Prognostic assessment following acute myocarditis requires convalescent scanning: neither peak troponin nor index scan T2 signal predicts convalescent late gadolinium enhancement

Funding Acknowledgements Type of funding sources: None. Background Cardiovascular magnetic resonance (CMR) is a key diagnostic investigation in acute myocarditis (1) and permits quantification of late gadolinium enhancement (LGE) and myocardial oedema. Follow-up CMR imaging is recommended to check for persistence of scar and oedema (2). Persistent late gadolinium enhancement is associated with a worse prognosis (3). It is not known whether all patients require follow-up scanning or whether the initial scan can provide useful information to identify which patients need convalescent assessment. Purpose In this study we considered whether extent of troponin elevation, extent of T2 elevation and initial late gadolinium enhancement burden predicted long-term late gadolinium enhancement at follow-up. Methods Index and follow-up CMR scans of consecutive patients presenting with a diagnosis of acute myocarditis between 2019 and 2020 across three hospitals were included. Inclusion criteria were: follow-up scan within 9 months of the index scan, CMR with LGE imaging and T2 mapping, and acute myocarditis being the primary diagnosis of the index scan. Myocardial T2 values in the area affected by myocarditis and percentage of LV myocardium showing late enhancement (using a threshold-based full height half width or manual region of interest strategy) were extracted. Results 20 patients were included in the study (80% male; mean age 37 years). Mean interval between the index and follow-up scan was 4.1 months. Peak troponin level during the acute illness was not associated with the proportion of LV myocardium affected by LGE in the index scan (R^2 <0.01) (Figure 1A). Myocardial T2 values in the first scan were not associated with the proportional resolution in LGE between the index and follow-up scans (R^2 0.02) (Figure 1B). The mean change in LGE was -61.7% (+/-22.8%) but the initial LGE burden did not predict the proportional degree of improvement in LGE between scans (R^2 <0.01)(Figure 1C). Conclusions The extent of troponin elevation and initial CMR phenotype was not a good predictor of the burden of long-term late gadolinium enhancement. Although most cases showed improvement in LGE scar burden between index and follow-up imaging, neither peak troponin level during the acute episode, nor T2 values at the first CMR scan were predictive of initial or change in scar burden. Serial CMR assessment is required to identify those patients who have residual long-term scarring.

Increased C-reactive protein concentrations in patients admitted to the emergency department with troponin level elevations decreases the probability of myocardial ischemia

Funding Acknowledgements Type of funding sources: None. Background Patients frequently present to the emergency department (ED) with chest pain, dyspnea, or other symptoms with elevated troponin level. This finding prompts a provisional diagnosis of myocardial ischemia and raises the need to exclude this possibility. However, elevated blood troponin may be the result of a systemic inflammatory or infectious state merely representing cardiac injury and not myocardial ischemia. Purpose We hypothesized that the ratio of CRP/troponin could reflect the extent of the systemic inflammatory state that induces an attendant cardiac injury, which if sufficiently high could exclude myocardial ischemia. Methods Study population included 10774 patients admitted to the ED during the years 2016-2019 with cTn level higher > 14 ng/liter. CRP level was measured in all patients and CRP/troponin ratio was assessed against discharge diagnosis of myocardial ischemia, in order to evaluate its ability to exclude ischemic etiology of symptoms. The incidence of myocardial ischemia among study patients decreased with increasing CRP/troponin value. Results The prevalence of myocardial ischemia was 760/2694 patients (28.2%), 415/2694 (15.4%), 294/2695 (10.9%) and 130/2694 (4.8%) with 1st-4th CRP/troponin quartile, respectively (p < 0.0001). Logistic regression has shown that the probability of myocardial ischemia decreased by 53%, 68%, and 87% in the second to fourth CRP/troponin quartile compared with the first quartile, respectively (p < 0.0001). Conclusion The present study has shown that increased CRP level seems to modulate the specificity of simultaneous troponin as a marker of ischemia. As CRP level increases, so increases the likelihood that concomitant elevated troponin is due to myocardial injury and not due to myocardial ischemia. The clinical implication is that in the presence of a high CRP/troponin ratio, admission to the cardiology department and coronary investigation are unnecessary, whereas appropriate investigation of the actual medical problem is warranted.

Nourin-Dependent miR-137 and miR-106b: Novel Early Inflammatory Diagnostic Biomarkers for Unstable Angina Patients

Background: Currently, no blood biomarkers exist that can diagnose unstable angina (UA) patients. Nourin is an early inflammatory mediator rapidly released within 5 min by reversible ischemic myocardium, and if ischemia persists, it is also released by necrosis. Nourin is elevated in acute coronary syndrome (ACS) patients but not in symptomatic noncardiac and healthy subjects. Recently, circulating microRNAs (miRNAs) have been established as markers of disease, including cardiac injury and inflammation. Objectives: To profile and validate the potential diagnostic value of Nourin-dependent miR-137 (marker of cell damage) and miR-106b-5p (marker of inflammation) as early biomarkers in suspected UA patients and to investigate the association of their target and regulating genes. Methods: Using Nourin amino acid sequence, an integrated bioinformatics analysis was conducted. Analysis indicated that Nourin is a direct target for miR-137 and miR-106b-5p in myocardial ischemic injury. Two linked molecular networks of lncRNA/miRNAs/mRNAs were also retrieved, including CTB89H12.4/miR-137/FTHL-17 and CTB89H12.4/miR-106b-5p/ANAPC11. Gene expression profiling was assessed in serum samples collected at presentation to an emergency department (ED) from: (1) UA patients (n = 30) (confirmed by invasive coronary angiography with stenosis greater than 50% and troponin level below the clinical decision limit); (2) patients with acute ST elevation myocardial infarction (STEMI) (n = 16) (confirmed by persistent ST-segment changes and elevated troponin level); and (3) healthy subjects (n = 16). Results: Gene expression profiles showed that miR-137 and miR-106b-5p were significantly upregulated by 1382-fold and 192-fold in UA compared to healthy, and by 2.5-fold and 4.6-fold in STEMI compared to UA, respectively. Healthy subjects showed minimal expression profile. Receiver operator characteristics (ROC) analysis revealed that the two miRNAs were sensitive and specific biomarkers for assessment of UA and STEMI patients. Additionally, Spearman’s correlation analysis revealed a significant association of miRNAs with the associated mRNA targets and the regulating lncRNA. Conclusions: Nourin-dependent gene expression of miR-137 and miR-106b-5p are novel blood-based biomarkers that can diagnose UA and STEMI patients at presentation and stratify severity of myocardial ischemia, with higher expression in STEMI compared to UA. Early diagnosis of suspected UA patients using the novel Nourin biomarkers is key for initiating guideline-based therapy that improves patients’ health outcomes.

PROSPECTIVE ANALYSIS OF IMPACT OF PHARMCOTHERAPY ADHERENCE ON TREATMENT EFFECTIVENESS IN POST OPERATIVE HEART PATIENTS

Myocardial infarction is the irreversible damage of myocardial tissue caused by prolonged ischemia and hypoxia. This most commonly occurs when a coronary artery becomese blocked following the rupture of an atherosclerotic plaque, which then leads to the formation of a blood clot (coronary thrombosis). This event can also trigger coronary vasospasm. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function. Prolonged myocardial ischemia activates a "wavefront" of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart. This prospective, pilot, observational study performed confirmed the hypothesis that systematic identifications and interventions administered through continued physician follow-up and patients counselling will improve adherence to therapy and therefore improvement in treatment effectiveness by lowering especially Troponin level ,CPK and quality of life in MI patients. Study was shown that lack of proper knowledge about disease and patients counseling and chronic treatment, most of patients takes disease and its treatment lightly and shows lower adherence attitude. The study analysis shown that female are generally more aware than males for adherence. Study analysis concluded that there was significant reduction in their Troponin level and CPK values in different comparison groups after each level of follow up. Statistical analysis concluded that patients with adherence ˃ 95% showed significant reduction in Troponin level and CPK values and patients with age group ≤50 shows more adherence than older. Most heart patients recorded with hypertension and Coronary Artery Diseases only few ones with diabetic complications. During study patients shows good control over their blood pressure and only few adverse events but no complications occur during study period.

Cardiovascular sequalae in uncomplicated COVID-19 survivors

Background A high proportion of COVID-19 patients were reported to have cardiac involvements. Data pertaining to cardiac sequalae is of urgent importance to define subsequent cardiac surveillance. Methods We performed a systematic cardiac screening for 97 consecutive COVID-19 survivors including electrocardiogram (ECG), echocardiography, serum troponin and NT-proBNP assay 1–4 weeks after hospital discharge. Treadmill exercise test and cardiac magnetic resonance imaging (CMR) were performed according to initial screening results. Results The mean age was 46.5 ± 18.6 years; 53.6% were men. All were classified with non-severe disease without overt cardiac manifestations and did not require intensive care. Median hospitalization stay was 17 days and median duration from discharge to screening was 11 days. Cardiac abnormalities were detected in 42.3% including sinus bradycardia (29.9%), newly detected T-wave abnormality (8.2%), elevated troponin level (6.2%), newly detected atrial fibrillation (1.0%), and newly detected left ventricular systolic dysfunction with elevated NT-proBNP level (1.0%). Significant sinus bradycardia with heart rate below 50 bpm was detected in 7.2% COVID-19 survivors, which appeared to be self-limiting and recovered over time. For COVID-19 survivors with persistent elevation of troponin level after discharge or newly detected T wave abnormality, echocardiography and CMR did not reveal any evidence of infarct, myocarditis, or left ventricular systolic dysfunction. Conclusion Cardiac abnormality is common amongst COVID-survivors with mild disease, which is mostly self-limiting. Nonetheless, cardiac surveillance in form of ECG and/or serum biomarkers may be advisable to detect more severe cardiac involvement including atrial fibrillation and left ventricular dysfunction.