%. EFV is an independent risk factor for LVSD in T2DM patients with normal LVEF and normal MPI, which could potentially serve as a novel imaging marker and a potential therapeutic target for subclinical myocardial damage.

A Multicentric Observational Study to Determine Myocardial Injury in Severe Community-Acquired Pneumonia (sCAP).

Background: Severe community-acquired pneumonia (sCAP) is the most frequent admission for acute respiratory failure in intensive care medicine. Observational studies have found a correlation between patients who were admitted with CAP and the development of cardiovascular events. The risk of acute myocardial damage in patients with CAP is particularly high within the first 30 days of hospitalization. Research design and methods: Multicenter prospective cohort analysis conducted in consecutive patients admitted to an ICU with microbiologically confirmed diagnoses of sCAP. The aim was to determine any structural cardiac damage detected by advanced imagining techniques (cardiac MRI) and cardiac biomarkers in patients with sCAP. The patients were stratified, according to their etiology, into pneumococcal or not-pneumococcal sCAP. The primary outcome was cardiac damage at day 5 and 7 of clinical presentation. Results: A total of 23 patients were consecutively and prospectively enrolled for two winter periods. No significant differences were observed between the median troponin when comparing the pneumococcal vs. non-pneumococcal. The incidence of myocardial damage was numerically higher in the pneumococcal subgroup (70% vs. 50%, p = 0.61) on day 5 and on day 7 (53% vs. 40%, p = 0.81) but did not achieve significance. Confirming a correlation between the biomarkers of cell damage and the biomarkers of myocardial damage, only a positive and significant correlation was observed between h-FABP and DNA on day 1 (r = 0.74; p < 0.01) and day 3 (r = 0.83; p < 0.010). Twenty cardiac MRIs were performed on the 23 patients (87%). No presence of fibrosis was observed in any of the studies carried out within the first 15 days of admission. Conclusions: No significant myocardial damage was found in patients with sCAP independent of the bacterial etiology in accordance with biomarker alterations (Troponin and/or h-FABP) or cardiac MRI. Using cardiac MRI, we could not find any presence of myocardial fibrosis within the first 15 days of admission.

Galectin-3 in Blood Serum and Lymphocytes as a Marker of Myocardial Damage in Patients with Arterial Hypertension and COVID-19.

The constant increase of arterial hypertension and the development of pathology at an earlier age are global healthcare problems that cause damage to vital organs and worsen patient prognosis. In recent years, studies have shown that galectin-3 plays a role in the development and progression of arterial hypertension and coronavirus disease (COVID-19). The explanatory research study aimed to analyze the prognostic value of galectin-3 determination in the serum blood and lymphocytes of patients with arterial hypertension and coronavirus disease (COVID-19). The patients were divided into two groups: Group 1 consisted of 36 individuals with AH, Group 2 included 35 patients with arterial hypertension and polysegmental COVID-19 pneumonia, and 16 practically healthy individuals were included in the control group. All patients underwent anthropometry, biochemical blood analysis, determination of galectin-3, level in serum and lymphocytes, IL-1β, IL-6, and echocardiography. The highest level of galectin-3 was found in patients of Group 1, while in patients of Group 2, the concentration of galectin-3 was significantly decreased, mostly due to the treatment of COVID-19, in addition to prolonged antihypertensive therapy. The level of galectin-3 in serum and lymphocytes was significantly higher in patients of both groups compared to the control group (p<0.05). Arterial hypertension causes structural changes in the cardiovascular system that are associated with elevated levels of galectin-3 in serum and lymphocytes. It can be used as a marker of myocardial damage in the context of arterial hypertension and COVID-19.

Troponin in cardiogenic shock not caused by acute myocardial infarction, a predictor of mortality

Abstract Background Cardiogenic shock is associated with a high mortality and morbidity due to organ damage and multi-organ failure including direct damage to the myocardium. Purpose This study aimed to assess troponin as a marker of myocardial damage in patients with cardiogenic shock outside of a myocardial infarction (e.g., non-ischaemic cardiogenic shock). Methods Data from unselected patients with cardiogenic shock not caused by myocardial infarction were anonymised and combined in a multicentre cohort study from 15 centres in 5 European countries (2011-2020). Cardiogenic shock was defined by clinical signs and symptoms, elevated lactate concentrations (arterial &amp;gt;2.0 mmol/l, venous &amp;gt;2.5 mmol/l), and hypotension (systolic &amp;lt;90 mmHg or need for vasopressors). Patients with need for urgent coronary revascularisation, predominant right heart failure, eCPR or cardiogenic shock after cardiotomy were excluded. Baseline was defined to reflect the worst clinical status within 6 hours before/after admission (for patients not treated with mechanical circulatory support) or after device implantation (for patients treated with mechanical circulatory support). Troponin concentrations at baseline as well as after 24 hours were quantified using the Elecsys® Troponin T high-sensitive assay by Roche (99th percentile 14 ng/l). Baseline troponin (displayed per 250 ng/l) and its increase within 24 hours were associated with 30-day mortality by fitting Cox regression models adjusted for age, sex, baseline creatinine, baseline lactate, baseline pH, prior cardiac arrest, duration of CPR, acute-on-chronic or de novo heart failure, and mechanical ventilation. Results Overall, 477 patients were analysed [mean age 62 (±15) years, 144 women (30.2%), acute-on-chronic heart failure in 255 (53.6%)]. Median LVEF was 20% (IQR 15-30%), CPR was performed in 196 cases (41.1%), median lactate at baseline was 7.3 mmol/l (IQR 4.2-10.8 mmol/l) and median baseline troponin T was 164 ng/l (IQR 77-678 ng/l). Patients with a higher troponin T at baseline (e.g., ≥median) more frequently presented with de novo heart failure (54.8 vs. 37.9%, p&amp;lt;0.01) or after prior CPR (47.7 vs. 34.3%, p&amp;lt;0.01) although other parameters reflecting cardiogenic shock severity (e.g., blood pressure, baseline lactate or LVEF) were not significantly different. Finally, troponin T at baseline showed a significant association with 30-day mortality (HR 1.006, 95% CI: 1.0-1.011, p = 0.041) while the relative troponin T increase within 24 hours did not (HR 1.005, 95% CI: 0.997-1.013, p = 0.212) (Figure 1). Conclusion Cardiac organ damage in cardiogenic shock outside of a myocardial infarction (e.g., non-ischaemic cardiogenic shock) is associated with increased risk of death within 30 days. Elevated troponin levels could identify a group of patients with cardiogenic shock in need for cardioprotective therapies.Figure 1

Abstract 13573: Association of Increased Eicosapentaenoic Acid to Arachidonic Acid Ratio With Early Restoration of Coronary Blood Flow in ST-Elevation Myocardial Infarction

Background: Early restoration of coronary blood flow is important to reduce myocardial damage in patients with ST-elevation myocardial infarction (STEMI). Cardiovascular protection of increased levels of eicosapentaenoic acid (EPA) to arachidonic acid (AA) has been shown in recent clinical trials. Therefore, this study examined whether increased EPA / AA ratio was related to early restoration of coronary blood flow in STEMI patients underwent primary percutaneous coronary intervention (PCI). Methods: Serum levels of EPA, AA, and EPA/AA ratio were measured in consecutive 216 STEMI patients. The angiographic findings of TIMI-flow grade in the infarct related artery before PCI were compared between patients with and without increased EPA / AA ratio (&amp;gt;0.291). Results: TIMI-flow grade 3 before PCI were obtained in 25 (11.6%) of all study patients. Smaller enzymatic infarct size was obtained in patients with TIMI-flow grade 3 before PCI compared with TIMI-flow grade 0-2 before PCI (Peak CK-MB; 358 &amp;plusmn; 252 mg/dL, vs. 280 &amp;plusmn; 260 mg/dL, p &amp;lt;0.05). There were significant differences between 2 groups in the distribution of TIMI-flow grade (p&amp;lt;0.05). Moreover, multivariate logistic regression analysis showed that patients with increased EPA/AA ratio was significantly associated with the presence of TIMI-flow grade 3 before PCI after adjustment for conventional risk factors (OR 5.0, 95% CI 1.92-12.8, p&amp;lt;0.01). Conclusions: Increased levels of EPA /AA ratio is independently associated with early restoration of coronary blood flow, leading to reduced myocardial damage in patients with STEMI. These results might support the new strategy of administration of EPA before PCI in STEMI care.

Cardiac manifestations of MIS-C: cardiac magnetic resonance and speckle-tracking data.

Cardiac involvement is central in MIS-C and represents the main cause of morbidity. In this study, we aimed to assess myocardial damage in patients with MIS-C using cardiac magnetic resonance (CMR) during the acute phase, as well as left ventricular and atrial longitudinal strain on admission, at discharge, and after 3 months. We performed a single-center prospective cohort study and case-control study. Between September 2020 and February 2022, we enrolled 39 patients hospitalized for MIS-C at our center. We performed left ventricular and atrial longitudinal 2D strain analysis on admission and during follow-up; echocardiographic data were compared to a matched control population. Patients above 4 years old with increased troponin underwent CMR. Of 24 patients (mean age: 8.2 ± 4.9 years) who underwent CMR, 14 (58%) presented myocardial edema and 6 (25%) late gadolinium enhancement (LGE). LGE was associated with older age (p < 0.01), increased BMI (p = 0.03), increased ferritin levels (p < 0.001), lower left ventricular (LV) ejection fraction (p < 0.001), LV longitudinal strain (p = 0.004), left atrial (LA) strain (p = 0.05), and prolonged hospital stay (p = 0.02). On admission, LV ejection fraction, LV longitudinal strain, and LA strain were impaired, but each improved gradually over time; LVEF was the fastest to recover, while global LV longitudinal strain was still impaired as compared to controls after 3 months (p = 0.01). Our study demonstrates that myocardial injury is present in a quarter of MIS-C patients, and impaired LA and LV myocardial deformation persist for at least several weeks after the acute phase. CMR and LV/LA strain could help us to individualize follow-up of MIS-C patients.

Retracted: Application Effect and Evaluation of Two-Dimensional Speckle Tracking Imaging on Myocardial Damage in Patients with Malignant Lymphoma Treated with Anthracyclines.

[This retracts the article DOI: 10.1155/2021/6355047.].

Fibroblast Growth Factor 23: Potential Marker of Invisible Heart Damage in Diabetic Population.

Two-dimensional speckle-tracking echocardiography (2DSTE) detects myocardial dysfunction despite a preserved left ventricular ejection fraction. Fibroblast growth factor 23 (FGF23) has become a promising biomarker of cardiovascular risk. This study aimed to determine whether FGF23 may be used as a marker of myocardial damage among patients with diabetes mellitus type 2 (T2DM) and no previous history of myocardial infarction. The study enrolled 71 patients with a median age of 70 years. Laboratory data were analyzed retrospectively. Serum FGF23 levels were determined using a sandwich enzyme-linked immunosorbent assay. All patients underwent conventional echocardiography and 2DSTE. Baseline characteristics indicated that the median time elapsed since diagnosis with T2DM was 19 years. All subjects were divided into two groups according to left ventricular diastolic function. Individuals with confirmed left ventricular diastolic dysfunction had significantly lower levels of estimated glomerular filtration rate and higher values of hemoglobin A1c. Global circumferential strain (GCS) was reduced in the majority of patients. Only an epicardial GCS correlated significantly with the FGF23 concentration in all patients. The study indicates that a cardiac strain is a reliable tool for a subtle myocardial damage assessment. It is possible that FGF23 may become an early diagnostic marker of myocardial damage in patients with T2DM.

Comparative Study of the Myocardium of Patients from Four COVID-19 Waves.

Few studies have compared COVID-19 patients from different waves. This study aims to conduct a clinical and morphological analysis of patients who died from COVID-19 during four waves. The study involved 276 patients who died from COVID-19 during four waves, including 77 patients in the first wave, 119 patients in the second wave, and 78 patients in the third wave. We performed a histological examination of myocardium samples from autopsies and additionally analyzed the samples by PCR. We conducted immunohistochemistry of the myocardium for 21 samples using antibodies against CD3, CD45, CD8, CD68, CD34, Ang1, VWF, VEGF, HLA-DR, MHC1, C1q, enteroviral VP1, and SARS-CoV-2 spike protein. We also did immunofluorescent staining of three myocardial specimens using VP1/SARS-CoV-2 antibody cocktails. Further, we ran RT-ddPCR analysis for 14 RNA samples extracted from paraffin-embedded myocardium. Electron microscopic studies of the myocardium were also performed for two samples from the fourth wave. Among the 276 cases, active myocarditis was diagnosed in 5% (15/276). Of these cases, 86% of samples expressed VP1, and individual cells contained SARS-CoV-2 spike protein in 22%. Immunofluorescence confirmed the co-localization of VP1 and SARS-CoV-2 spike proteins. ddPCR did not confidently detect SARS-CoV-2 RNA in the myocardium in any myocarditis cases. However, the myocardium sample from wave IV detected a sub-threshold signal of SARS-CoV-2 by qPCR, but myocarditis in this patient was not confirmed. Electron microscopy showed several single particles similar to SARS-CoV-2 virions on the surface of the endothelium of myocardial vessels. A comparison of the cardiovascular complication incidence between three waves revealed that the incidence of hemorrhage (48 vs. 24 vs. 17%), myocardial necrosis (18 vs. 11 vs. 4%), blood clots in the intramural arteries (12 vs. 7 vs. 0%), and myocarditis (19 vs. 1 vs. 6%) decreased over time, and CD8-T-killers appeared. Immunohistochemistry confirmed the presence of endotheliitis in all 21 studied cases. This study compared myocardial damage in patients who died during three COVID-19 waves and showed a decrease in the incidence of endotheliitis complications (thrombosis, hemorrhage, necrosis) and myocarditis over time. However, the connection between myocarditis and SARS-CoV-2 infection remains unproven.

Protective Effect of Nicorandil Injection on Myocardial Damage in Patients with Acute ST-Elevation Myocardial Infarction

Protective Effect of Nicorandil Injection on Myocardial Damage in Patients with Acute ST-Elevation Myocardial Infarction

Galectin-3, Acute Kidney Injury and Myocardial Damage in Patients With Acute Heart Failure

Galectin-3, a biomarker of inflammation and fibrosis, can be associated with renal and myocardial damage and dysfunction in patients with acute heart failure (AHF). We retrospectively analyzed 790 patients with AHF who were enrolled in the AKINESIS study. During hospitalization, patients with galectin-3 elevation (> 25.9 ng/mL) on admission more commonly had acute kidney injury (assessed by KDIGO criteria), renal tubular damage (peak urine neutrophil gelatinase-associated lipocalin [uNGAL] > 150 ng/dL) and myocardial injury (≥ 20% increase in the peak high-sensitivity cardiac troponin I [hs-cTnI] values compared to admission). They less commonly had ≥ 30% reduction in B-type natriuretic peptide from admission to last measured value. In multivariable linear regression analysis, galectin-3 was negatively associated with estimated glomerular filtration rate and positively associated with uNGAL and hs-cTnI. Higher galectin-3 was associated with renal replacement therapy, inotrope use and mortality during hospitalization. In univariable Cox regression analysis, higher galectin-3 was associated with increased risk for the composite of death or rehospitalization due to HF and death alone at 1 year. After multivariable adjustment, higher galectin-3 levels were associated only with death. In patients with AHF, higher galectin-3 values were associated with renal dysfunction, renal tubular damage and myocardial injury, and they predicted worse outcomes.

Thrombin receptor protease-activated receptor 1 (PAR1) related cytotoxic CD8+ T cell activity is associated with atrial myopathy and pro-inflammatory immune response in early atrial fibrillation

Abstract Background and aims Cytotoxic CD8+ T cells mediate myocardial damage in patients with virus induced myocarditis, plaque erosion during acute coronary syndrome, and promote adverse post-ischemic cardiac remodeling. There is emerging evidence to support a link between inflammation and atrial fibrillation (AF). Protease-activated receptor 1 (PAR1) is the thrombin receptor expressed on platelets, but it is also expressed in endothelial cells, vascular smooth muscle cells, cardiac fibroblasts, and CD8+ T cells. The role of CD8+ T cells and PAR1 in atrial myopathy and early AF have not been studied. Methods In 80 non-anticoagulated patients with a first documented episode of AF, and 20 control subjects without AF but with a comparable cardiovascular risk profile (e.g. SCORE2, CHA2DS2-VASc, p&amp;gt;0.05), we studied PAR1-related cytotoxic T cell activity in the first hours (up to 24 h) of AF clinical manifestation. The Apolipoprotein E–knock out (ApoEko) mouse is a commonly used model of metabolic syndrome that develops atrial myopathy (structural correlate of AF). ApoEko male mice (Apoetm1Unc with a C57BL/6 genetic background) were fed for six weeks with a standard chew, western-type diet (high fat and high sucrose = WD) ± the specific PAR1 inhibitor vorapaxar. Results High levels of circulating, activated CD8+ T cells (CD8+CD57+ T cells with pro-inflammatory and high cytotoxic properties) were present in patients with early AF (flow cytometry). Stimulation of cytotoxic T cells, that expressed the thrombin receptor PAR1, that were isolated from patients with new onset of AF, released pro-inflammatory cytokines (e.g. IFN-γ, TNF-α). Enhanced cytotoxic activity of CD8+ T cells was suggested by elevated plasma levels of effector molecules (e.g. granulysin and granzyme). In ApoEko mice fed a WD, atrial myopathy as the structural correlate for AF, was paralleled by increased expression of effector molecules that were associated with CD8+ T cell activity (like perforin, granzyme A, granzyme B, IFN-γ). Cytotoxic T cell activity disrupted the release of the potective atrial natriuretic peptide, ANP, and increased signaling pathways associated with atrial fibrosis (e.g. TGF-β, cTGF, TGF-β receptor). The specific PAR1 inhibitor, vorapaxar, reduced inflammatory T cell activity, transcription of fibrotic mediators, and reconstituted ANP secretion in atria of ApoEko mice. Conclusions Targeting the FXa/FIIa-PAR1-CD8+ axis might be a promising approach to reduce atrial fibrosis and inflammation. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): BIH Charité Clinician Scientist Program

Global longitudinal strain to predict myocardial fibrosis in patients in carbon monoxide poisoning

Abstract Background Carbon monoxide (CO) inhibits oxygen delivery and subsequently causes ischemic changes that can lead to myocardial damage. Late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR) reflects myocardial fibrosis and detects subclinical myocardial damage in patients with acute CO poisoning. However, CMR is expensive and hard to perform in patients with neurologic deficit. Therefore, this study aims to investigate which echocardiographic parameters could predict the presence of myocardial fibrosis represented by LGE in CO intoxication patients. Methods This prospective observational study included 128 consecutive patients (Mean age: 52.2±16.2) with acute CO poisoning and elevated troponin I (defined as &amp;gt;0.045 ng/mL) at the emergency department of a tertiary university hospital. All participants underwent hyperbaric oxygen therapy (HBOT). CMR and conventional echocardiography with 2D speckle-tracking were performed within 7 days. Subjects were categorized into late gadolinium enhancement (LGE) and no LGE group according to the CMR findings. Results Mean left ventricular (LV) ejection fraction (EF) and global longitudinal strain (GLS) were 57.0±10.0% and −16.3±3.7% respectively. LGE was observed in 89 (69.5%) patients and the most common pattern was mid-wall involvement. Clinical characteristics such as age, sex, shock, time elapsed from rescue to HBOT, and the level of troponin I were not different between groups with LGE and without LGE. Among echocardiographic parameters, LV EF was not significantly different between groups (LGE: 56.0±10.5% vs 59.3±8.1%, p=0.089). LV GLS was more impaired in patients with LGE compared to those without LGE (−15.7±3.8% vs −17.9±3.0%, p=0.003). In multivariate logistic analysis, LV GLS was independently associated with the presence of LGE [Odds ratio (OR) 1.279, 95% confidence interval (CI) (1.047–1.563), p=0.016], but not LV EF. Conclusion In patients with acute CO poisoning and elevated troponin I, LV GLS predicted the presence of LGE in CMR. These finding suggest that subclinical myocardial dysfunction represented by LV GLS may reflect the burden of CO induced myocardial fibrosis. Funding Acknowledgement Type of funding sources: None.

Blood serum concentration of troponin in patients with COVID-19 of various severities

BACKGROUND: The search for available predictors of hospital survival and mortality rates during the COVID-19 pandemic is an urgent problem.&#x0D; AIM: The study aimed to determine the role of troponin in the immediate prognosis of patients with COVID-19.&#x0D; MATERIALS AND METHODS: The study included 85 patients with a new coronavirus infection upon admission, who underwent a blood test for troponin. All patients underwent an echocardiographic study according to a standard protocol, and the effect of troponin levels on nosocomial survival and mortality rates, correlation of this indicator with the left ventricular ejection fraction, degree of pulmonary hypertension, laboratory parameters, and degree of respiratory failure determined by computed tomography of the lungs and oxygen saturation indicators were analyzed. Correlation analysis with autopsy parameters was performed.&#x0D; RESULTS: A high level of troponin indicated the worst prognosis of patients during hospitalization. The laboratory marker level correlated significantly with the parameters of the left ventricular ejection fraction. Its highest level was determined in patients with type 1 myocardial infarction. Troponin was not correlated with the degree of respiratory failure, as well as the state of the myocardium in the autopsy material.&#x0D; CONCLUSIONS: Determining the troponin levels as a routine laboratory marker can be recommended for stratifying the risk of myocardial damage in patients with COVID-19 during hospitalization.

Different Impacts on the Heart After COVID-19 Infection and Vaccination: Insights From Cardiovascular Magnetic Resonance.

IntroductionMyocarditis-like findings after COVID-19 (coronavirus disease 2019) infection and vaccination were reported by applying cardiovascular magnetic resonance (CMR). These results are very heterogenous and dependent on several factors such as hospital admission or outpatient treatment, timing of CMR, and symptomatic load. This retrospective study aimed to identify differences in myocardial damage in patients with persistent symptoms both after COVID-19 infection and vaccine by applying CMR.Materials and MethodsThis study entails a retrospective analysis of consecutive patients referred for CMR between August 2020 and November 2021 with persistent symptoms after COVID-19 infection or vaccination. Patients were compared to healthy controls (HC). All patients underwent a CMR examination in a 1.5-T scanner with a scan protocol including: cine imaging for biventricular function and strain assessment using feature tracking, T2 mapping for the quantification of edema, and T1 mapping for diffuse fibrosis and late gadolinium enhancement (LGE) for the detection and quantification of focal fibrosis. Patients were divided into a subacute COVID-19 (sCov) group with symptoms lasting < 12 weeks, post-COVID-19 (pCov) group with symptoms > 12 weeks, and patients after COVID-19 vaccination (CovVac).ResultsA total of 162 patients were recruited of whom 141 were included for analysis. The median age in years (interquartile range (IQR)) of the entire cohort was 45 (37–56) which included 83 women and 58 men. Subgroups were as follows (total patients per subgroup, median age in years (IQR), main gender): 34 sCov, 43 (37–52), 19 women; 63 pCov, 52 (39–58), 43 women; 44 CovVac, 43 (32–56), 23 men; 44 HC (41 (28–52), 24 women). The biventricular function was preserved and revealed no differences between the groups. No active inflammation was detected by T2 mapping. Global T1 values were higher in pCov in comparison with HC (median (IQR) in ms: pCov 1002ms (981–1023) vs. HC 987ms (963–1009; p = 0.005) with other parings revealing no differences. In 49/141 (34.6%) of patients, focal fibrosis was detectable with the majority having a non-ischemic pattern (43/141; 30.4%; patients) with the subgroups after infection having more often a subepicardial pattern compared with CovVac (total (% of group): sCov: 7/34(21%); pCov 13/63(21%); CovVac 2/44(5%); p = 0.04).ConclusionPatients after COVID-19 infection showed more focal fibrosis in comparison with patients after COVID-19 vaccination without alterations in the biventricular function.

P411 MINOCA OR NOT MINOCA? THE DECISIVE ROLE OF CARDIAC MAGNETIC RESONANCE IN THE DIFFERENTIAL DIAGNOSIS OF MYOCARDIAL DAMAGE

Abstract Cardiac MRI can facilitate the differential diagnosis of myocardial damage in patients without coronary artery disease. Our case report is about a 50–year–old man who was admitted to the Emergency Department of the Maggiore Hospital in Bologna in October 2021 for oppressive chest pain at rest; previously he had experienced a similar episode but of minor intensity. He had not previous medical records. When the patient arrived at the emergency department chest pain had regressed, blood pressure was elevated (170/110 mmHg). The ECG showed sinus tachycardia at 100 bpm without electrocardiographic abnormalities suggestive of acute ischemia. Cardiac biomarkers were elevated (hsTnI 312 ng / L –&amp;gt; 975 ng / L – n.v. &amp;lt;19.8 ng / L); blood gas analysis showed pH 7.42, pO2 47 mmHg and pCO2 33 mmHg. Chest CT scan excluded pulmonary embolism and acute aortic syndrome. The patient was transferred to Cardiology Ward in the suspicion of acute coronary syndrome, where echocardiogram showed normal biventricular volumes, mild wall hypertrophy and hypokinesia of the lower middle wall (EF 52%). Coronary angiography didn’t showed any obstructive stenosis in any epicardial vessels. In consideration of the clinical presentation and instrumental evidences, the patient was discharged with a diagnosis of myocardial infarction with non–obstructive coronary arteries (MINOCA), but a cardiac MRI was scheduled in the post–discharge to clarify its genesis. MRI didn’t showed any areas of signal hyperintensity, any perfusion deficits in the first pass study and any areas of late gadolinium enhancement (LGE). Those images permitted to exclude areas of necrosis or inflammation, orienting the diagnosis to myocardial damage during hypertensive crisis. Therefore, the antiplatelet therapy recommended at discharge was suspended. In this case report, cardiac magnetic resonance showed that it can improve the etiological diagnosis of MINOCA, allowing for better clinical and therapeutic management.

Biventricular Myocardial Strain Analysis in Patients with Pulmonary Arterial Hypertension Using Cardiac Magnetic Resonance Tissue-Tracking Technology.

: ObjectivesTo evaluate both left and right ventricular (LV and RV) function in patients with pulmonary arterial hypertension (PAH) using cardiac magnetic resonance tissue-tracking (CMR-TT) technology and explore its clinical value. Methods: A total of 79 participants (including 47 patients with PAH and 32 healthy controls) underwent cardiac magnetic resonance imaging (CMRI) with a short-axis balanced steady-state free precession (SSFP) sequence. The biventricular cardiac function parameters and strain parameters were obtained by postprocessing with CVI42 software. A comparative analysis was performed between the LV and RV strain parameters in all PAH patients and in PAH patients with reduced or preserved cardiac function. Results: The results showed preferable repeatability of CMR-TT in analyzing the global radial strain (GRS), circumferential strain (GCS), and longitudinal strain (GLS) of the left and right ventricles in the PAH group. The GRS, GCS, and GLS of the left and right ventricles except for LV GRS (LVGRS) of PAH patients were significantly lower than those of healthy controls (p < 0.05 for all). The GRS and GCS of the left and right ventricles showed a moderate correlation in the PAH group (r = 0.323, p = 0.02; r = 0.301, p = 0.04, respectively). PAH patients with preserved RV function (n = 9) showed significantly decreased global and segmental RS, CS, and LS of the right ventricles than healthy controls (p < 0.05 for all), except for basal RVGCS (RVGCS-b, p = 0.996). Only the LVGLS was significantly different between the PAH patients with preserved LV function (n = 32) and the healthy controls (−14.23 ± 3.01% vs. −16.79 ± 2.86%, p < 0.01). Conclusions: As a nonradioactive and noninvasive technique, CMR-TT has preferable feasibility and repeatability in quantitatively evaluating LV and RV strain parameters in PAH patients and can be used to effectively detect early biventricular myocardial damage in patients with PAH.

Magnetic resonance syndromes of myocardial damage in patients after new coronavirus infection (COVID-19) – two typical clinical cases

Clinical examples for variants of cardiovascular complications of a new coronavirus infection (COVID-19) are presented when they are visualized by means of magnetic resonance imaging (MRI) of the heart and chest organs with paramagnetic contrast enhancement and synchronization with ECG and respiration signal. The syndromes of post-COVID focal infarct injury and diffuse inflammatory lesion are identified. The picture of MRI visualization of coronary atherosclerotic plaque is presented. The results of quantitative processing of cardiac MRI in these two different syndromes of post-COVID cardiological complications are presented. The presented clinical examples indicate the need for cardiac MRI to monitor patients and assess the long-term cardiovascular effects of COVID-19.

Non-invasive left ventricular myocardial work in patients with chronic aortic regurgitation and preserved left ventricular ejection fraction

Abstract Funding Acknowledgements Type of funding sources: None. Background Left ventricular global longitudinal strain (LV GLS) has been proposed as sensitive marker of myocardial damage in patients with chronic severe aortic regurgitation (AR) and preserved left ventricular ejection fraction (LVEF). However, LV GLS does not take into account the afterload. Non-invasive LV myocardial work is a novel parameter of LV myocardial performance, which integrates measurements of myocardial deformation and non-invasive blood pressure (afterload). Purpose The aims of this study were: 1) to assess non-invasive LV myocardial work in patients with chronic AR and preserved LVEF and its correlation with other echocardiographic parameters, 2) to evaluate changes of LV myocardial work after aortic valve replacement or repair (AVR) and 3) to assess the relationship between LV myocardial work and post-operative LV reverse remodeling. Methods This retrospective study included fifty patients (53 ± 16 years; 68% men) with moderate or severe chronic AR and preserved LVEF, who underwent AVR. Non-invasive LV myocardial work indices were measured at baseline and post-operatively (between 2 and 12 months after surgery) and compared with previously reported normal reference ranges. Results Based on normal reference values, patients with chronic AR and preserved LVEF had preserved or increased values of LV global work index (LV GWI) (84% and 16%, respectively) and LV global constructive work (LV GCW) (78% and 22%, respectively) (Figure 1). In addition, LV global work efficiency (LV GWE) was preserved in all patients, despite 16 (32%) subjects had impaired values of LV GLS (&amp;lt;16.7.% in men and &amp;lt;17.8% in women). LV GWI and GCW showed a positive correlation with markers of AR severity and parameters of LV systolic function. AVR results in a significant reduction of myocardial work indices (p &amp;lt; 0.0001), with the exception of LV global wasted work, that did not change (p = 0.29). According to normal reference ranges, 15 (30%) patients had impaired values of LV GWI and LV GCW post-operatively, while LV GLS was impaired in 37 (74%) patients. The post-operative impairment of LV GWI demonstrated a stronger association with reduced LV reverse remodeling, as compared to the impairment of LV GLS (Figure 2). Conclusions Compared to afterload-dependent echocardiographic parameters, non-invasive LV myocardial work indices allow a better understanding of myocardial performance and energetics in the setting of chronic AR with preserved LVEF and could improve risk stratification. Abstract Figure. Abstract Figure.